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Who Is at Risk?

For the great majority of people, the major factor that increases a person’s risk for colorectal cancer (CRC) is increasing age. Risk increases dramatically after age 50 years; 90% of all CRCs are diagnosed after this age. Incidence and mortality rates are higher in African American individuals compared with other races; however, a meta-analysis found no evidence that African American individuals have higher rates of precancerous lesions.[1,2] The history of CRC in a first-degree relative, especially if before the age of 55 years, roughly doubles the risk. A personal history of CRC, high-risk adenomas, or ovarian cancer also increases the risk.[3] Other risk factors are weaker than age and family history. People with an inflammatory bowel disease, such as ulcerative colitis or Crohn disease, have a much higher risk of CRC starting about 8 years after disease onset and are recommended to have frequent colonoscopic surveillance.[4] A small percentage (<5%) of CRCs occur in people with a genetic predisposition, including familial adenomatous polyposis and hereditary nonpolyposis coli.

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The treatment information given here is not official policy of the American Cancer Society and is not intended as medical advice to replace the expertise and judgment of your cancer care team. It is intended to help you and your family make informed decisions, together with your doctor. Your doctor may have reasons for suggesting a treatment plan different from these general treatment options. Don't hesitate to ask him or her questions about your treatment options.

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Colorectal Cancer Treatment | How to Treat Colorectal Cancer

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The treatment information given here is not official policy of the American Cancer Society and is not intended as medical advice to replace the expertise and judgment of your cancer care team. It is intended to help you and your family make informed decisions, together with your doctor.

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Statistics at a Glance

At a Glance

Estimated New Cases in 2021 149,500

% of All New Cancer Cases 7.9%

Estimated Deaths in 2021 52,980

% of All Cancer Deaths 8.7%

5-Year
Relative Survival

64.7% 2011-2017

Year

Rate of New Cases - SEER 9

Rate of New Cases - SEER 13

Death Rate - U.S.

5-Year Relative Survival - SEER 9

Observed

Modeled Trend

Observed

Modeled Trend

Observed

Modeled Trend

Observed

Modeled Trend

New cases are also referred to as incident cases in other publications. Rates of new cases are also referred to as incidence rates.

View Data Table

Rate of New Cases and Deaths per 100,000: The rate of new cases of colorectal cancer was 37.8 per 100,000 men and women per year. The death rate was 13.7 per 100,000 men and women per year. These rates are age-adjusted and based on 2014-2018 cases and deaths.

Lifetime Risk of Developing Cancer: Approximately 4.1 percent of men and women will be diagnosed with colorectal cancer at some point during their lifetime, based on 2016-2018 data.

Prevalence of This Cancer: In 2018, there were an estimated 1,365,135 people living with colorectal cancer in the United States.

Survival Statistics

How Many People Survive 5 Years Or More after Being Diagnosed with Colorectal Cancer?

Relative survival is an estimate of the percentage of patients who would be expected to survive the effects of their cancer. It excludes the risk of dying from other causes. Because survival statistics are based on large groups of people, they cannot be used to predict exactly what will happen to an individual patient. No two patients are entirely alike, and treatment and responses to treatment can vary greatly.

5-Year
Relative Survival

64.7%

Survival by Stage

Cancer stage at diagnosis, which refers to extent of a cancer in the body, determines treatment options and has a strong influence on the length of survival. In general, if the cancer is found only in the part of the body where it started it is localized (sometimes referred to as stage 1). If it has spread to a different part of the body, the stage is regional or distant. The earlier colorectal cancer is caught, the better chance a person has of surviving five years after being diagnosed. For colorectal cancer, 37.5% are diagnosed at the local stage. The 5-year relative survival for localized colorectal cancer is 90.6%.

Percent of Cases & 5-Year Relative Survival by Stage at Diagnosis: Colorectal Cancer

Stage

Percent of Cases

5-Year Relative Survival

Percent of Cases by Stage

New Cases and Deaths

How Common Is This Cancer?

Compared to other cancers, colorectal cancer is fairly common.

Rank

Common Types of Cancer

Estimated New
Cases 2021

Estimated
Deaths 2021

Colorectal cancer represents 7.9% of all new cancer cases in the U.S.
7.9%

In 2021, it is estimated that there will be 149,500 new cases of colorectal cancer and an estimated 52,980 people will die of this disease.

Who Gets This Cancer?

Colorectal cancer is more common in men than women and among those of African American descent. The rate of new cases of colorectal cancer was 37.8 per 100,000 men and women per year based on 2014-2018 cases, age-adjusted.

Rate of New Cases per 100,000 Persons by Race/Ethnicity & Sex: Colorectal Cancer

Percent of New Cases by Age Group: Colorectal Cancer

Age Range

Percent of New Cases

<20

0.3%

20-34

1.9%

35-44

4.6%

45-54

15.1%

55-64

22.4%

65-74

24.8%

75-84

19.6%

>84

11.2%

Colorectal cancer is most frequently diagnosed among people aged 65-74.

Median Age
At Diagnosis

67

Who Dies From This Cancer?

For colorectal cancer, death rates increase with age. Colorectal cancer is the second leading cause of cancer death in the United States. The death rate was 13.7 per 100,000 men and women per year based on 2014-2018 deaths, age-adjusted.

Death Rate per 100,000 Persons by Race/Ethnicity & Sex: Colorectal Cancer

Percent of Deaths by Age Group: Colorectal Cancer

Age Range

Percent of Deaths

<20

0.0%

20-34

0.7%

35-44

2.7%

45-54

9.3%

55-64

19.1%

65-74

23.9%

75-84

23.7%

>84

20.6%

The percent of colorectal cancer deaths is highest among people aged 65-74.

Trends in Rates

Changes Over Time

Keeping track of new cases, deaths, and survival over time (trends) can help scientists understand whether progress is being made and where additional research is needed to address challenges, such as improving screening or finding better treatments.

Using statistical models for analysis, age-adjusted rates for new colorectal cancer cases have been falling on average 2.0% each year over 2009-2018. Age-adjusted death rates have been falling on average 2.1% each year over 2009-2018. 5-year relative survival trends are shown below.

New Cases, Deaths and 5-Year Relative Survival

Interactive Statistics with SEER*Explorer

With SEER*Explorer, you can...

Create custom graphs and tables

Download data and images

Share links to results

SEER*Explorer is an interactive website that provides easy access to a wide range of SEER cancer statistics. It provides detailed statistics for a cancer site by gender, race, calendar year, age, and for a selected number of cancer sites, by stage and histology.

Explore Additional Colorectal Cancer Statistics

More About This Cancer

Cancer and the Colon and Rectum

Cancer that begins in the colon is called colon cancer, and cancer that begins in the rectum is called rectal cancer. Cancer that starts in either of these organs may also be called colorectal cancer.

The digestive system is made up of the esophagus, stomach, and the small and large intestines. The first 6 feet of the large intestine are called the large bowel or colon. The last 6 inches are the rectum and the anal canal.
Additional Information
More Information

Here are some resources for learning more about colorectal cancer.

References

All statistics in this report are based on statistics from SEER and the Centers for Disease Control and Prevention's National Center for Health Statistics. Most can be found within SEER*Explorer.

Suggested Citation

All material in this report is in the public domain and may be reproduced or copied without permission; citation as to source, however, is appreciated.

SEER Cancer Stat Facts: Colorectal Cancer. National Cancer Institute. Bethesda, MD, https://seer.cancer.gov/statfacts/html/colorect.html

These stat facts focus on population statistics that are based on the U.S. population. Because these statistics are based on large groups of people, they cannot be used to predict exactly what will happen to an individual patient. To see tailored statistics, browse SEER*Explorer. To see statistics for a specific state, go to the State Cancer Profiles.

The statistics presented in these stat facts are based on the most recent data available, most of which can be found in SEER*Explorer. In some cases, different year spans may be used.

Estimates of new cases and deaths for 2021 are projections made by the American Cancer Society (ACS), based on earlier reported data.

Cancer is a complex topic. There is a wide range of information available. These stat facts do not address causes, symptoms, diagnosis, treatment, follow-up care, or decision making, although links are provided to information in many of these areas.

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Cancer of the Colon and Rectum - Cancer Stat Facts

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Estimated New Cases in 2021 149,500 % of All New Cancer Cases 7.9% Estimated Deaths in 2021 52,980 % of All Cancer Deaths 8.7% 5-YearRelative Survival 64.7% 2011-2017 Year Rate of New Cases - SEER 9 Rate of New Cases - SEER 13 Death Rate - U.S.

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Main

Colorectal carcinoma (CRC) is a major cause of cancer-related mortality in Western countries ( Parkin et al, 2003). Evidence from twin studies indicates that inherited susceptibility is responsible for ∼30% of CRC ( Lichtenstein et al, 2000). While germline mutations in APC, the mismatch repair (MMR) genes, MUTYH/MYH, SMAD4, ALK3 and STK11/LKB1 confer a high risk of CRC, collectively, such mutations account for <5% of disease ( Aaltonen et al, 2007) with much of the remaining variation in genetic risk likely to be explained by combinations of more common, lower penetrance variants. This 'common disease-common variant' hypothesis implies that conducting association analyses based on scans of single nucleotide polymorphisms (SNPs) should be a powerful strategy for identifying low-penetrance genes ( Risch and Merikangas, 1996; Botstein and Risch, 2003). Such an assertion is supported by recent data showing an association between 8q24 variants and CRC risk ( Haiman et al, 2007; Tomlinson et al, 2007; Zanke et al, 2007).

Despite much research, few definitive low-penetrance susceptibility alleles have been unequivocally identified through association studies. As with many other diseases, positive associations have been reported for various polymorphisms of genes such as NAT2, GSTM1, CYP1A1, STK15 and TP53 from small studies, but few of the initial positive results have been replicated in subsequent studies ( Vinesis et al, 1999; Houlston and Tomlinson, 2001; Ye and Parry, 2003; Borlak and Reamon-Buettner, 2006; Webb et al, 2006a). The inherent statistical uncertainty of case-control studies involving just a few hundred cases and controls seriously limits the power of such studies to identify reliably genetic determinants conferring modest but potentially important risks. Hence, the identification of genes associated with CRC predisposition and determination of their contribution to disease incidence is, however, contingent on having DNA samples from large, systematic series of cancer patients.

The National Cancer Research Network (NCRN) was established to provide support for clinical cancer research in England and is one of the most substantial and constructive developments in the area of cancer research to be made in the United Kingdom in recent years. The NCRN is made up of 40 geographically distinct Networks covering the entire country (33 in England, 3 in Scotland, 3 in Wales and 1 in Northern Ireland). Within each Network there are clinical research support staff and infrastructure to promote accrual of patients into trials and studies, and the collection of high-quality clinicopathological data and appropriate biological samples. Hence, the NCRN presents a major scientific initiative not only in the field of clinical trials but also in the field of genetic epidemiology.

To create a resource for identifying low-penetrance predisposition alleles for CRC, we established the National Study of Colorectal Cancer Genetics (NSCCG) in March 2003 to collect DNA and clinicopathological data from 20 000 cases. Through linkage with the NCRN, it has been possible to create a world-class resource with samples from over 8500 patients in less than 4 years.

Materials and methods

Eligibility criteria

All patients with colon or rectal cancer (International Classification of Diseases (ICD) ninth edition codes 153 and 154, respectively) within 5 years of diagnosis were deemed eligible for the study. To ensure that data and samples were only collected from bona fide adenocarcinoma cases histological confirmation of disease was a prerequisite. The upper limit was initially 75 years at diagnosis, but this was subsequently reduced to 69 years in the light of excellent ascertainment to increase the proportion of younger patients whose cancers are more likely to be due to inherited susceptibility ( Houlston and Peto, 2004). Coupled with patient recruitment, spouses/partners who had no known past or current history of malignancy were invited to participate for the purposes of contributing to the generation of a control series. No age limit was imposed for these individuals.

Procedural outline

A standardised questionnaire administered to patients is being used to collect demographic characteristics - sex, date of birth, ethnic group (White, Black-Caribbean, Black-African, Black-other, Indian, Pakistani, Chinese, and Other), country of birth and current area of residence. In addition, detailed identifiable information is being collected on all first-degree relatives (parents, siblings and offspring) on cancer diagnoses. An open question is being used to illicit information on cancer diagnoses in second-degree relatives. All questionnaires are self-administered and no surrogate responders were used. Clinicopathological details of CRCs (site, stage and grade at presentation) were obtained from the referring clinician using a standardised registration form. For controls, details of sex, date of birth, ethnic group, place of birth and current area of residence were collected through a self-administrated questionnaire. Ethylenediaminetetraacetic acid-venous blood samples (10-20 ml) were collected from all participants. In addition to blood samples, archival blocks representative of patients' CRC were routinely being sought.

Consent forms, questionnaires, registration forms and blood samples were returned to the Institute of Cancer Research (ICR) by mail. Blood samples collected were stored at −80°C prior to DNA extraction and quantification. Extraction of genomic DNA from whole blood is being undertaken by means of either a conventional salt lysis procedure or Chemagic Magnetic Separation Module 1™ methodology.

Colorectal cancer develops along at least two biologically distinct pathways characterised by genetic abnormalities, which can reflect different underlying predispositions ( Ilyas and Tomlinson, 1996). The chromosome instability pathway is typified by chromosomal abnormalities resulting in loss of heterozygosity and tumour suppressor gene inactivation, while cancers exhibiting microsatellite instability (MSI) have defective DNA mismatch repair. In view of this, we are routinely evaluating CRCs for MSI using the following methodology: 10  μm sections are cut from formalin-fixed paraffin-embedded tumours, lightly stained with toluidine blue, and regions containing at least 60% tumour are micro-dissected. Tumour DNA is being extracted using the QIAamp DNA Mini kit (Qiagen, Crawley, UK) according to the manufacturer's instructions and genotyped for the mononucleotide microsatellite loci BAT25 and BAT26, which are highly sensitive markers of MSI ( Zhou et al, 1998). Samples showing novel alleles at either BAT26 or BAT25 or both markers are assigned as MSI (corresponding to a high level of instability, MSI-H Boland et al, 1998).

Statistical considerations

The primary aim of establishing NSCCG was to generate a DNA resource of CRC patients of sufficient size to robustly identify low-penetrance alleles by association studies of genetic polymorphisms. From the outset, it was envisaged that such searches would be conducted on a genome-wide basis. It is well-recognised that as such studies involve genotyping a vast number of markers, a large number of false-positive associations will inevitably be generated and only a small number will be truly associated with disease susceptibility. Hence, associations need to attain a high level of statistical significance to be established beyond reasonable doubt and significance levels of ∼10 −7 have been proposed as being appropriate ( Risch and Merikangas, 1996). The original target of NSCCG was to assemble a series that will include 2000 cases. This figure had been based upon contemporaneous preconceptions on the probable impact of common alleles on disease risk. Recent data from association studies, however, indicate that common disease alleles are likely to be associated with risks typically <1.5 ( Easton et al, 2007; Gudmundsson et al, 2007; Haiman et al, 2007; Tomlinson et al, 2007; Zanke et al, 2007). To identify alleles conferring such risks to have 80% power-stipulating statistical thresholds of 10 −7 necessitates having access to sample sets of at least 10 000 cases and 10 000 controls. These statistical considerations led us to significantly revise our target sample size to ensure that we would generate a resource adequately powered to identify such disease-causing alleles and to examine for epistatic interactions.

Ethical considerations

In generating DNA registries, ethical considerations are central to study design. One of the particular strengths of studies such as NSCCG is that once constructed the DNA database can be probed repeatedly for different existing and newly identified candidate risk factor genes. It is not feasible to contact all study entrants to seek further written consent for each specific test, therefore, the information sheet study discussion and consent is centred on the general concept of 'genetic analyses'. As these investigations were to be solely for research to find new gene(s) predisposing to cancer, it was implicit that no individual results will be conveyed to persons. In publications of findings no study entrant would be identifiable. As with all studies of this nature, we clearly stated that if a study entrant wished to withdraw, then their DNA sample and all information held on them would be destroyed. To ensure confidentiality, data are held under secure conditions at the Institute of Cancer Research (ICR) in accordance with the Data Protection Act (1998).

All clinical information and biological samples were obtained only after fully informed consent was obtained from participating individuals, and in accordance with the tenets of the Declaration of Helsinki. Ethical approval for the study was obtained from the Multi-Centre Research Ethics Committees (MREC/98/2/67; MREC02/0/97).

Results

After securing ethical permissions at national level through the Multi-Centre Research Ethics Committee, the study was incorporated into the NCRN (National Cancer Research Network) portfolio in March 2003. It was subsequently rolled out across England after individual hospitals had obtained relevant local ethical permissions. As the number of centres becoming active participants in NSCCG widened, accrual of both patients and controls significantly increased ( Figure 1). Currently, 148 sites are participating in NSCCG ( Figure 2) and recruitment stands at approximately 160 cases and 40 controls per month. Although most hospitals entering subjects into NSCCG are located in England, centres in Wales and Northern Ireland are now participating and a number in Scotland are in the process of gaining local ethical permissions to participate, thereby, making the study UK-wide.

Accrual rate of patients and controls to NSCCG.

Sites of centres in the United Kingdom recruiting to NSCCG as of March 2007.

To date, blood samples and completed questionnaires have been collected from 8722 cases and 2185 controls. The NSCCG collection will continue until samples from 20 000 CRC cases has been assembled. The number of male patients ascertained or included (59% of cohort) reflects the slight sex preponderance of the disease. In terms of ethnicity, over 90% of patients entered into NSCCG were self reported as White Caucasians. Although controls were of similar age in comparison to cases (mean age 59 years; s.d.=9.5) and 90% were self-reported as White Caucasians not surprisingly, the majority (64%) were female.

A high proportion of the cases have been diagnosed at a young age, reflecting the criterion for ascertainment ( Table 1) ; specifically, 29% of the cases were aged <55 years old at diagnosis, compared with <10% in the general population. Approximately 15% of patients have a family history of CRC defined by having at least one affected first-degree relative. The 60 : 40 ratio of colonic (ICD 153) to rectal disease (ICD 154) of cases recruited to date is in keeping with that observed in the general UK population ( Table 1). Similarly, stage at presentation is comparable to that generally observed. To date, 3088 tumour blocks have been collected and 2516 evaluated for MSI; 12% showing MMR deficiency, concordant with the frequency of this phenotype in unselected CRC ( Storojeva et al, 2005).

Table 1 Clinicopathological characteristics of colorectal cancer patients recruited to the National Study of Colorectal Cancer Genetics

Discussion

Over the coming years our expanding knowledge of cancer genetics will have a major impact on our ability to predict an individual's level of risk of developing cancer, detect and diagnose cancer early and select treatments which are most likely to be effective. Ultimately the genetic revolution may lead to ways of preventing cancer. Advances in genetics will lead to a greater understanding of inherited susceptibility to cancer. The relative influence of genes on cancer development is variable and ranges from situations where genetic factors predominate and are highly predictive of disease development, to others where they play only a minor role in modifying the effect of environmental exposure to toxic substances.

(NHS Cancer Plan, 2000)

Following the sequencing of the human genome, large-scale harvests of SNPs have been conducted, and there are currently >10 million documented human SNPs (dbSNP). Patterns of linkage disequilibrium (LD) between polymorphisms have been characterised allowing subsets of tagging SNPs to be selected that, through LD with other variants, capture a large proportion of the common sequence variation in the human genome. These comprehensive sets of tagging SNPs, which capture most of the common sequence variation, coupled with the development of highly efficient analytical platforms allow whole-genome studies for disease associations to be conducted cost effectively. This approach is unbiased and does not depend upon prior knowledge of function or presumptive involvement of any gene in disease causation. Moreover, it avoids the possibility of missing the identification of important variants in hitherto unstudied genes or regions of the gene-harbouring and gene-controlling elements. The relationship between patients' genotype and aetiology of cancer is, thus, now open for further exploration.

Here, we have demonstrated that the centralisation of cancer services in the United Kingdom offers an opportunity to establish large, well-characterised cohorts by targeting collection to the largest centres. Moreover, mobilising NCRN networks provides a means of consistently delivering the data and sample collection needed to complete genetic epidemiology studies on the required scale.

Ascertainment of cases through NCRN has been directed towards those diagnosed at young age and this serves to empower the resource for identifying disease-causing alleles by virtue of genetic enrichment. The possibility of population stratification leading to false inference of disease-genotype association can be addressed by adjusting for known region/ethnicity or by using information on unlinked genetic markers. In NSCCG, the geographical area of birth and area of residence within the United Kingdom is known for all of the individuals, and this information can be used to allow analyses stratified by region of residence, reducing any effects of population stratification.

For some analyses, family history information on cancer diagnosis in relatives is required. In our study, participants are providing information on cancer diagnosis in relatives without verification of the diagnosis through medical sources or health records. Subject to ethical approval, there is a possibility of verifying cancer diagnoses verified through national registries. While such verification is theoretically desirable since studies have shown that CRC patients correctly report ∼80% of positive family histories and >95% of negative family histories in first-degree relatives ( Aitken et al, 1995; Ziogas and Anton-Culver, 2003), self-reported data still has great utility and is unlikely to systematically bias many types of analyses.

As blood samples have been ascertained from many clinical centres in the United Kingdom, we are cognisant of the potential problem of differential bias in genotyping. We have however, no evidence of differences in DNA quality as we have previously documented call rates of 99.8% in 1526 of samples ascertained through NSCCG ( Webb et al, 2006b).

The NCRN research networks are established within cancer care networks where access to partners is readily available and direct. They are not designed to collect samples from the general population or the unrelated population so our choice of collecting samples from partners was a pragmatic one appropriate for the NCRN. Inevitably, in studies such as NSCCG, a smaller number of samples from controls will be collected than from cases since in addition to lack of compliance many patients do not have a current partner. While the sex of controls ascertained through initiatives such as NSCCG will usually be of the opposite gender to cases by pooling samples from other similar studies, it is possible to develop large control data sets such as a 1958 Birth Cohort established in the United Kingdom currently being used by the Wellcome Trust Case Control Consortium (WTCCC). Because of the difficulty of obtaining sufficiently detailed and accurate data on environmental exposure in studies such as NSCCG, and because there are issues to do with comparability of exposure data from controls assembled from different studies, it is acknowledged that studies of environmental risk factors including gene-environment interaction will be limited in resources such as NSCCG.

Given the projected size of NSCCG, the main value of collections such as this will be in studies of common genetic risk factors and gene-gene interactions, hypotheses regarding gene-environment interaction will require alternative data sets. Accepting the limitations of NSCCG, our experience in developing this resource serves to illustrate how large DNA databases for genetic analyses can rapidly be developed in the United Kingdom.

Change history

16 November 2011

This paper was modified 12 months after initial publication to switch to Creative Commons licence terms, as noted at publication

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National study of colorectal cancer genetics - British Journal of Cancer

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Approximately, a third of all colorectal cancer (CRC) is due to inherited susceptibility. However, high-risk mutations in APC, the mismatch repair (MMR) genes, MUTYH/MYH, SMAD4, ALK3 and STK11/LKB1 are rare and account for <5% of cases. Much of the remaining variation in genetic risk is likely to be explained by combinations of more common gene variants that modestly increase risk.

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Survivorship Care Plans in Colorectal Cancer

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Treatment for colon cancer is based largely on the stage (extent) of the cancer, but other factors can also be important.

People with colon cancers that have not spread to distant sites usually have surgery as the main or first treatment. Chemotherapy may also be used after surgery (called adjuvant treatment). Most adjuvant treatment is given for about 6 months.

Treating stage 0 colon cancer

Since stage 0 colon cancers have not grown beyond the inner lining of the colon, surgery to take out the cancer is often the only treatment needed. In most cases this can be done by removing the polyp or taking out the area with cancer through a colonoscope (local excision). Removing part of the colon (partial colectomy) may be needed if a tumor is too big to be removed by local excision.

Treating stage I colon cancer

Stage I colon cancers have grown deeper into the layers of the colon wall, but they have not spread outside the colon wall itself or into the nearby lymph nodes.

Stage I includes cancers that were part of a polyp. If the polyp is removed completely during colonoscopy, with no cancer cells at the edges (margins) of the removed piece, no other treatment may be needed.

If the cancer in the polyp is high grade (see Colorectal Cancer Stages for more on this), or there are cancer cells at the edges of the polyp, more surgery might be recommended. You might also be advised to have more surgery if the polyp couldn't be removed completely or if it had to be removed in many pieces, making it hard to see if cancer cells were at the edges.

For cancers not in a polyp, partial colectomy ─ surgery to remove the section of colon that has cancer and nearby lymph nodes ─ is the standard treatment. You typically won't need any more treatment.

Treating stage II colon cancer

Many stage II colon cancers have grown through the wall of the colon, and maybe into nearby tissue, but they have not spread to the lymph nodes.

Surgery to remove the section of the colon containing the cancer (partial colectomy) along with nearby lymph nodes may be the only treatment needed. But your doctor may recommend adjuvant chemotherapy (chemo after surgery) if your cancer has a higher risk of coming back (recurring) because of certain factors, such as:

The cancer looks very abnormal (is high grade) when viewed under a microscope.

The cancer has grown into nearby blood or lymph vessels.

The surgeon did not remove at least 12 lymph nodes.

Cancer was found in or near the margin (edge) of the removed tissue, meaning that some cancer may have been left behind.

The cancer had blocked off (obstructed) the colon.

The cancer caused a perforation (hole) in the wall of the colon.

Not all doctors agree on when chemo should be used for stage II colon cancers. It's important for you to discuss the pros and cons of chemo with your doctor, including how much it might reduce your risk of recurrence and what the likely side effects will be.

If chemo is used, the main options include 5-FU and leucovorin, oxaliplatin, or capecitabine, but other combinations may also be used.

Treating stage III colon cancer

Stage III colon cancers have spread to nearby lymph nodes, but they have not yet spread to other parts of the body.

Surgery to remove the section of the colon with the cancer (partial colectomy) along with nearby lymph nodes, followed by adjuvant chemo is the standard treatment for this stage.

For chemo, either the FOLFOX (5-FU, leucovorin, and oxaliplatin) or CapeOx (capecitabine and oxaliplatin) regimens are used most often, but some patients may get 5-FU with leucovorin or capecitabine alone based on their age and health needs.

Radiation therapy and/or chemo may be options for people who aren't healthy enough for surgery.

Treating stage IV colon cancer

Stage IV colon cancers have spread from the colon to distant organs and tissues. Colon cancer most often spreads to the liver, but it can also spread to other places like the lungs, brain, peritoneum (the lining of the abdominal cavity), or to distant lymph nodes.

In most cases surgery is unlikely to cure these cancers. But if there are only a few small areas of cancer spread (metastases) in the liver or lungs and they can be removed along with the colon cancer, surgery may help you live longer. This would mean having surgery to remove the section of the colon containing the cancer along with nearby lymph nodes, plus surgery to remove the areas of cancer spread. Chemo is typically given as well, before and/or after surgery. In some cases, hepatic artery infusion may be used if the cancer has spread to the liver.

If the metastases cannot be removed because they're too big or there are too many of them, chemo may be given before any surgery (neoadjuvant chemo). Then, if the tumors shrink, surgery to remove them may be tried. Chemo would then be given again after surgery. For tumors in the liver, another option may be to destroy them with ablation or embolization.

If the cancer has spread too much to try to cure it with surgery, chemo is the main treatment. Surgery might still be needed if the cancer is blocking the colon or is likely to do so. Sometimes, such surgery can be avoided by putting a stent (a hollow metal or plastic tube) into the colon during a colonoscopy to keep it open. Otherwise, operations such as a colectomy or diverting colostomy (cutting the colon above the level of the cancer and attaching the end to an opening in the skin on the belly to allow waste out) may be used.

If you have stage IV cancer and your doctor recommends surgery, it's very important to understand the goal of the surgery ─ whether it's to try to cure the cancer or to prevent or relieve symptoms of the disease.

Most people with stage IV cancer will get chemo and/or targeted therapies to control the cancer. Some of the most commonly used regimens include:

FOLFOX: leucovorin, 5-FU, and oxaliplatin (Eloxatin)

FOLFIRI: leucovorin, 5-FU, and irinotecan (Camptosar)

CAPEOX or CAPOX : capecitabine (Xeloda) and oxaliplatin

FOLFOXIRI: leucovorin, 5-FU, oxaliplatin, and irinotecan

One of the above combinations plus either a drug that targets VEGF, (bevacizumab [Avastin], ziv-aflibercept [Zaltrap], or ramucirumab [Cyramza]), or a drug that targets EGFR (cetuximab [Erbitux] or panitumumab [Vectibix])

5-FU and leucovorin, with or without a targeted drug

Capecitabine, with or without a targeted drug

Irinotecan, with or without a targeted drug

Cetuximab alone

Panitumumab alone

Regorafenib (Stivarga) alone

Trifluridine and tipiracil (Lonsurf)

The choice of regimens depends on several factors, including any previous treatments you've had and your overall health.

If one of these regimens is no longer working, another may be tried. For people with certain gene changes in their cancer cells, another option after initial chemotherapy might be treatment with an immunotherapy drug such as pembrolizumab (Keytruda).

For advanced cancers, radiation therapy can also be used to help prevent or relieve symptoms such as pain. It may shrink tumors for a time, but it's not likely to cure the cancer. If your doctor recommends radiation therapy, it's important that you understand the goal of treatment.

Treating recurrent colon cancer

Recurrent cancer means that the cancer has come back after treatment. The recurrence may be local (near the area of the initial tumor), or it may be in distant organs.

Local recurrence

If the cancer comes back locally, surgery (often followed by chemo) can sometimes help you live longer and may even cure you. If the cancer can't be removed surgically, chemo might be tried first. If it shrinks the tumor enough, surgery might be an option. This would again be followed by more chemo.

Distant recurrence

If the cancer comes back in a distant site, it's most likely to appear in the liver first. Surgery might be an option for some people. If not, chemo may be tried to shrink the tumor(s), which may then be followed by surgery to remove them. Ablation or embolization techniques might also be an option to treat some liver tumors.

If the cancer has spread too much to be treated with surgery, chemo and/or targeted therapies may be used. Possible regimens are the same as for stage IV disease.

For people whose cancers are found to have certain traits on lab tests, another option might be treatment with immunotherapy.

Your options depend on which, if any, drugs you had before the cancer came back and how long ago you got them, as well as your overall health. You may still need surgery at some point to relieve or prevent blockage of the colon or other local problems. Radiation therapy may be an option to relieve symptoms as well.

Recurrent cancers can often be hard to treat, so you might also want to ask your doctor if clinical trials of newer treatments are available.

For more on recurrence, see Understanding Recurrence.

The treatment information given here is not official policy of the American Cancer Society and is not intended as medical advice to replace the expertise and judgment of your cancer care team. It is intended to help you and your family make informed decisions, together with your doctor. Your doctor may have reasons for suggesting a treatment plan different from these general treatment options. Don't hesitate to ask him or her questions about your treatment options.

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Treatment for colon cancer is based largely on the stage (extent) of the cancer, but other factors can also be important. People with colon cancers that have not spread to distant sites usually have surgery as the main or first treatment. Chemotherapy may also be used after surgery (called adjuvant treatment).

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Three measures of cancer survival can be calculated in SEER*Stat software:

Observed all cause survival - Observed survival is an estimate of the probability of surviving all causes of death.

Net cancer-specific survival (policy-based statistic) - This is the probability of surviving cancer in the absence of other causes of death. It is a measure that is not influenced by changes in mortality from other causes and, therefore, provides a useful measure for tracking survival across time, and comparisons between racial/ethnic groups or between registries.

Crude probability of death (patient prognosis measure) - This is the probability of dying of cancer in the presence of other causes of death. It is a better measure to assess the impact of cancer diagnosis at an individual level since mortality from other causes play a key role. It measures mortality patterns actually experienced in a cohort of cancer patients on which many possible causes of death are acting simultaneously. The crude measure is reported as a cumulative probability of death from cancer rather than survival.

The SEER*Stat help system includes several frequently asked questions to clarify when net survival and crude probability of death would be used.

Approaches to Estimation of Cancer-Specific Survival

Relationship of the Survival Measure to the Estimation Method

Net cancer-specific survival and crude probability of death have two methods in which they can be estimated: using cause of death information or expected survival tables. When using cause of death information, there has been much debate over what is the right endpoint. If death certification were perfect, one would just use the specific form of cancer as the endpoint. However, if a cancer metastasizes, there are instances where the death certificate incorrectly lists the underlying cause of death as the metastatic site. In this instance, it may be best to use all cancers as the end point, especially if the patient only has one cancer. Work is ongoing to define more sophisticated algorithms for defining endpoints based on common sites of metastases for each cancer.

Regardless of whether one uses an approach which utilizes cause of death or expected lifetables, careful consideration should be given to exclusions from the analysis. A technical report from Boer et al., 2003 (PDF, 879 KB), summarizes various approaches to exclusions for survival analyses, as well as the choice of endpoints when death certificate information is utilized. The figure above illustrates the survival statistics that result from the combination of the two measures and twoestimation methods. A description of each is given below.

Relative survival - Cancer survival in the absence of other causes of death is calculated using survival life tables. Relative survival is defined as the ratio of the proportion of observed survivors (all causes of death) in a cohort of cancer patients to the proportion of expected survivors in a comparable cohort of cancer-free individuals. The formulation is based on the assumption of independent competing causes of death. Since a cohort of cancer-free individuals is difficult to obtain, we use expected life tables and assume that the cancer deaths are a negligible proportion of all deaths. (See the technical report from Cho et al., 2011 (PDF, 638 KB))

Cause-specific survival is a net survival measure representing survival of a specified cause of death in the absence of other causes of death. Estimates are calculated by specifying the cause of death. Individuals who die of causes other than those specified are considered to be censored. (See Marubini & Valsecchi, 1995)

Crude Probability of Death Using Expected Survival - This crude measure uses expected survival (obtained from the expected life tables) to estimate the probability of dying from other causes in each interval. Since a cohort of cancer-free individuals is difficult to obtain, we use expected life tables and assume that the cancer deaths are a negligible proportion of all deaths. (See Cronin & Feuer, 2000)

Crude Probability of Death Using Cause of Death Information - The probability of dying from cancer and dying from other causes in a cohort of cancer patients is calculated using cause of death information. (See Marubini & Valsecchi, 1995; Schairer et al., 2004)

Example: This figure shows crude and net probability of death from localized colorectal cancer for men and women diagnosed over the age of 70. Crude probability of death (cancer) is lower than net probability of death because localized colorectal cancer has good prognosis, and because mortality for other causes is high for that age group.

Cumulative Probability of Death in Men and Women Age 70+ Diagnosed with Localized Colorectal Cancer, 1996-2012, SEER 13 Registries

The SEER*Stat matrix file used to obtain the percentages for the Cumulative Probability of Death figure shown above is available for download. You must have the SEER*Stat software in order to open this file - crude.vs.net.ssm.

SEER*Stat Features in Survival Analysis

Presentation from SEER*Stat Technical Webinar (July 14, 2011) (PDF, 909 KB)

These are slides from a webinar highlighting two features in the calculation of cancer survival added to SEER*Stat version 7.0:

Ederer II method to estimate expected survival in relative survival

Improved algorithm to specify the underlying cause of death: the SEER cause-specific death classification variable

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Three measures of cancer survival can be calculated in SEER*Stat software: Observed all cause survival - Observed survival is an estimate of the probability of surviving all causes of death. Net cancer-specific survival (policy-based statistic) - This is the probability of surviving cancer in the absence of other causes of death.

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Evidence of Benefit Associated With Colorectal Cancer Screening

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Evidence of Benefit Associated With Colorectal Cancer Screening

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Based on solid evidence, screening for colorectal cancer (CRC) reduces CRC mortality. In addition, there is solid evidence that some CRC screening modalities also reduce CRC incidence. A meta-analysis of flexible sigmoidoscopy randomized controlled trials found that screening with sigmoidoscopy reduces all-cause mortality.

https://www.cancer.gov/types/colorectal/hp/colorectal-screening-pdq#_342_toc

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Dr. Marcos Rejtman: Palliative Care - Memorial Cancer System

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Not counting some kinds of skin cancer, colorectal cancer is the third most common cancer in men and women. It is the third leading cause of cancer-related deaths in the United States.

U.S. Cancer Statistics Data Visualizations Tool

The Data Visualizations tool makes it easy for anyone to explore and use the latest official federal government cancer data from United States Cancer Statistics. It includes the latest cancer data covering the U.S. population.

See rates or numbers of new colorectal cancers or colorectal cancer deaths for the entire United States and individual states. Also, see the top 10 cancers for men and women.

See rates or numbers of new colorectal cancers or colorectal cancer deaths by race/ethnicity, sex, and age group.

See how the rates of new colorectal cancers or colorectal cancer deaths changed over time for the entire United States and individual states.

The percentage of U.S. adults aged 50 to 75 years who were up-to-date with colorectal cancer screening increased 1.4 percentage points, from 67.4% in 2016 to 68.8% in 2018. This represents an additional 3.5 million adults screened for colorectal cancer.

Page last reviewed:

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Not counting some kinds of skin cancer, colorectal cancer is the third most common cancer in men and women. It is the third leading cause of cancer-related deaths in the United States. The Data Visualizations tool makes it easy for anyone to explore and use the latest official federal government cancer data from United States Cancer Statistics.

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There's no sure way to prevent colorectal cancer. But there are things you can do that might help lower your risk, such as changing the risk factors that you can control.

Colorectal cancer screening

Screening is the process of looking for cancer or pre-cancer in people who have no symptoms of the disease. Regular colorectal cancer screening is one of the most powerful tools for preventing colorectal cancer.

From the time the first abnormal cells start to grow into polyps, it usually takes about 10 to 15 years for them to develop into colorectal cancer. With regular screening, most polyps can be found and removed before they have the chance to turn into cancer. Screening can also find colorectal cancer early, when it's small and easier to treat.

If you're age 45 or older, you should start getting screened for colorectal cancer. Several types of tests can be used. Talk to your health care provider about which ones might be good options for you. No matter which test you choose, the most important thing is to get tested.

If you have a strong family history of colorectal polyps or cancer, talk with your doctor about your risk. You might benefit from genetic counseling to review your family medical tree to see how likely it is that you have a family cancer syndrome.

Body weight, physical activity, and diet

You might be able to lower your risk of colorectal cancer by managing your diet and physical activity.

Weight: Being overweight or obese increases the risk of colorectal cancer in both men and women, but the link seems to be stronger in men. Staying at a healthy weight may help lower your risk.

Physical activity: Being more active lowers your risk of colorectal cancer and polyps. Regular moderate to vigorous activity can lower the risk. Limiting your sitting and lying down time may also lower your risk. Increasing the amount and intensity of your physical activity may help reduce your risk.

Diet: Overall, diets that are high in vegetables, fruits, and whole grains, and low in red and processed meats, probably lower colorectal cancer risk, although it's not exactly clear which factors are important. Many studies have found a link between red meats (beef, pork, and lamb) or processed meats (such as hot dogs, sausage, and lunch meats) and increased colorectal cancer risk.

In recent years, some large studies have shown conflicting evidence that fiber in the diet probably lowers colorectal cancer risk. Research in this area is still under way. Recent studies looking specifically at whole grain intake, however, show that colorectal cancer risk appears to go down as you add more whole grains to your diet.

Limiting red and processed meats and eating more vegetables, fruits, and whole grains may help lower your risk.

Alcohol: Several studies have found a higher risk of colorectal cancer with increased alcohol intake, especially among men.It is best not to drink alcohol. For people who do drink, they should have no more than 1 drink per day for women or two drinks per day for men. Not drinking alcohol may help reduce your risk.

For more about diet and physical activity, see the American Cancer Society Guidelines for Diet and Physical Activity for Cancer Prevention.

Not smoking

Long-term smoking is linked to an increased risk of colorectal cancer, as well as many other cancers and health problems. Quitting smoking may help lower you risk of colorectal cancer and many other types of cancer, too.If you smoke and would like help quitting, call the American Cancer Society at 1-800-227-2345.

Vitamins, calcium, and magnesium

Some studies suggest that taking a daily multi-vitamin containing folic acid, or folate, may lower colorectal cancer risk, but not all studies have found this. In fact, some studies have hinted that folic acid might help existing tumors grow. More research is needed in this area.

Some studies have suggested that vitamin D, which you can get from sun exposure, in certain foods, or in a vitamin pill, might lower colorectal cancer risk. Studies have shown that low vitamin D levels are associated with an increased risk of colorectal cancer as well as other cancers. Because of concerns that excess sun exposure can cause skin cancer, most experts do not recommend this as a way to lower colorectal cancer risk at this time. More studies are needed to determine if increasing vitamin D intake from a supplement can help prevent colorectal cancer. Avoiding a low vitamin D level may be helpful; it is best to talk with your doctor about whether your vitamin D level should be tested.

Low levels of dietary calcium have been linked with an increased risk of colorectal cancer in some studies. Other studies suggest that increasing calcium intake may lower colorectal cancer risk. Calcium is important for a number of health reasons aside from possible effects on cancer risk. But because of the possible increased risk of prostate cancer in men with high calcium/dairy product intake, and the possible lower risk of other cancers like colorectal cancer and breast cancer, the American Cancer Society does not have any specific recommendations regarding dairy food consumption for cancer prevention.

Calcium and vitamin D might work together to reduce colorectal cancer risk, as vitamin D aids in the body's absorption of calcium. Still, not all studies have found that supplements of these nutrients reduce risk.

A few studies have found a possible link between a diet that's high in magnesium and reduced colorectal cancer risk, especially among women. More research is needed to determine if this link exists.

Non-steroidal anti-inflammatory drugs (NSAIDs)

Many studies have found that people who regularly take aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen (Motrin, Advil) and naproxen (Aleve), have a lower risk of colorectal cancer and polyps.

But aspirin and other NSAIDs can cause serious or even life-threatening side effects, such as bleeding from stomach irritation or stomach ulcers, which may outweigh the benefits of these medicines for the general public. For this reason, the American Cancer Society does not recommend taking NSAIDs just to lower colorectal cancer risk if you are someone at average risk.

Still, for some people in their 50s who have a high risk of heart disease, where low-dose aspirin is found to be beneficial, the aspirin may also have the added benefit of reducing the risk of colorectal cancer.

Because aspirin or other NSAIDs can have serious side effects, check with your doctor before starting any of them on a regular basis.

Hormone replacement therapy for women

Some studies have shown that taking estrogen and progesterone after menopause (sometimes called menopausal hormone therapy or combined hormone replacement therapy) may reduce a woman's risk of developing colorectal cancer, but other studies have not.

Because taking estrogen and progesterone after menopause can also increase a woman's risk of heart disease, blood clots, and cancers of the breast and lung, it's not commonly recommended just to lower colorectal cancer risk.

If you're considering using menopausal hormone therapy, be sure to discuss the risks and benefits with your doctor.

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Colorectal Cancer Prevention | How to Prevent Colorectal Cancer

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There's no sure way to prevent colorectal cancer. But there are things you can do that might help lower your risk, such as changing the risk factors that you can control. Screening is the process of looking for cancer or pre-cancer in people who have no symptoms of the disease.

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INTRODUCTION

Epidemiology and background

Colorectal cancer (CRC) is the third most common cancer (estimated 1.23 million cases per year) and the fourth cancer-related cause of death (609 thousands deaths per year) in world population[ 1]. Ten-fold differences in incidence between the different regions of the world, being the highest in Australia, Western Europe and North America, are reported[ 1].

Traditionally managed surgically, by resection of the primitive tumor, intestinal bypass or stoma[ 6- 8], the palliative approach to incurable stage IV CRC patients has significantly changed over the last three decades and is nowadays multidisciplinary, with a pivotal role played by chemotherapy (CHT)[ 9- 11]. Such a multimodal management of incurable CRC is responsible for a significant increase in survival of patients affected by incurable CRC in general, which has passed from 8 to 14 mo over the last two decades[ 3], but has been reported to exceed two years in selected populations following the sequential use of various lines of treatment including the newest chemotherapeutic agents[ 12, 13].

Differently from potentially curable patients, where overall survival and disease-free survival are the main outcome and measured variable of any treatment, the short residual life of these patients radically change the perspective. Although the overall survival (or "quantity of residual life") is still one of the main endpoint of any palliative treatment, indeed, it should be emphasized that the other main endpoint of management is the "quality of residual life", which can be severely affected by surgery, CHT, and any other palliative treatment. From such a changed point of view, individual, psychological, ethical issues gain importance in deciding for the best management of any singular patient.

Evolving concepts and "gray zones" between curative and palliative

Traditionally used to define the management of patients with CRC disease not curable with radical intent and inevitably leading the patient to death in a matter of months/few years, the concept itself of "palliative" has changed in recent years, following the progress of CHT and surgery of CRC and distant metastasis.

The multimodal approach to initially non-resectable liver metastasis, including systemic CHT[ 12, 14, 15], intraarterial CHT[ 16, 17], portal embolization[ 18, 19] and secondary surgery[ 20, 21], and its impact on survival[ 22], will be treated in a dedicated paragraph.

Extrahepatic CRC metastasis do not systematically imply a palliative management anymore, either. Synchronous/metachronous lung metastasis are nowadays considered suitable of surgical resection[ 23- 25]. The indication to resection of CRC liver metastasis with local lymph node involvement is currently under debate[ 25], but specialized centers report patients with liver pedicle node involvement to have a 25%-5-year-survival after surgery[ 26]. The indication to surgical resection of other extrahepatic CRC disease, in particular peritoneal metastasis, is also matter of debate: peritoneal carcinomatosis, once considered a prognostic criterion of dismal prognosis and a contraindication to surgery[ 27, 28], may be nowadays managed by a multidisciplinary approach including cytoreductive surgery and perioperative intraperitoneal chemotherapy[ 29, 30], thus achieving a 5-year-survival rate of 10%-30%[ 30- 32].

Significantly, the latest version of the National Comprehensive Cancer Group[ 33] and very recent guidelines[ 25, 34], propose a systematic re-evaluation for "conversion to resectable" every 2 mo during CHT course of patients with initially unresectable synchronous liver and/or lung metastases. Although such new perspectives and modalities of treatment have a potentially curative purpose and are not treated in the present paper, nevertheless, they represent the paradigm of a "moving frontier" between curative and palliative management of advanced CRC patients.

Assessment of resectabilty (or palliation)

Although it is not among the aims of the present paper, imaging modalities for resectability assessment are briefly summarized. Liver assessment is usually performed by several examinations, including Magnetic Resonance Imaging (MRI), computed tomography (CT), contrast-enhanced ultrasounds (CEUS), ¹⁸F-fluorodeoxyglucose Positron Emission Tomography (PET) and PET/CT[ 35- 38], as surgical decision-making requires information from multiple imaging modalities. MRI is reported to be superior to CT in the preoperative evaluation of colorectal metastasis both in normal liver[ 35], where it has higher sensitivity (95.6% vs 74.8%) and specificity (97.2% vs 81.1%), and in post-CHT liver[ 36], where MRI is reported to have a sensitivity of 85.7% compared to 69.9% of CT. MRI also shows the best effectiveness in nature characterization of hepatic lesions together with CEUS[ 37]. PET, PET/CT and transparietal US are also diffusely used for diagnosis, staging and follow up[ 35, 36].

Usually diagnosed endoscopically, primary CRC resectability is normally assessed by CT[ 38], endoscopic ultrasound[ 39] and MRI[ 40], these two latter having a pivotal role in defining the resectability of rectal cancer. Identifying peritoneal metastasis by imaging is one of the major issues in advanced CRC. Although recent efforts in defining new radiologic criteria for diagnosis[ 41], the performance of CT scan[ 42, 43] and PET/CT[ 43] is limited in the absence of ascites and obvious supra-centimetric tumor deposits on the peritoneum. Thus, peritoneal metastasis is still, often, an intraoperative diagnosis.

Limits of past and present literature

First appeared in scientific literature in the mid-twentieth century[ 46, 47], the management of incurable metastatic CRC still represent a matter of debate among oncologists, and surgeons. Through seven decades, several "surgery-focused" papers addressed the issue of efficacy of primary CRC resection in prolonging survival. Unfortunately, most of those papers were single-center, small-sized, retrospective series, extremely heterogeneous concerning patients, clinical scenarios and setting, metastatic pattern, primary tumor location, and management (surgery, CHT, stenting etc.)[ 27, 47- 53]. In the absence of randomized trials, in recent years, the efficacy of colonic resection has been assessed by larger retrospective series, metanalysis and literature reviews[ 54- 56]. More recently, since the late eighties, the introduction of new chemotherapic agents in stage IV patients has given rise to a prolific "CHT-focused" literature, evaluating CHT regimens by high-quality, multi-centric, prospective randomized trials[ 9, 11- 13, 57].

Interestingly, in "surgery-focused" papers, also owing to the retrospective nature, CHT is often analysed as one of the possible variables potentially affecting survival, but it is usually considered as a whole (regardless of the CHT regimen administered)[ 5, 27, 50, 58- 62]. On the contrary, "CHT-focused" articles do not even report whether patients undergo surgery (resective or non-resective) of primary CRC, and consequently do not evaluate surgical resection as a parameter potentially prolonging survival[ 9- 13].

As a matter of fact, such a various literature on the subject, prevent even nowadays from definitive conclusions concerning the best approach to incurable stage IV patients, in particular concerning the role of palliative resection of the primary CRC.

Clinical relevance and management of incurable CRC

Patients with incurable CRC may be asymptomatic or present with a variety of symptoms and clinical scenarios ranging from moderate anaemia to digestive troubles, to lower gastrointestinal (GI) bleeding to life-threatening conditions, including obstruction and perforation, needing emergency management.

In order to allow a rational and practical organisation of the present review, here we present two flow charts (Figures and ) based on clinical relevance of CRC at presentation, since the approach to the patient changes radically. In fact, in asymptomatic patients, the management is aimed to slow down cancer progression, thus prolonging long-term survival and preventing cancer-related complications. Differently, in emergency and severely symptomatic patients, it is focused in solving cancer-related complications, which may be rapidly fatal or imply intolerable symptoms. Obviously, the two proposed managements are not indefinitely exclusive, as an emergency patient may become asymptomatic after a life-threatening condition has been treated, and, conversely, an asymptomatic patient may become severely symptomatic under CHT.

This simplification does not to consider rarer, non emergency symptoms that may become invalidating and finally lead to surgery, including hyperpyrexia or pain due to compression ("bulk-effect of tumor") or infiltration of nervous plexuses or contiguous organs (ureters etc.). Moreover, this review does not consider comorbidities, which can finally play a determinant role in deciding the management, and does not consider that the majority of patients presents with an intermediate clinical picture, where often the greatest challenge is "to decide the right timing" to turn to a more aggressive management, indeed. This paper is aimed to address the issue of "what" to do according to a specific clinical situation, whereas "when" to proceed is still (and probably will ever be) a medical decision on a case by case basis.

ASYMPTOMATIC (OR MINIMALLY SYMPTOMATIC) PATIENTS

Role of surgery

In recent times, the main role in the management of non-emergency patients affected by incurable CRC has passed from surgery to CHT. Accordingly, international guidelines suggest nowadays to avoid surgery in the case of patients with incurable metastasis from CRC, unless in the presence of (or in the imminent risk of) complications such as obstruction or significant bleeding[ 33].

Nevertheless, the approach to patients with incurable CRC is extremely various, as two thirds of them undergo surgery in United States[ 63], whereas they are mostly non-operated on in the Netherlands[ 64]. Probably, several factors play a role in deciding to explore surgically (and to resect the tumor, if feasible) patients with such a dismal prognosis, including the belief/perception of prolonging survival, preventing complications, improving quality of life, and having a positive psychological effect on the patient[ 27].

Although the purpose of the paper is not technical, here we present a brief summary of the surgical procedures performed for palliation.

Non-resective procedures

Non-resective procedures performed for advanced CRC may be summarized in so-called "exploration" laparotomy/laparoscopy, stomas and internal by-passes.

Laparotomy/laparoscopy exploration: Usually performed in the midline, laparotomy is aimed to verify the correctness of preoperative CRC diagnosis/staging and to manage cancer. Not rarely, laparotomy is performed as the last "diagnostic tool" before renouncing to any other procedure[ 27, 28] and eventually results in the only surgical act performed (as the indication to surgery is not confirmed intraoperatively). Laparotomy may allow for intraoperative diagnostic procedures (such as US or biopsy of primary CRC, nodes or carcinosis) aimed to better define CRC stage/histology and further therapeutic strategy. Although, in these cases, laparotomy just addresses the first purpose of surgery (diagnosis/staging), nevertheless, it generally implies a general anaesthesia and an abdominal incision (port-site incisions for laparoscopy), which are not negligible acts in end-stage CRC patients. Since healing process may be poor in end-stage CRC, and neoplastic ascites may predispose to eventrations and early ventral hernias, the abdominal wall should be accurately closed plane by plane. In general, it should be reminded that any complication, even minor, may significantly affect the short residual life. Laparoscopy may be as effective as laparotomy[ 65] with better early outcome and less long-term complications[ 66, 67].

Stomas: Stomas are usually fashioned as "loop stomas" (one exception is after Hartmann procedure) by pulling the ileum or the colon through a full-thickness incision preferably passing through the rectum muscle. It is ideally placed at an adequate distance from the umbilicus, the superior iliac spine and the 10 th rib, where it carries the lesser risk of parastomal hernia/prolapsus and allows for the best postoperative management.

Differently from ileal stomas, that present the main drawback of high volume, very irritating, liquid stools, colonic stomas have the advantage of lower-volume, solid stools, are normally easier to manage postoperatively and have lower morbidity, thus representing the ideal solution for palliation[ 68]. Normally performed in the transverse colon or sigma, stoma fashioning may be preceded by laparoscopic exploration, which can facilitate the dissection of the chosen segment and the identification of the colostomy placement[ 69]. Whenever general anaesthesia is contraindicated, stomas may also be performed under spinal or loco-regional anaesthesia in the lower abdomen.

Internal by-passes: Internal by-passes are usually performed for colon cancer through laparotomy by manual (or partially mechanical) latero-lateral anastomosis between the ileum/colon proximal to obstructing tumor and the colon distal to tumor. Since colonic obstruction is normally associated to ileal and/or colonic distension, performing laparoscopically such an anastomosis should be considered a very demanding procedure and reserved to experienced laparoscopic surgeons[ 66].

Resective procedures

Nevertheless, the "safety rules" to perform a leakage-free anastomosis have to be respected. The vascularisation of the colonic remnant must be respected, and any manoeuvre aimed to avoid any tension at the anastomosis-site should be performed, including colonic dissection and inferior mesentery vein division, if needed. The anastomosis should be performed avoiding any contamination of the abdomen and abdominal wall, which should be adequately protected, since both neoplastic cell dissemination and infectious complications may occur.

Extended resections for CRC infiltrating contiguous organs, including anterior and posterior pelvic exenteration[ 72, 73], and hemicorporectomy[ 74] are not indicated in a palliative context anymore.

Transanal procedures are discussed in the paragraph dedicated to bleeding and other symptoms.

Strategy in surgical palliation: Several variables play a role in deciding the procedure, including patient's status, clinical scenario and setting, need/availability/timing of adjuvant treatments, R0 resectability of the primary CRC, site of primary CRC, attitude and beliefs of medical team. Importantly, if the non-resectability is due to distant metastasis, technical difficulty of resection is comparable to curative surgery, whereas, if the reason of non resectability is the primary, surgery may results in a very challenging situation. CRC site also influences the surgical strategy also concerning the type of surgery (resective vs non-resective). In fact, clinical impact and morbidity of CRC resection are generally considered to increase from proximal to distal, being maximum for the lower third of the rectum. Palliative ileocecal resection is considered a low-complexity, short-lasting procedure which may be accomplished even under spinal anaesthesia, thus reducing the stress of surgery. On the contrary, left-sided procedures are more time-consuming and associated to higher morbidity[ 75], including leakage and pelvic abscess[ 76].

Rectal cancer deserves a particular mention. Also owing to intrinsic technical difficulty and morbidity of surgery, and the fact that stoma is often necessary (thus cancelling one advantage of resection), deciding to perform a palliative resection of low rectal tumors should be carefully pondered. The resective options are: Hartmann procedure (HP), low anterior resection (LAR), and abdomino-perineal resection (APR). Since APR implies a perineal wound which is associated to healing complications in roughly one half of the patients[ 77], sphincter-preserving techniques are generally preferred. Differently from HP and APR, which imply a colostomy, this latter is not systematically performed after LAR for cancer of the upper rectum, whereas it is preferably fashioned (with protective purpose) after high-risk, "low" colorectal anastomosis. According to Fazio[ 78], in any case stoma is not avoided, the indication to resection should be carefully pondered against palliative stoma (without resection) whenever patient's supposed survival is not superior to 6 mo. For all these reasons, the general attitude is to be more aggressive for proximal tumors, and more oriented towards non-resective procedures for distal tumors.

CRC extirpation and survival: In patients presenting without significant clinical symptoms or emergency conditions, the main question is whether they may benefit from primary CRC resection or a less aggressive management should be preferred.

Since 1949[ 6], the debate as to the real effectiveness of palliative resection of primary CRC in prolonging survival has not given a definitive answer. Although, in the pre-CHT era, most authors[ 8, 47, 79, 80] described a 10.6-15 mo and 3.4-7 mo mean survival after resective and non-resective management, respectively, selection biases challenge the validity of those results, since non-resective procedures were mostly performed whenever resective surgery was not technically feasible or contraindicated by poor general conditions, thus resulting as being the only option allowed[ 6, 8, 29, 47, 79- 81]. In order to overcome such bias and answer the question regarding the indication to surgical resection when possible, our group selectively, although retrospectively, compared the overall survival of primitive CRC resection vs non-resective procedures in resectable patients, finding that resection was related to a 46% 1-year-survival ( vs 17%)[ 28].

Since the nineties, the massive introduction of CHT in this class of patients, and the development of more and more effective CHT regimens, has rekindled the debate regarding the indication to palliative surgery in patients already undergoing a potentially non-inferior, less aggressive management. Significantly, in their systematic review of papers comparing survival of patients undergoing the resection vs non-resection of the primary tumor, Verhoef et al[ 82] found that the resection of primary CRC was related to better prognosis in all papers including no (or very few) patients undergoing CHT[ 27, 47, 79], whereas results were more ambiguous in series including patients undergoing CHT, where resective surgery resulted as being related to survival in some papers[ 50, 83- 85] but not in others[ 48, 52, 53, 61, 70, 86]. Since then, other papers specifically addressing this issue (is CHT + resective surgery superior to CHT alone) somehow confirmed such an incertitude, concluding in favour[ 5] or against[ 62] the use of surgery in such a class of patients. In particular, our group[ 62] analysed the prognosis of four groups of patients selected by coupling type of surgery (resective/non-resective) and CHT policy (CHT/non-CHT); interestingly, resective surgery associated to CHT did not show any advantage over CHT alone in terms of survival. Since the results were confirmed in "technically" resectable patients, we concluded that, even when feasible, surgical resection is not indicated in asymptomatic patients. An ongoing randomized controlled multicenter trial (SYNCHRONOUS - ISRCTN30964555)[ 87] is now addressing the issue of short- and long-term outcome after the resection of the primary tumor vs no resection prior to systemic therapy in patients with colon cancer and synchronous unresectable metastases (UICC stage IV).

Differently from procedures achieving an R0 resection (no residual neoplastic tissue left after resection), leaving residual neoplastic tissue (R1, R2) is related to the same dismal prognosis as no resection[ 5]. Since, in this latter case, the patient should suffer the drawbacks of both major colonic resection (high morbidity) and non-operative management (short survival), the abstention from CRC resection should be strongly recommended whenever an R0 resection may not be achieved.

Several others criteria have been found to be related to a poor prognosis or poor surgical outcome, thus being considered to be arguments against major surgical resection. Major liver involvement[ 5, 8, 50, 86], otherwise described as extensive (bilobar) liver involvement[ 27], hepatic parenchymal replacement by tumor > 25%[ 88] or > 50%[ 47], and old age, variously intended as ≥ 65 years[ 27, 88], ≥ 70 years[ 3], ≥ 80 years[ 89], have been related to a poor survival and are currently proposed as a strong contraindication to major colonic surgery. Other parameters, including poor differentiation[ 5, 25], high serum levels of CEA[ 47, 88] or lactic dehydrogenase[ 85, 88] have been also related to poor outcome.

Perioperative mortality and morbidity: Higher perioperative mortality and morbidity of CRC resection represent the counterpart of a supposed longer survival. Such an issue may be supposed as being even underestimated, since an intrinsic distress due to major colonic surgery with respect of clinical observation is undeniable (although never measured) and may be supposed to significantly affect the residual life. Excluding emergency surgery, perioperative mortality for colonic resection for incurable CRC is reported to vary widely, ranging from 0% to 14%[ 5, 27, 47, 53, 59, 79, 90], and exceeding 8% in several studies[ 27, 47, 59, 90, 91]. Morbidity of elective resective surgery varies widely through series, too, ranging from 18% to 50%[ 27, 48, 53, 79, 85, 86].

Since 2000, laparoscopic surgery has been widely adopted in order to reduce the aggressiveness of surgery in incurable CRC patients[ 92- 99]. Although a minimally invasive approach may seem intuitively not the main issue in patients with dismal prognosis, on the contrary, a prompt recovery during the weeks following surgery may significantly improve the quality of residual life. As already observed in other fields of laparoscopy, a recent systematic review[ 56] found that laparoscopy allowed, in front of a prolonged operative time time (median 180.5 min vs 148 min), lesser blood loss (127.5 cc vs 180 cc) and a shorter hospital stay (9.3 d vs 15 d). Although only two of reviewed papers[ 96, 97] found a difference in postoperative complication-rate, the pooled odd ratio allowed the authors to report a significantly lower morbidity after laparoscopy (19.5% vs 26.9%), whereas mortality was the same[ 56]. Altered anatomy and tissues due to advanced CRC disease (and intrinsic technical limits of laparoscopy in dealing with them) represent a potential critical issue of laparoscopy, potentially increasing the rate of procedures "converted" to laparotomy, with the following significant reduction in the benefits of a mini-invasive approach. Interestingly enough, although in some cases it is reported to reach 26.5%[ 93], the median 13% conversion-to-laparotomy rate is consistent with the 14%-17% reported for "curable patients"[ 100, 101], thus confirming that laparoscopy may have a role in advanced CRC management.

Moreover, it should be considered that surgical resection of the primary CRC may affect the following management by modifying CHT administration schedule: on one hand, complications of surgery may lead to a delay in CHT administration, in some cases out of the "therapeutic window" of CHT after surgery (usually 4 to 6 wk), with the consequent potential impact on survival; on the other hand, in the case of an uneventful recovery after surgery, the patient may be supposed to avoid any primary CRC-related complication during CHT administration, when a suspension of CHT may lead to a reduced response and an emergency procedure may carry the highest perioperative risk. Pros and cons of operative and non-operative attitudes are difficult to assess, as they are likely to be related to the peculiar characteristics of the patient, tumor, and planned surgery.

Secondary surgery after CHT-induced "conversion" from non-resectable to resectable liver metastasis: Although curative management is not the aim of this review, nevertheless, the possibility to switch from a palliative context to a curative one is the most intriguing aspect of metastatic CRC management and will be briefly treated. Since, in 2004, Adam et al[ 20] first showed that the 5-year-survival rate of patients undergoing secondary resection was comparable to that of primary resection, resectability of liver meatastasis has become one of the purpose of new CHT agents. Since, liver metastasis resectability has been reported to increase to 30%-32% under doublet regimens (FOLFOX or FOLFIRI)[ 20, 103], to 36% under FOLFOXIRI[ 14], to 40% when bevacizumab is added to XELODA (oxaliplatin and capecitabine)[ 104]. Conversion rate of non-resectable, non-WT-KRAS patients was retrospectively reported to be as high as 60% when Cetuximab is added to FOLFIRI[ 105], but more recent randomized trials have reported a more realistic 16%-27.9% when Cetuximab is associated to FOLFOX/FOLFIRI/XELODA regimens[ 106, 107].

Finally, the improvement of liver surgery[ 20, 21] has allowed a 20%-64% morbidity and 0%-2% mortality of secondary resection of CRC metastasis on post-CHT liver, which is comparable to those achieved after primary surgery. Significantly, 5-year-survival of patients undergoing secondary liver surgery after downstaging is comparable, although not the same, to that of primary surgery of resectable disease (33% vs 46%) according to an international database[ 22], although very wide ranges of 5 years survival (33%-50%), disease-free survival (8.7-17 mo) and overall survival (36-60 mo) are reported in the literature following various CHT regimens[ 21].

Role of chemotherapy

Medical treatment for colon cancer has been radically modified in its aims and modalities in the last 30 years: the dramatic evolution of researches and discoveries in this field led to significant improvements on overall survival (OS) (Figure ) and strongly modified the concept of curability of the disease.

From the eighties to the nineties, with studies on fluoropyrimidines, some steps have been made towards a chemotherapeutic regimen active in advanced CRC[ 9, 108- 111]. These trials analyzed the use of infusional or bolus 5-fluorouracil (5-FU) combined with folinic acid (FA) or levamisole, with different modulations; the results showed an enhanced effectiveness of 5-FU when combined with high-dose folinic acid, finally identifying a bimonthly schedule with continuous infusion of 5-FU after bolus as the more effective and less toxic schedule[ 111]. The same trials showed an overall response rates (RR) of 39%-54.1% with a median overall survival (mOS) of 12-18 mo and a progression free survival (PFS) of 14.5 mo[ 9, 108- 111]. A further trial showed the equivalence between oral 5-FU (capecitabine) and infusional 5-FU[ 112]. During this long period of time, chemotherapy was considered as a palliative treatment and was administered only when surgery was no longer possible due to the presence of locally advanced or metastatic disease.

After years of attempts and modulation of approaches with fluoropyrimidines, a turning point was determined by the introduction of new drugs to be administered in association. The exploration of the activity of chemotherapeutic doublets with irinotecan and 5-FU was performed since the early 2000s in large randomized phase III trials[ 10, 113- 115], establishing a new survival standard for metastatic CRC. Douillard et al[ 113] and Saltz et al[ 10, 114] showed the superiority of FOLFIRI regimen compared to 5-FU bolus plus FA[ 10, 113] and to irinotecan alone[ 114] in terms of PFS and OS. Saltz et al[ 114] reported a PFS of 7 mo and a mOS of 14.8 mo (ORR = 39%), whereas, similarly, Douillard et al[ 113] obtained a TTP of 6.7 mo, an OS of 17.4 mo and an ORR of 35% and Fuchs et al[ 115] reported a PFS of 7.6 mo and a mOS of 23.1 mo.

In 2007, Falcone et al[ 14] first compared the association of 5-FU, irinotecan and oxaliplatin (FOLFOXIRI) with FOLFIRI, showing an increased RR (66% vs 41%), PFS (9.8 mo vs 6.9 mo) and OS (22.6 mo vs 16.7 mo), in spite of a slightly increased toxicity (mostly neurotoxicity, neutropenia and diarrhea). Interestingly, a significantly higher number of patients undergoing FOLFOXIRI regimen underwent secondary resection of pre-treatment non-resectable liver metastasis (36% vs 12%). Such a study represented a turning point, suggesting this regimen as a valid option to improve the outcome of a selected group of patients with good performance status, also by converting metastatic disease from non-operable to operable.

From target to tailored therapy: In the last decade, the intrinsic and acquired resistance of metastatic colon cancer to chemotherapy, on one hand, and the evolution of target identification through translational medicine, on the other, are paving the road to patient-tailored therapy for metastatic CRC, aiming to cure patients basing on the complex interactions among patient's characteristics, disease physiopathology and drugs' metabolism.

The understanding of biological mechanisms at the basis of the disease and the discovery of molecular pathways leading to CRC progression have led to the development of new targeted drugs against CRC. In particular, bevacizumab (a humanized antibody anti-circulating vascular endothelial growth factor - VEGF-A) and cetuximab (a recombinant antibody anti- epidermal growth factor receptor - EGFR) have been introduced in advanced CRC in association with poli-chemotherapic regimens. The first performed trials evidenced statistically significant and clinically meaningful improvement in terms of OS, PFS and RR, by adding bevacizumab to oxaliplatin- or irinotecan-based regimens with an easily manageable additional toxicity[ 15, 120, 121]. Hurwitz et al[ 15] first studied the association of bevacizumab with 5-FU bolus with FA ( vs 5-FU bolus with FA alone), showing an increase in RR (44.8% vs 34.8%), PFS (10.6 vs 6.2) and mOS (20.3 mo vs 15.6 mo). Saltz et al[ 120] also showed an increase of PFS following the administration of bevacizumab in patients receiving FOLFOX.

Since 2009, the association of cetuximab with FOLFIRI[ 12] or with FOLFOX regimens[ 122] was reported to increase PFS whereas the increase of OS did not reach statistical significance in metastatic colon cancer. More recently, the OPUS study[ 106] showed that the benefit was limited to patients with KRAS wild-type (WT) tumors, confirming KRAS mutation status as a predictive biomarker. This latter result was confirmed by a pooled analysis[ 123], which also reported a significant improvement in OS (HR = 0.81; P = 0.0062), PFS (HR = 0.66; P < 0.001) and ORR (OR = 2.16; P < 0.0001). Some new evidence in favour of cetuximab in a prospectively selected series of WT-KRAS patients emerged from a very recent study presented at the American Society of Clinical Oncology 2013 Annual Meeting[ 13]. From this large trial, the combination of cetuximab and FOLFIRI resulted more effective than the combination of bevacizumab and FOLFIRI in a population of WT-KRAS metastatic colon cancer patients, both considering ORR and OS (28.7 mo vs 25 mo).

An alternative agent proposed in the first line therapy for WT-KRAS patients is panitumubab[ 107], which has been observed to prolong overall survival from 20.2 mo in the FOLFOX4-alone group to 26.0 mo in the panitumumab-FOLFOX4 group.

Future development and open issues: New agents have already showed promising results after the failure of conventional CHT. Aflibercept[ 124], a soluble fusion protein with high affinity for VEGF-A, -B and PlGF, has been associated to a 1.5-mo-increase of OS after first line FOLFIRI. Regorafenib[ 125], a multi Tyrosin Kynase Inhibitor (TKI), in association with FOLFIRI has been found to prolong survival by 1.4 mo in heavily treated patients: trials are ongoing to identify the best management of these drugs.

The extensive study of genoma in CRC is ongoing. Several genes, including BRAF[ 101], NRAS[ 126], PI3K[ 126, 127], MEK 1/2[ 127] and PTEN[ 128] are currently studied as their mutation seems to be related to poor prognosis in CRC patients undergoing CHT. New agents, including pimasertib, have been evaluated by preclinical studies, showing promising results[ 127].

As a natural consequence of the recent trend towards multifaceted treatment and patient-tailoring, different strategies and sequencing of chemotherapy have been explored in the advanced disease. "Treatment until progression or unacceptable toxicity" has been the standard practice until now, but a new approach is challenging this paradigm[ 129], proposing to temporarily quit CHT administration until clear progression, with no difference in terms of OS and better quality of life.

The encouraging and continuously improving results of CHT in advanced CRC management has led to extend its use to earlier CRC classes, including stage III[ 130] and, more recently, stage II[ 131, 132], in accordance with the hypothesis that recurrence was likely to be due to residual cancer existing at microscopic stage. Since 1990, Moertel et al[ 130] reported an overall recurrence rate reduction of 41%, establishing infusional 5-FU and FA as the new standard of care for adjuvant CRC therapy, thus hypothesizing that CRC was a more chemosensitive disease than previously thought. In 2004 the MOSAIC trial[ 131], recently updated[ 132], showed an increase of 5-year DFS rates (from 67.4% to 73.3%) and 6-year OS rates (from 76% to 78.5%) when oxaliplatin is added (bolus + infusional) to 5-FU (FOLFOX) in resected stage III colon cancer. Those encouraging results in stage III CRC seem to suggest a similar benefit of fluorouracil-based adjuvant chemotherapy in Stage II, high risk patients (T4, < 12 lymph nodes harvested, emergency setting)[ 132, 133], whereas targeted therapy seems useless in this setting[ 134].

EMERGENCY/SEVERELY SYMPTOMATIC CRC

The most commonly reported life-threatening complications of advanced CRC are obstruction and perforation[ 27, 51], but also bleeding and other minor symptoms will be discussed. Indeed, unless the patient presents the typical features of acute obstruction or acute diffuse peritonitis by colonic perforation, it is often difficult to assess the real threaten to life and consequently the real need and timing of emergency surgery in the case of patients with a very limited life expectancy. Therefore, it is difficult to make any generalization and any patient should be evaluated on a case by case basis. Moreover, data from literature are extremely debatable and non-concordant, as study series are non-homogeneous concerning patients, tumors and management; nevertheless, for practical reasons, those conditions are discussed separately.

Obstruction

Surgery: Even more than in asymptomatic patients, the main issue of incurable CRC resection performed for colic obstruction, is not a complete lymphadenectomy, but removing the obstruction as soon as possible not causing any colonic leak in order to avoid any dissemination of neoplastic cells and infectious complications. The choice of derivative surgery also depends on tumor characteristics and location indeed, being any internal by-pass non possible for tumors arising distally to the sigmoid colon. Resective surgery is usually preferred in proximal CRC, where colostomy is not an option and internal by pass by ileo-colonic (transverse or sigmoid) anastomosis is performed for locally infiltrating tumors or carcinosis. For obstructing distal tumors, the choice between CRC resection and stoma (usually in the sigmoid/transverse colon) is more challenging (see above).

In some cases, colonic obstruction distal to the cecum usually causes a distension of the cecum itself (according to the law of Laplace), which may be increased by the continence of the ileo-cecal valve: in such a case, a concomitant ischemia/perforation of the proximal colon due to distension may occur and require multiple/extensive colonic resections or stomas. Although CRC palliative resection performed in such a setting implies the highest mortality (up to 18%[ 47, 51, 59, 79, 90, 91]), it is often the option preferred by the surgeon especially in presence of a concomitant perforation and consequent pericolonic abscess/stercoral peritonitis (see below).

Stenting: Since the mid-90s, self-expanding metallic stents have shown to be more effective than other treatments (argon laser, plastic stent) and have been proposed in the management of colorectal stenosis in order to avoid emergency surgery[ 141]. Since then, stent use has been proposed with three purposes: (1) allowing a delayed, elective (rather than emergency) colonic resection in the case of "curable CRC patients"; (2) allowing a definitive, palliative solution for "non-curable patients"; and (3) avoiding a stoma. Modern self-expandable metallic stents are conceived to be incorporated into the tumor by exercising a pressure and inducing a partial necrosis in surrounding neoplastic tissue. In order to anchor the stent and to prevent any migration, colonic stents are usually clepsydra-shaped and may have various diameters and length in order to fit any neoplastic stricture. The reported rate of successful positioning of the stent is 75%-98%[ 137, 142- 146], being the main cause of failure the impossibility to pass a guidewire through the tumor, whereas the effectiveness in relieving a neoplastic obstruction is as high as 93.1%-98.7%[ 143- 145].

Short-term complications are reported up to 14.8%[ 143] of cases, with a median perioperative perforation rate of 3.9%-4.5%[ 137, 138]. Although not the most frequent, perforation is the most relevant, since it could give rise to a life-threatening acute peritonitis, with a 20%-100% mortality[ 138, 144]. Moreover, perforation may cause the transcelomatic diffusion of CRC by dissemination of neoplastic cells[ 143]. According to clinical picture and entity of perforation, the management of such complication include surgery (stoma, resection) unless contraindicated by prohibitive general conditions. Other common perioperative complications are stent migration/occlusion (1.8%-9%), and bleeding (0.5%-4%), normally managed endoscopically by stent replacement and hemostasis[ 138, 143].

Long-term morbidity of palliative stents may exceed 40%[ 143, 144, 146], with a rehospitalisation rate of 34%, and include bleeding (21%[ 143]) stent migration (12.5%-22%[ 143, 144]) or occlusion (9.4%-17%[ 137, 143, 144]), whereas perforation is 3%-7%[ 143, 144]. Late stent occlusion is usually due to cancer progression and colonization of stent neo-lumen, and therefore is manageable endoscopically and suitable of re-stenting or laser ablation. Abdominal pain and tenesmus are also observed both perioperatively and as a late complication, and are generally managed conservatively[ 138, 143, 144].

When compared to palliative, emergency surgery, CRC stenting has showed a lesser perioperative mortality (0%-4.2% vs 5%-10.5%), lower perioperative morbidity, shorter hospital stay (9.5-10 d vs 15-18.8 d)[ 137, 143, 145] and lower rate of stoma formation (54% vs 12.7%)[ 145]. Nevertheless, it should be remarked that every fifth patient undergoing palliative stenting finally needs some other reintervention, including re-stenting, laser ablation or colonic surgery[ 137, 146]. Although encouraging, the retrospective nature of present literature on the subject prevents from definitive conclusions. Significantly, a high rate of severe complications following stage IV CRC stenting led to the early closure of a multicenter trial[ 147].

Although it may be considered a fine mini-invasive, low morbidity option for patients with limited life expectancy, nevertheless, stents' use still has some open issues to be addressed. First, the success rate and morbidity of stenting seems to be different between the sigmoid-rectum and the remaining colon, where the intraperitoneal location and anatomic variability may be supposed to cause lower success rate and higher morbidity, including perforation[ 143]. The fact that, in their extended review of patients treated by stenting, Watt et al[ 137] found only 2% and 1% with transverse and right-sided CRCs, somehow confirms a more common use for left tumors. If we add that, owing to technical reasons, it may be difficult or impossible to stent low rectum cancers approaching to the anus, we can deduce that a not negligible part of CRCs are not suitable for stenting. Second, the long-term effectiveness of CRC stenting still have to be confirmed on a long-term basis. Stent-patency has generally been evaluated within few mo from positioning, whereas its median duration is three and half mo (106 d)[ 137]. Indeed, in pre-CHT era, the short life expectancy of advanced CRC led to consider stent positioning an effective, definitive palliation[ 48], allowing the prompt start of CHT. Nowadays, the reported long survival associated to new CHT regimens, rekindle the debate about long-term effectiveness of stents, which are also associated with a high late morbidity, also exceeding 40%[ 143] or even 50%[ 144]. Significantly, a recent meta-analysis[ 145] shows how the early morbidity rate is significantly higher after surgery (13.7% vs 33.7%) whereas late complications are more frequent after stenting (32.35% vs 12.7%). Such long-term results of stents prompt a double dilemma: (1) should palliative surgical resection to be preferred to stent, at least in supposed long-survivors[ 146] and (2) should elective palliative surgery be considered after successful stenting, or should simple observation be preferred This latter hypothesis may become even more interesting if we consider that emergency (rather than elective) surgery notably carries higher colostomy rates and that rates of primary anastomosis after elective surgery following stenting are at least twice that of those after emergency surgery[ 137]. The recent development of a sequential management of obstructing CRC by "bridge stenting" followed by laparoscopic colonic resection[ 148, 149] may be considered as a feasible mini-invasive option somehow fitting the need of advanced CRC patients.

Last but not least, the positive psychological effect of not having a temporary or permanent colostomy is another positive effect of stent positioning[ 150].

Laser therapy and endocavitary radiation: Initially proposed for small polyps, bleeding[ 151] and palliation[ 152] in the late 70s, Neodymium yttrium-aluminum-garnet (Nd:YAG) laser therapy (also called high-powered diode laser therapy) is decreasingly proposed for the palliative treatment of obstructing rectal cancer (by vaporizing neoplastic tissue) and bleeding (by inducing coagulative necrosis) in patients unfit for surgery. Laser therapy normally needs up to 5 session to be effective and has a 78%-91% success rate in treating obstruction[ 139, 140]. A 2%-5.3%[ 138- 140] morbidity and 1.8% mortality[ 140] have been reported, being colonic perforation the most feared complication. Somehow accordingly, lower morbidity and no mortality are observed when only rectal tumors are examined[ 139]. Some concern has been expressed about long-term results of palliation, since obstruction is reported to recur at a median of 24 wk after initial treatment, thus requiring delayed surgical palliation[ 139]. Such a consideration may gain interest in the light of long-survival recently observed with last generation CHT.

Perforation

Colonic perforation is mostly a potential life-threatening condition requiring emergency surgery. The mechanism of perforation in advanced CRC includes tumor necrosis[ 48, 156, 157], colonic (usually cecum) distension secondary to obstruction by distal CRC[ 156, 157], other treatment complications, including stenting[ 143, 144], laser therapy[ 139, 140], transanal resection[ 158, 159]. Such a complication has a significant mortality rate[ 138, 140, 143, 156, 157]. Indeed, colonic perforation may present with a wide variety of clinical scenarios, ranging from ongoing acute stercoral peritonitis to more ambiguous clinical pictures, whenever the perforation is limited or "covered"[ 156, 157]. Although symptoms and management vary widely, also owing to site and mechanism of perforation, here we describe such two extreme scenarios. In general, sudden onset abdominal pain is a key-symptom, and should be investigated in any patient with advanced CRC even in the absence of signs of acute peritonitis or hyperpyrexia. CT scan is mandatory, possibly associated with contrast mean rectal administration, unless plane X-rays has already shown "free" intra-abdominal air.

Surgery: Colonic perforation may occur as "free" perforation causing an acute, diffuse stercoral peritonitis, which is normally associated with symptoms of generalized sepsis. Such a picture needs emergency surgery by laparotomy. Obviously, the main purpose of surgery for colonic perforation is not avoiding colonic leak, since stools have already diffused in the abdomen, nor performing an oncologically complete lymphadenectomy. In the case of perforation, surgeon's first concern is removing the cause of acute peritonitis by resecting the perforated segment and cleaning the abdomen by lavage. It should not be forgotten that obstruction by CRC may turn into acute peritonitis by perforation of proximal colon (usually the caecum) following long-term distension[ 156, 157]. Moreover, performing an anastomosis after the resection of perforated CRC in a generalized peritonitis context carries a high risk of postoperative leakage, and deciding to perform a temporary stoma is often the preferred option. Alternatively, the anastomosis may be fashioned together with a so-called "protective", proximal loop stoma. As this option normally implies a second surgery in order to close the stoma, it is rarely performed in a palliative setting (potential "long-survivors").

In some cases, colonic perforation is small-sized or "covered" by other organs or perirectal fat, thus stools spilling results as being limited. In such cases, signs/symptoms of acute peritonitis may be localized, reduced or even absent, if the perforation site is deep in the abdomen or in the under-peritoneal rectum. In the absence of deteriorating septic state, perforation may be managed by conservative treatment (including antibiotics) and/or derivative procedures (stomas) rather than major resections. Perforations resulting in localized abscesses may also be managed by surgical drainage of the collection or US- or CT-scan guided procedure. Obviously, high ASA score patients or short-survivors may be supposed to benefit most by such a low mini-invasive attitude.

Bleeding and other invalidating symptoms (pain, tenesmus)

Although usually it is not an emergency situation, bleeding may represent a major issue of advanced CRC, especially in patients needing anticoagulant/antiaggregant therapy for any reason. Pain and tenesmus are typical symptoms of rectal tumors but are rarely treated by surgical resection, since they are usually associated to a locally infiltrating, already non resectable rectal cancer. If we consider that those symptoms are also reported to reduce under CHT[ 160, 161], we can understand why they are usually managed conservatively by radiotherapy or transanal procedures.

Surgery: Resective surgery, obviously allows definitively treating chronic haemorrhage and other CRC -related symptoms by extirpation of tumor. The pros, cons and timing of resective surgery need to be discussed with the patient and in multidisciplinary meeting. Surgery intrinsic morbidity/mortality[ 27, 47, 59, 90, 91] and the possible spontaneous reduction of non-emergency symptoms owing to CRC response to CHT[ 55, 160, 161] should be balanced with the risk of performing a late, possibly emergency procedure after CHT has started, when it may carry the highest risk of complications. As reported before, resection is generally proposed for proximal tumors, whereas it is attentively pondered for rectal tumors (see above for surgical options).

Radiotherapy (RT): RT is one of the mostly adopted treatment for rectal bleeding and other invalidating symptoms. Although it is reported to relief in particular pain and bleeding in 75%-80% of patients[ 162, 163], unfortunately, the results of studies are difficult to compare, as RT is often part of a multimodal treatment including surgery and CHT, patients are heterogeneous as well as administered RT doses, varying from 10 to 80 Gy[ 162, 163]. Bae et al[ 162], analysing a series of patients with advanced symptomatic (mostly pain and bleeding) CRC undergoing various managements, including surgery, CHT and RT, found the association between CT and RT to be significantly associated to symptoms' control[ 162]. The main limitations of RT is the recurrence of symptoms in roughly one half of the patients within 6 mo[ 59, 162]; thus, it is best indicated in short survivors[ 59].

Laser therapy: Success rate of Nd:YAG laser (see above for general principles of endoscopic laser treatment) in managing rectal bleeding is 73%-97%[ 140, 151, 164]. Since the median symptom-free survival after the procedure(s) is 10 mo[ 164], its effectiveness in long-survivors is also questionable.

Transanal resection techniques: Various techniques for transanal resection have been proposed for the palliative treatment of symptomatic rectal cancer, including endoscopic transanal resection (ETAR)[ 156, 165- 167] and transanal endoscopic microsurgery (TEM)[ 159].

Performed since the early 1990s with various approaches, ETAR consists in the endorectal management of rectal tumor complications by several manoeuvres, including tumor resection/debulking and haemostasis. ETAR is reported to have a 73%-87% overall success rate in achieving symptoms relief[ 165, 166], with a specific 50% success rate for incontinence, rectal pain and tenesmus, 66% for bleeding and 77% for diarrhoea[ 167]. Chen et al[ 156] found ETAR to be related to the same long term outcome as traditional surgery (LAR/APR) with lower morbidity (4% vs 24%), although others reported an higher 8%-17% complication rate[ 165, 166]. Such low morbidity and a 15%-23% rate of colostomy finally performed[ 156, 165, 166] led to consider ETAR as a feasible option in palliative management of rectal cancer.

More recently introduced[ 168], TEM implies the full-thickness resection of the rectum including the perirectal mesorectum until reaching the recto-vaginal septum or the prostate capsule (anteriorly) or the mesorectal fascia posteriorly, followed by rectum closure. Although it is nowadays mostly reported for the management of T1-T2 rectal tumors[ 158, 169], TEM has been also proposed for the palliative management of advanced rectal tumors[ 159, 170]. Overrall, a 6.3%-21% morbidity is reported (mostly due to urinary retention) with a 2.3%-5% rate of severe complications requiring management[ 158, 159, 170].

Argon plasma coagulation: Initially proposed as complementary to endoscopic piecemeal resection of sessile rectal polyps in order to reduce recurrence[ 171], argon plasma coagulation (APC) has also a coagulative effect and has been proposed in the mid-2000s for the treatment of low entity haemorrhage[ 172]. The argon ionized by electrodes determines an effective but superficial fulguration of neoplastic tissue (normally less than 3 mm in depth). Also owing to the limited penetration in neoplastic tissue, complications including colonic perforation, are presumably lower than that reported after Nd:YAG laser[ 55].

All non-resective procedures (radiotherapy, laser therapy, APC and transanal procedures) should not be considered as excluding each other, but as multiple options to be used whenever other managements have failed.

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Palliative care and end-stage colorectal cancer management: The surgeon meets the oncologist

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Colorectal cancer (CRC) is the third most common cancer (estimated 1.23 million cases per year) and the fourth cancer-related cause of death (609 thousands deaths per year) in world population[ 1]. Ten-fold differences in incidence between the different regions of the world, being the highest in Australia, Western Europe and North America, are reported[ 1].

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How common is colorectal cancer?

Excluding skin cancers, colorectal cancer is the third most common cancer diagnosed in both men and women in the United States. The American Cancer Society's estimates for the number of colorectal cancer cases in the United States for 2021 are:

104,270 new cases of colon cancer

45,230 new cases of rectal cancer

The rate of people being diagnosed with colon or rectal cancer each year has dropped overall since the mid-1980s, mainly because more people are getting screened and changing their lifestyle-related risk factors. From 2013 to 2017, incidence rates dropped by about 1% each year. But this downward trend is mostly in older adults and masks rising incidence among younger adults since at least the mid-1990s. From 2012 through 2016, it increased every year by 2% in people younger than 50 and 1% in people 50 to 64.

Lifetime risk of colorectal cancer

Overall, the lifetime risk of developing colorectal cancer is: about 1 in 23 (4.3%) for men and 1 in 25 (4.0%) for women. A number of other factors (described in Colorectal Cancer Risk Factors) can also affect your risk for developing colorectal cancer.

Deaths from colorectal cancer

In the United States, colorectal cancer is the third leading cause of cancer-related deaths in men and in women, and the second most common cause of cancer deaths when men and women are combined. It's expected to cause about 52,980 deaths during 2021.

The death rate (the number of deaths per 100,000 people per year) from colorectal cancer has been dropping in both men and women for several decades. There are a number of likely reasons for this. One reason is that colorectal polyps are now being found more often by screening and removed before they can develop into cancers, or cancers are being found earlier when they are easier to treat. In addition, treatments for colorectal cancer have improved over the last few decades. As a result, there are now more than 1.5 million survivors of colorectal cancer in the United States. Although the overall death rate has continued to drop, deaths from colorectal cancer among people younger than 55 have increased 1% per year from 2008 to 2017.

Statistics related to survival among people with colorectal cancer are discussed in Survival Rates for Colorectal Cancer.
Visit the American Cancer Society's Cancer Statistics Center for more key statistics.

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Colorectal Cancer Statistics | How Common Is Colorectal Cancer?

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Excluding skin cancers, colorectal cancer is the third most common cancer diagnosed in both men and women in the United States.

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On This Page

Key Points

Colon cancer is a disease in which malignant (cancer) cells form in the tissues of the colon.

Health history affects the risk of developing colon cancer.

Signs of colon cancer include blood in the stool or a change in bowel habits.

Tests that examine the colon and rectum are used to diagnose colon cancer.

Certain factors affect prognosis (chance of recovery) and treatment options.

Colon cancer is a disease in which malignant (cancer) cells form in the tissues of the colon.

The colon is part of the body's digestive system. The digestive system removes and processes nutrients ( vitamins, minerals, carbohydrates, fats, proteins, and water) from foods and helps pass waste material out of the body. The digestive system is made up of the esophagus, stomach, and the small and large intestines. The colon (large bowel) is the main part of the large intestine and is about 5 feet long. Together, the rectum and anal canal make up the last part of the large intestine and are about 6-8 inches long. The anal canal ends at the anus (the opening of the large intestine to the outside of the body).

Gastrointestinal stromal tumors can occur in the colon. See the PDQ summary on Gastrointestinal Stromal Tumors Treatment (Adult) for more information.

See the PDQ summary about Childhood Colorectal Cancer Treatment for information about colorectal cancer in children.

Health history affects the risk of developing colon cancer.

Anything that increases your chance of getting a disease is called a risk factor. Having a risk factor does not mean that you will get cancer; not having risk factors doesn't mean that you will not get cancer. Talk to your doctor if you think you may be at risk for colorectal cancer.

Risk factors for colorectal cancer include the following:

Older age is a main risk factor for most cancers. The chance of getting cancer increases as you get older.

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Signs of colon cancer include blood in the stool or a change in bowel habits.

These and other signs and symptoms may be caused by colon cancer or by other conditions. Check with your doctor if you have any of the following:

A change in bowel habits.

Blood (either bright red or very dark) in thestool.

Diarrhea, constipation, or feeling that the bowel does not empty all the way.

Stools that are narrower than usual.

Frequent gas pains, bloating, fullness, or cramps.

Weight loss for no known reason.

Feeling very tired.

Vomiting.

Tests that examine the colon and rectum are used to diagnose colon cancer.

The following tests and procedures may be used:

Certain factors affect prognosis (chance of recovery) and treatment options.

The prognosis and treatment options depend on the following:

The stage of the cancer (whether the cancer is in the inner lining of the colon only or has spread through the colon wall, or has spread tolymph nodes or other places in the body).

Whether the cancer has blocked or made a hole in the colon.

Whether there are any cancer cells left after surgery.

Whether the cancer has recurred.

The patient's general health.

The prognosis also depends on the blood levels of carcinoembryonic antigen (CEA) before treatment begins. CEA is a substance in the blood that may be increased when cancer is present.

Key Points

After colon cancer has been diagnosed, tests are done to find out if cancer cells have spread within the colon or to other parts of the body.

There are three ways that cancer spreads in the body.

Cancer may spread from where it began to other parts of the body.

The following stages are used for colon cancer:

Stage 0 (Carcinoma in Situ)

Stage I

Stage II

Stage III

Stage IV

Sometimes colon cancer recurs (comes back) after treatment.

After colon cancer has been diagnosed, tests are done to find out if cancer cells have spread within the colon or to other parts of the body.

The process used to find out if cancer has spread within the colon or to other parts of the body is called staging. The information gathered from the staging process determines the stage of the disease. It is important to know the stage in order to plan treatment.

The following tests and procedures may be used in the staging process:

CT scan (CAT scan): A procedure that makes a series of detailed pictures of areas inside the body, such as the abdomen, pelvis, or chest, taken from different angles. The pictures are made by a computer linked to an x-ray machine. A dye may be injected into a vein or swallowed to help the organs or tissues show up more clearly. This procedure is also called computed tomography, computerized tomography, or computerized axial tomography.

MRI (magnetic resonance imaging): A procedure that uses a magnet, radio waves, and a computer to make a series of detailed pictures of areas inside the colon. A substance called gadolinium is injected into the patient through a vein. The gadolinium collects around the cancer cells so they show up brighter in the picture. This procedure is also called nuclear magnetic resonance imaging (NMRI).

PET scan (positron emission tomography scan): A procedure to find malignant tumor cells in the body. A small amount of radioactive glucose (sugar) is injected into a vein. The PET scanner rotates around the body and makes a picture of where glucose is being used in the body. Malignant tumor cells show up brighter in the picture because they are more active and take up more glucose than normal cells do.

Chest x-ray: An x-ray of the organs and bones inside the chest. An x-ray is a type of energy beam that can go through the body and onto film, making a picture of areas inside the body.

Surgery: A procedure to remove the tumor and see how far it has spread through the colon.

Lymph node biopsy: The removal of all or part of a lymph node. A pathologist views the lymph node tissue under a microscope to check for cancer cells. This may be done during surgery or by endoscopic ultrasound-guided fine needle aspiration biopsy.

Complete blood count (CBC): A procedure in which a sample of blood is drawn and checked for the following:

Carcinoembryonic antigen (CEA) assay: A test that measures the level of CEA in the blood. CEA is released into the bloodstream from both cancer cells and normal cells. When found in higher than normal amounts, it can be a sign of colon cancer or other conditions.

There are three ways that cancer spreads in the body.

Cancer can spread through tissue, the lymph system, and the blood:

Tissue. The cancer spreads from where it began by growing into nearby areas.

Lymph system. The cancer spreads from where it began by getting into the lymph system. The cancer travels through the lymph vessels to other parts of the body.

Blood. The cancer spreads from where it began by getting into the blood. The cancer travels through the blood vessels to other parts of the body.

Cancer may spread from where it began to other parts of the body.

When cancer spreads to another part of the body, it is called metastasis. Cancer cells break away from where they began (the primary tumor) and travel through the lymph system or blood.

Lymph system. The cancer gets into the lymph system, travels through the lymph vessels, and forms a tumor (metastatic tumor) in another part of the body.

Blood. The cancer gets into the blood, travels through the blood vessels, and forms a tumor (metastatic tumor) in another part of the body.

The metastatic tumor is the same type of cancer as the primary tumor. For example, if colon cancer spreads to the lung, the cancer cells in the lung are actually colon cancer cells. The disease is metastatic colon cancer, not lung cancer.

The following stages are used for colon cancer:

Stage 0 (Carcinoma in Situ)

In stage 0, abnormal cells are found in the mucosa (innermost layer) of the colon wall. These abnormal cells may become cancer and spread into nearby normal tissue. Stage 0 is also called carcinoma in situ.

Stage I

In stage I colon cancer, cancer has formed in the mucosa (innermost layer) of the colon wall and has spread to the submucosa (layer of tissue next to the mucosa) or to the muscle layer of the colon wall.

Stage II

Stage II colon cancer is divided into stages IIA, IIB, and IIC.

Stage IIA: Cancer has spread through the muscle layer of the colon wall to the serosa (outermost layer) of the colon wall.

Stage IIC: Cancer has spread through the serosa (outermost layer) of the colon wall to nearby organs.

Stage III

Stage III colon cancer is divided into stages IIIA, IIIB, and IIIC.

In stage IIIA, cancer has spread:

through the mucosa (innermost layer) of the colon wall to the submucosa (layer of tissue next to the mucosa) or to the muscle layer of the colon wall. Cancer has spread to one to three nearby lymph nodes or cancer cells have formed in tissue near the lymph nodes; or

through the mucosa (innermost layer) of the colon wall to the submucosa (layer of tissue next to the mucosa). Cancer has spread to four to six nearby lymph nodes.

In stage IIIB, cancer has spread:

through the muscle layer of the colon wall to the serosa (outermost layer) of the colon wall or has spread through the serosa to the tissue that lines the organs in the abdomen (visceral peritoneum). Cancer has spread to one to three nearby lymph nodes or cancer cells have formed in tissue near the lymph nodes; or

to the muscle layer or to the serosa (outermost layer) of the colon wall. Cancer has spread to four to six nearby lymph nodes; or

through the mucosa (innermost layer) of the colon wall to the submucosa (layer of tissue next to the mucosa) or to the muscle layer of the colon wall. Cancer has spread to seven or more nearby lymph nodes.

In stage IIIC, cancer has spread:

through the muscle layer of the colon wall to the serosa (outermost layer) of the colon wall or has spread through the serosa to the tissue that lines the organs in the abdomen (visceral peritoneum). Cancer has spread to seven or more nearby lymph nodes; or

through the serosa (outermost layer) of the colon wall to nearby organs. Cancer has spread to one or more nearby lymph nodes or cancer cells have formed in tissue near the lymph nodes.

Stage IV

Stage IV colon cancer is divided into stages IVA, IVB, and IVC.

Sometimes colon cancer recurs (comes back) after treatment.

Colon cancer may come back in the colon or in other parts of the body, such as the liver, lungs, or both.

Key Points

There are different types of treatment for patients with colon cancer.

Seven types of standard treatment are used:

Surgery

Radiofrequency ablation

Cryosurgery

Chemotherapy

Radiation therapy

Targeted therapy

Immunotherapy

New types of treatment are being tested in clinical trials.

Treatment for colon cancer may cause side effects.

Patients may want to think about taking part in a clinical trial.

Patients can enter clinical trials before, during, or after starting their cancer treatment.

Follow-up tests may be needed.

There are different types of treatment for patients with colon cancer.

Different types of treatment are available for patients with colon cancer. Some treatments are standard (the currently used treatment), and some are being tested in clinical trials. A treatment clinical trial is a research study meant to help improve current treatments or obtain information on new treatments for patients with cancer. When clinical trials show that a new treatment is better than the standard treatment, the new treatment may become the standard treatment. Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.

Seven types of standard treatment are used:

Surgery

Surgery (removing the cancer in an operation) is the most common treatment for all stages of colon cancer. A doctor may remove the cancer using one of the following types of surgery:

After the doctor removes all the cancer that can be seen at the time of the surgery, some patients may be given chemotherapy or radiation therapy after surgery to kill any cancer cells that are left. Treatment given after the surgery, to lower the risk that the cancer will come back, is called adjuvant therapy.

Radiofrequency ablation

Radiofrequency ablation is the use of a special probe with tiny electrodes that kill cancer cells. Sometimes the probe is inserted directly through the skin and only local anesthesia is needed. In other cases, the probe is inserted through an incision in the abdomen. This is done in the hospital with general anesthesia.

Cryosurgery

Cryosurgery is a treatment that uses an instrument to freeze and destroy abnormal tissue. This type of treatment is also called cryotherapy.

Chemotherapy

Chemotherapy is a cancer treatment that uses drugs to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. When chemotherapy is taken by mouth or injected into a vein or muscle, the drugs enter the bloodstream and can reach cancer cells throughout the body ( systemic chemotherapy). When chemotherapy is placed directly into the cerebrospinal fluid, an organ, or a body cavity such as the abdomen, the drugs mainly affect cancer cells in those areas ( regional chemotherapy).

Chemoembolization of the hepatic artery may be used to treat cancer that has spread to the liver. This involves blocking the hepatic artery (the main artery that supplies blood to the liver) and injecting anticancer drugs between the blockage and the liver. The liver's arteries then deliver the drugs throughout the liver. Only a small amount of the drug reaches other parts of the body. The blockage may be temporary or permanent, depending on what is used to block the artery. The liver continues to receive some blood from the hepatic portal vein, which carries blood from the stomach and intestine.

The way the chemotherapy is given depends on the type and stage of the cancer being treated.

See Drugs Approved for Colon and Rectal Cancer for more information.

Radiation therapy

Radiation therapy is a cancer treatment that uses high-energy x-rays or other types of radiation to kill cancer cells or keep them from growing. There are two types of radiation therapy:

The way the radiation therapy is given depends on the type and stage of the cancer being treated. External radiation therapy is used as palliative therapy to relieve symptoms and improve quality of life.

Targeted therapy

Targeted therapy is a type of treatment that uses drugs or other substances to identify and attack specific cancer cells. Targeted therapies usually cause less harm to normal cells than chemotherapy or radiation therapy do.

Types of targeted therapies used in the treatment of colon cancer include the following:

See Drugs Approved for Colon and Rectal Cancer for more information.

Immunotherapy

Immunotherapy is a treatment that uses the patient's immune system to fight cancer. Substances made by the body or made in a laboratory are used to boost, direct, or restore the body's natural defenses against cancer. This cancer treatment is a type of biologic therapy.

Immune checkpoint inhibitor therapy is a type of immunotherapy:

PD-1 and PD-L1 inhibitor therapy: PD-1 is a protein on the surface of T cells that helps keep the body's immune responses in check. PD-L1 is a protein found on some types of cancer cells. When PD-1 attaches to PD-L1, it stops the T cell from killing the cancer cell. PD-1 and PD-L1 inhibitors keep PD-1 and PD-L1 proteins from attaching to each other. This allows the T cells to kill cancer cells. Pembrolizumab is a type of PD-1 inhibitor.

See Drugs Approved for Colon and Rectal Cancer for more information.

New types of treatment are being tested in clinical trials.

Information about clinical trials is available from the NCI website.

Treatment for colon cancer may cause side effects.

For information about side effects caused by treatment for cancer, see our Side Effects page.

Patients may want to think about taking part in a clinical trial.

For some patients, taking part in a clinical trial may be the best treatment choice. Clinical trials are part of the cancer research process. Clinical trials are done to find out if new cancer treatments are safe and effective or better than the standard treatment.

Many of today's standard treatments for cancer are based on earlier clinical trials. Patients who take part in a clinical trial may receive the standard treatment or be among the first to receive a new treatment.

Patients who take part in clinical trials also help improve the way cancer will be treated in the future. Even when clinical trials do not lead to effective new treatments, they often answer important questions and help move research forward.

Patients can enter clinical trials before, during, or after starting their cancer treatment.

Some clinical trials only include patients who have not yet received treatment. Other trials test treatments for patients whose cancer has not gotten better. There are also clinical trials that test new ways to stop cancer from recurring (coming back) or reduce the side effects of cancer treatment.

Clinical trials are taking place in many parts of the country. Information about clinical trials supported by NCI can be found on NCI's clinical trials search webpage. Clinical trials supported by other organizations can be found on the ClinicalTrials.gov website.

Follow-up tests may be needed.

Some of the tests that were done to diagnose the cancer or to find out the stage of the cancer may be repeated. Some tests will be repeated in order to see how well the treatment is working. Decisions about whether to continue, change, or stop treatment may be based on the results of these tests.

Some of the tests will continue to be done from time to time after treatment has ended. The results of these tests can show if your condition has changed or if the cancer has recurred (come back). These tests are sometimes called follow-up tests or check-ups.

For information about the treatments listed below, see the Treatment Option Overview section.

Treatment of stage I colon cancer usually includes the following:

Use our clinical trial search to find NCI-supported cancer clinical trials that are accepting patients. You can search for trials based on the type of cancer, the age of the patient, and where the trials are being done. General information about clinical trials is also available.

For information about the treatments listed below, see the Treatment Option Overview section.

Treatment of stage II colon cancer may include the following:

Use our clinical trial search to find NCI-supported cancer clinical trials that are accepting patients. You can search for trials based on the type of cancer, the age of the patient, and where the trials are being done. General information about clinical trials is also available.

For information about the treatments listed below, see the Treatment Option Overview section.

Treatment of stage III colon cancer may include the following:

Use our clinical trial search to find NCI-supported cancer clinical trials that are accepting patients. You can search for trials based on the type of cancer, the age of the patient, and where the trials are being done. General information about clinical trials is also available.

For more information from the National Cancer Institute about colon cancer, see the following:

For general cancer information and other resources from the National Cancer Institute, see the following:

About PDQ

Physician Data Query (PDQ) is the National Cancer Institute's (NCI's) comprehensive cancer information database. The PDQ database contains summaries of the latest published information on cancer prevention, detection, genetics, treatment, supportive care, and complementary and alternative medicine. Most summaries come in two versions. The health professional versions have detailed information written in technical language. The patient versions are written in easy-to-understand, nontechnical language. Both versions have cancer information that is accurate and up to date and most versions are also available in Spanish.

PDQ is a service of the NCI. The NCI is part of the National Institutes of Health (NIH). NIH is the federal government's center of biomedical research. The PDQ summaries are based on an independent review of the medical literature. They are not policy statements of the NCI or the NIH.

Purpose of This Summary

This PDQ cancer information summary has current information about the treatment of colon cancer. It is meant to inform and help patients, families, and caregivers. It does not give formal guidelines or recommendations for making decisions about health care.

Reviewers and Updates

Editorial Boards write the PDQ cancer information summaries and keep them up to date. These Boards are made up of experts in cancer treatment and other specialties related to cancer. The summaries are reviewed regularly and changes are made when there is new information. The date on each summary ("Updated") is the date of the most recent change.

The information in this patient summary was taken from the health professional version, which is reviewed regularly and updated as needed, by the PDQ Adult Treatment Editorial Board.

Clinical Trial Information

A clinical trial is a study to answer a scientific question, such as whether one treatment is better than another. Trials are based on past studies and what has been learned in the laboratory. Each trial answers certain scientific questions in order to find new and better ways to help cancer patients. During treatment clinical trials, information is collected about the effects of a new treatment and how well it works. If a clinical trial shows that a new treatment is better than one currently being used, the new treatment may become "standard." Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.

Clinical trials can be found online at NCI's website. For more information, call the Cancer Information Service (CIS), NCI's contact center, at 1-800-4-CANCER (1-800-422-6237).

Permission to Use This Summary

PDQ is a registered trademark. The content of PDQ documents can be used freely as text. It cannot be identified as an NCI PDQ cancer information summary unless the whole summary is shown and it is updated regularly. However, a user would be allowed to write a sentence such as "NCI's PDQ cancer information summary about breast cancer prevention states the risks in the following way: [include excerpt from the summary]."

The best way to cite this PDQ summary is:

PDQ® Adult Treatment Editorial Board. PDQ Colon Cancer Treatment. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: https://www.cancer.gov/types/colorectal/patient/colon-treatment-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389319]

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The information in these summaries should not be used to make decisions about insurance reimbursement. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.

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More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website's E-mail Us.

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Colon Cancer Treatment (PDQ®)-Patient Version

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On This Page Colon cancer is a disease in which malignant (cancer) cells form in the tissues of the colon. Health history affects the risk of developing colon cancer. Signs of colon cancer include blood in the stool or a change in bowel habits.

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Researchers have found several factors that can increase a person's risk of colorectal cancer, but it's not yet clear exactly how all of these factors might cause this cancer.

Cancer is caused by changes in the DNA inside our cells. DNA is the chemical in our cells that makes up our genes, which control how our cells function. We usually look like our parents because they are the source of our DNA. But DNA affects more than just how we look.

Some genes help control when our cells grow, divide into new cells, and die:

Certain genes that help cells grow, divide, and stay alive are called oncogenes.

Genes that help keep cell division under control or cause cells to die at the right time are called tumor suppressor genes.

Cancers can be caused by DNAmutations (changes) that turn on oncogenes or turn off tumor suppressor genes. This leads to cells growing out of control. Changes in many different genes are usually needed to cause colorectal cancer.

For more about how genes changes can lead to cancer, see Genes and Cancer.

Inherited gene ﻿mutations

Some DNA mutations can be passed on in families and are found in all of a person's cells. These are called inherited mutations. A very small portion of colorectal cancers are caused by inherited gene mutations. Many of these DNA changes and their effects on the growth of cells are now known. For example:

Familialadenomatous polyposis (FAP), attenuated FAP (AFAP), and Gardner syndrome are caused by inherited changes in the APC gene. The APC gene is a tumor suppressor gene; it normally helps keep cell growth in check. In people with inherited changes in the APC gene, this "brake" on cell growth is turned off, causing hundreds of polyps to form in the colon. Over time, cancer will nearly always develop in one or more of these polyps.

Lynch syndrome (hereditary non-polyposis colon cancer, or HNPCC) is caused by changes in genes that normally help a cell repair damaged DNA. A mutation in one of the DNA repair genes like MLH1, MSH2, MSH6, PMS2, and can allow DNA errors to go unfixed. These errors will sometimes affect growth-regulating genes, which may lead to the development of cancer.

Peutz-Jeghers syndrome is caused by inherited changes in the STK11 (LKB1) gene, a tumor suppressor gene.

MUTYH-associated polyposis (MAP) is caused bymutations in the MUTYH gene, which is involved in how the cell "proofreads" or checks the DNA and fixes errors when cells divide.

Special genetic tests can find gene mutations linked to these inherited syndromes. If you have a family history of colorectal polyps or cancer or other symptoms linked to these syndromes, you may want to ask your doctor about genetic counseling and genetic testing. The American Cancer Society recommends discussing genetic testing with a qualified cancer genetics professional before any genetic testing is done. For more on this, see Understanding Genetic Testing for Cancer and What Happens during Genetic Testing for Cancer?

Acquired gene mutations

Most gene mutations that lead to cancer are ﻿ acquired mutations. They happen during a person's lifetime and are not passed on to their children. These DNA changes affect only cells that come from the original mutated cell.

In most cases of colorectal cancer, the DNA mutations that lead to cancer are acquired during a person's life rather than having been inherited. Certain risk factors probably play a role in causing these acquired mutations, but so far it's not known what causes most of them.

There doesn't seem to be a single genetic pathway to colorectal cancer that's the same in all cases. In many cases, the first mutation occurs in the APC gene. This leads to an increased growth of colorectal cells because of the loss of this "brake" on cell growth. Further mutations may then occur in other genes, which can lead the cells to grow and spread uncontrollably. Other genes that aren't known yet are probably involved as well.

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Causes of Colorectal Cancer | Is Colon Cancer Hereditary?

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Researchers have found several factors that can increase a person's risk of colorectal cancer, but it's not yet clear exactly how all of these factors might cause this cancer. Cancer is caused by changes in the DNA inside our cells. DNA is the chemical in our cells that makes up our genes, which control how our cells function.

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United States Cancer Statistics Data Visualizations

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Palliative care is used to manage a disease or medical condition that is serious or life threatening by easing pain and other associated physical, emotional, or psychosocial symptoms.

Palliative care also eases other distressing symptoms, like depression, anxiety, fatigue, insomnia, and shortness of breath. Palliative care provides advanced care planning and a support system to help you live a life that is as active, fulfilling, and as pain-free as possible.

Palliative care may last for weeks, months, or years, and the relief of moderate to severe pain during that time can greatly improve quality of life. The biggest problem with palliative care is that many people are referred for care too late. By starting this type of care early, and by using the right type of pain management, nearly all pain problems can be relieved or reduced.

Principles of palliative care and pain medicine

The first step in managing pain is to do a total pain assessment. You may be asked to choose a number from 0 to 10 to rank your pain, with 0 being very mild pain and 10 being the worst possible pain you could have.

Keep in mind 3 important principles when deciding how to manage pain. First, pain should always be treated right away. A delay allows pain to get worse. Second, you should not be afraid of becoming addicted to pain medicine. If medicines are used in the right way under close supervision of a healthcare provider, this is rarely a problem. Of course, if you believe that you are losing control of how you are using pain medicines, you should discuss this with your healthcare provider right away. Third, most pain problems can be controlled by using the World Health Organization's step-care approach:

Step 1. Start with a nonsteroidal anti-inflammatory drug (NSAID). Examples of NSAIDs include over-the-counter drugs like ibuprofen and stronger NSAIDs that your healthcare provider may prescribe. An alternative to NSAIDs for step 1 pain is acetaminophen.

Step 2. If pain continues or gets worse, your healthcare provider may prescribe a weak opioid medicine, like hydrocodone. A weak opioid may be combined with a nonopioid pain reliever.

Step 3. If pain continues or gets worse, your healthcare provider may prescribe a stronger opiate. Examples of strong opioids include morphine and fentanyl.

Understanding opioid drugs

Opioid drugs are the most effective and commonly used drugs for moderate to severe pain. A wide range of opioid drugs is available, and they can be taken in a variety of ways. One drawback of these medicines is that, over time, you will almost certainly develop a tolerance to the one you're taking and need higher doses to get the same effect. One way your healthcare provider may get around this problem is by switching the type, dose, or the way the drug is given.

These are common ways in which opioid drugs can be given:

Oral medicines. These can be taken in pill or liquid form and can be short acting or long acting (sustained release).

Adhesive patch. This can be applied to the skin to release medicine over time. An example of this is a fentanyl patch.

Opioid drug injection. This shot may be given under the skin or into a muscle.

Opioid drug IV. An opiate may be given directly into the blood through an intravenous line.

Medicine pump. Opiate medicine can be given through a pump attached to an IV line that you control. This is called patient-controlled analgesia.

Spinal injection. For pain that's hard to control, a pain-control specialist may give an opioid drug directly into the spinal cord area.

Understanding helper drugs

These medicines, called adjuvant analgesics, can help control pain in certain situations. These are commonly used adjuvant drugs:

Steroids. These are strong anti-inflammatory medicines that may help relieve pain by decreasing inflammation. They may be used along with other pain relievers for nerve, bone, or other types of pain.

Antidepressants. Treating any existing depression or anxiety can make pain easier to control. These drugs may also be useful in pain caused by nerve damage.

Anticonvulsants. These medicines are usually used to control seizures, but they can also help control nerve-related pain.

Local anesthetics. These are medicines that can block pain signals in the body. A pain specialist may inject a local anesthetic to block pain.

Muscle relaxants. Antianxiety medicines and muscle relaxants may be used along with pain medicine if pain is aggravated by tension or muscle spasms.

Bisphosphonates. These medicines are sometimes used to prevent fractures in people whose cancer has spread to the bone. They can play a key role in relieving bone injury and pain.

Other pain control interventions

Surgery is often the last thing a patient or his or her healthcare provider would consider at end of life. But at times surgery can provide pain relief and increase function. Surgery's primary goal can be to relieve specific symptoms. For instance, a healthcare provider may recommend surgery to stabilize a hip fracture in someone with advanced cancer. The surgery is not going to treat the cancer or lengthen the patient's life, but it may be the best way to reduce hip pain and improve mobility. Radiation therapy can also be used to improve pain and control symptoms. Because surgery involves risk, the healthcare provider must clearly define treatment goals for both the patient and the patient's family.

If you or a loved one needs palliative care, many options are available. Work with your healthcare provider to find the right approach. You can also get help from a pain medicine specialist or a palliative care specialist. Remember: You have a right to be as free of pain as possible. There is no reason to let pain decrease your quality of life.

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Palliative Care Methods for Controlling Pain

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Palliative care is used to manage a disease or medical condition that is serious or life threatening by easing pain and other associated physical, emotional, or psychosocial symptoms. Palliative care also eases other distressing symptoms, like depression, anxiety, fatigue, insomnia, and shortness of breath.

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Once treatments meant to halt colon cancer are no longer working, and is considered terminal, it is important to know what to expect. Despite having an advancing condition, the timing of death is very unpredictable.

Usually, in the context of cancer, patients do not experience a "sudden death." Instead, death comes over a period of days to weeks. However, some symptoms are synonymous with the end of life and can be anticipated for comfort.

If you choose, you can discuss palliative care or hospice with your loved one's doctor-these professionals are trained to anticipate and provide symptom relief during the last stages of life and can make a world of difference in the last days and hours.

One of the most feared symptoms of death is pain. If your loved one is dying from colon cancer, they most likely have diffuse ​ metastases -or the spread of cancer outside of their colon to other organs and lymph nodes, as well as tumors in and around their colon.

Pain is anticipated, and opioid narcotics, or very strong pain medicines, are most commonly administered. If your loved one is unable to swallow medicine at this point, certain preparations can be ordered and given sublingually (under the tongue) or rectally, as a suppository.​﻿﻿

Many people ask how to tell if someone is in pain if they are asleep, as many people are towards the end of life. Even in rest, there are signs of discomfort that loved ones can watch for:﻿﻿

Grimacing and frowning

Breathing quickly

Fidgety movements of the arms, legs, and feet

Be sure to check your loved one's environment before assuming they are in pain. For instance, there may be simple reasons for these signs of discomfort, such as wet bedclothes or a fever.

Complete Withdrawal

Although you may see this symptom wax and wane during the weeks prior to the end of life, most people enter a sleeping or almost comatose-like state in the days and hours preceding death.﻿﻿

This is not a voluntary choice-your loved one is not ignoring you. Similarly, this withdrawal is also not an effect of the medications being provided for comfort, as many family members fear.

It is not completely understood why people withdraw, but it is assumed that it is a combination of physical and mental exhaustion from fighting illness.

Changes in Breathing

Changes in the way your loved one breathes might be a signal that the end of life is approaching. If you start to see pauses between breaths or hear an audible gurgling noise, also known as the death rattle, your loved one is most likely within hours of passing on.﻿﻿

To make them more comfortable, try elevating the head of the bed and do not offer any more fluids at this point. The fluids will add to the saliva pooled in the back of the throat and increase the sound of gurgling.﻿﻿

Agitation and Confusion

Symptoms at the end of life can include periods of confusion, agitation, and even hallucinations. Your loved one may see insects in the room, angels, or even people that you cannot see. They may not recognize you or may seem upset and out of sorts for no apparent reason.

Medications may help calm them and decrease these symptoms. Try not to escalate the situation. It's best not to argue with your loved one-try calm, gentle reassurance.﻿﻿

Not everyone will experience a rally at the end of life, but if they do, it can be confusing to ​family. During a rally, many people develop moments of complete clarity, alertness, and might even request food after abstaining for days.

Some family members might see this as a hopeful sign that their loved one is improving.﻿﻿ No one knows why some people experience this and other people do not. A rally may last up to a few days or occur just for a moment or two prior to death.

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What to Expect When Losing a Loved One to Colon Cancer

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Once treatments meant to halt colon cancer are no longer working, and is considered terminal, it is important to know what to expect. Despite having an advancing condition, the timing of death is very unpredictable. Usually, in the context of cancer, patients do not experience a "sudden death."

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Centers for Disease Control and Prevention

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What Is Colorectal Cancer Screening?

If you are 45 to 75 years old, you should get screened for colorectal cancer.

Millions of people in the United States are not getting screened as recommended. They are missing the chance to prevent colorectal cancer or find it early, when treatment works best.

If you think you may be at increased risk for colorectal cancer, speak with your doctor about when to begin screening, which test is right for you, and how often to get tested.

A screening test is used to look for a disease when a person doesn't have symptoms. (When a person has symptoms, diagnostic tests are used to find out the cause of the symptoms.)

Colorectal cancer almost always develops from precancerous polyps (abnormal growths) in the colon or rectum. Screening tests can find precancerous polyps, so that they can be removed before they turn into cancer. Screening tests can also find colorectal cancer early, when treatment works best.

Screening Guidelines

Regular screening, beginning at age 45, is the key to preventing colorectal cancer and finding it early. The U.S. Preventive Services Task Force (USPSTF) recommendsexternal icon that adults age 45 to 75 be screened for colorectal cancer. The Task Force recommends that adults age 76 to 85 ask their doctor if they should be screened.

The Task Force recommends several colorectal cancer screening strategies, including stool tests, flexible sigmoidoscopy, colonoscopy, and CT colonography (virtual colonoscopy). Learn about these screening tests.

When Should I Begin to Get Screened?

Most people should begin screening for colorectal cancer soon after turning 45, then continue getting screened at regular intervals. However, you may need to be tested earlier than 45, or more often than other people, if-

If you think you are at increased risk for colorectal cancer, speak with your doctor about-

When to begin screening.

Which test is right for you.

How often to get tested.

Insurance and Medicare Coverage

Most insurance plans and Medicare help pay for colorectal cancer screening for people who are 50 years old or older. Colorectal cancer screening tests may be covered by your health insurance policy without a deductible or co-pay. For more information about Medicare coverage, visit www.medicare.govexternal icon or call 1-800-MEDICARE (1-800-633-4227). TTY users should call 1 (877) 486-2048. Check with your insurance plan to find out what benefits are covered for colorectal cancer screening.

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What Should I Know About Screening for Colorectal Cancer?

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What Is Colorectal Cancer Screening? If you are 45 to 75 years old, you should get screened for colorectal cancer. Millions of people in the United States are not getting screened as recommended. They are missing the chance to prevent colorectal cancer or find it early, when treatment works best.

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https://www.cancer.gov/types/colorectal/hp/colon-treatment-pdq#_74

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Diagnosis

Screening for colon cancer

Doctors recommend certain screening tests for healthy people with no signs or symptoms in order to look for signs of colon cancer or noncancerous colon polyps. Finding colon cancer at its earliest stage provides the greatest chance for a cure. Screening has been shown to reduce your risk of dying of colon cancer.

Doctors generally recommend that people with an average risk of colon cancer begin screening around age 50. But people with an increased risk, such as those with a family history of colon cancer or African-American heritage, should consider screening sooner.

Several screening options exist - each with its own benefits and drawbacks. Talk about your options with your doctor, and together you can decide which tests are appropriate for you. If a colonoscopy is used for screening, polyps can be removed during the procedure before they turn into cancer.

Diagnosing colon cancer

If your signs and symptoms indicate that you could have colon cancer, your doctor may recommend one or more tests and procedures, including:

Using a scope to examine the inside of your colon (colonoscopy). Colonoscopy uses a long, flexible and slender tube attached to a video camera and monitor to view your entire colon and rectum. If any suspicious areas are found, your doctor can pass surgical tools through the tube to take tissue samples (biopsies) for analysis and remove polyps.

Blood tests. No blood test can tell you if you have colon cancer. But your doctor may test your blood for clues about your overall health, such as kidney and liver function tests.

Your doctor may also test your blood for a chemical sometimes produced by colon cancers (carcinoembryonic antigen, or CEA). Tracked over time, the level of CEA in your blood may help your doctor understand your prognosis and whether your cancer is responding to treatment.

Determining the extent of the cancer

If you've been diagnosed with colon cancer, your doctor may recommend tests to determine the extent (stage) of your cancer. Staging helps determine what treatments are most appropriate for you.

Staging tests may include imaging procedures such as abdominal, pelvic and chest CT scans. In many cases, the stage of your cancer may not be fully determined until after colon cancer surgery.

The stages of colon cancer are indicated by Roman numerals that range from 0 to IV, with the lowest stages indicating cancer that is limited to the lining of the inside of the colon. By stage IV, the cancer is considered advanced and has spread (metastasized) to other areas of the body.

Treatment

Which treatments are most likely to help you depends on your particular situation, including the location of your cancer, its stage and your other health concerns. Treatment for colon cancer usually involves surgery to remove the cancer. Other treatments, such as radiation therapy and chemotherapy, might also be recommended.

Surgery for early-stage colon cancer

If your colon cancer is very small, your doctor may recommend a minimally invasive approach to surgery, such as:

Removing polyps during a colonoscopy (polypectomy). If your cancer is small, localized, completely contained within a polyp and in a very early stage, your doctor may be able to remove it completely during a colonoscopy.

Endoscopic mucosal resection. Larger polyps might be removed during colonoscopy using special tools to remove the polyp and a small amount of the inner lining of the colon in a procedure called an endoscopic mucosal resection.

Minimally invasive surgery (laparoscopic surgery). Polyps that can't be removed during a colonoscopy may be removed using laparoscopic surgery. In this procedure, your surgeon performs the operation through several small incisions in your abdominal wall, inserting instruments with attached cameras that display your colon on a video monitor. The surgeon may also take samples from lymph nodes in the area where the cancer is located.

Surgery for more advanced colon cancer

If the cancer has grown into or through your colon, your surgeon may recommend:

Partial colectomy. During this procedure, the surgeon removes the part of your colon that contains the cancer, along with a margin of normal tissue on either side of the cancer. Your surgeon is often able to reconnect the healthy portions of your colon or rectum. This procedure can commonly be done by a minimally invasive approach (laparoscopy).

Surgery to create a way for waste to leave your body. When it's not possible to reconnect the healthy portions of your colon or rectum, you may need an ostomy. This involves creating an opening in the wall of your abdomen from a portion of the remaining bowel for the elimination of stool into a bag that fits securely over the opening.

Sometimes the ostomy is only temporary, allowing your colon or rectum time to heal after surgery. In some cases, however, the colostomy may be permanent.

Lymph node removal. Nearby lymph nodes are usually also removed during colon cancer surgery and tested for cancer.

Surgery for advanced cancer

If your cancer is very advanced or your overall health very poor, your surgeon may recommend an operation to relieve a blockage of your colon or other conditions in order to improve your symptoms. This surgery isn't done to cure cancer, but instead to relieve signs and symptoms, such as a blockage, bleeding or pain.

In specific cases where the cancer has spread only to the liver or lung but your overall health is otherwise good, your doctor may recommend surgery or other localized treatments to remove the cancer. Chemotherapy may be used before or after this type of procedure. This approach provides a chance to be free of cancer over the long term.

Chemotherapy

Chemotherapy uses drugs to destroy cancer cells. Chemotherapy for colon cancer is usually given after surgery if the cancer is larger or has spread to the lymph nodes. In this way, chemotherapy may kill any cancer cells that remain in the body and help reduce the risk of cancer recurrence.

Chemotherapy might also be used before an operation to shrink a large cancer so that it's easier to remove with surgery.

Chemotherapy can also be used to relieve symptoms of colon cancer that can't be removed with surgery or that has spread to other areas of the body. Sometimes it's combined with radiation therapy.

Radiation therapy

Radiation therapy uses powerful energy sources, such as X-rays and protons, to kill cancer cells. It might be used to shrink a large cancer before an operation so that it can be removed more easily.

When surgery isn't an option, radiation therapy might be used to relieve symptoms, such as pain. Sometimes radiation is combined with chemotherapy.

Targeted drug therapy

Targeted drug treatments focus on specific abnormalities present within cancer cells. By blocking these abnormalities, targeted drug treatments can cause cancer cells to die.

Targeted drugs are usually combined with chemotherapy. Targeted drugs are typically reserved for people with advanced colon cancer.

Immunotherapy

Immunotherapy is a drug treatment that uses your immune system to fight cancer. Your body's disease-fighting immune system may not attack your cancer because the cancer cells produce proteins that blind the immune system cells from recognizing the cancer cells. Immunotherapy works by interfering with that process.

Immunotherapy is usually reserved for advanced colon cancer. Your doctor might have your cancer cells tested to see if they're likely to respond to this treatment.

Supportive (palliative) care

Palliative care is specialized medical care that focuses on providing relief from pain and other symptoms of a serious illness. Palliative care is provided by a team of doctors, nurses and other specially trained professionals that work with you, your family and your other doctors to provide an extra layer of support that complements your ongoing care.

Palliative care teams aim to improve the quality of life for people with cancer and their families. This form of care is offered alongside curative or other treatments you may be receiving.

When palliative care is used along with all of the other appropriate treatments, people with cancer may feel better and live longer.

Clinical trials

Explore Mayo Clinic studies testing new treatments, interventions and tests as a means to prevent, detect, treat or manage this disease.

Coping and support

A cancer diagnosis can be emotionally challenging. In time, people learn to cope in their own unique ways. Until you find what works for you, you might try to:

Learn enough about your cancer to feel comfortable making treatment decisions. Ask your doctor to tell you the type and stage of your cancer, as well as your treatment options and their side effects. The more you know, the more confident you'll be when it comes to making decisions about your own care. Look for information in your local library and on reliable websites.

Keep friends and family close. Keeping your close relationships strong will help you deal with cancer. Friends and family can provide the practical support you'll need, such as helping take care of your home if you're in the hospital. And they can serve as emotional support when you feel overwhelmed.

Find someone to talk with. Find a good listener who is willing to listen to you talk about your hopes and fears. This may be a friend or family member. The concern and understanding of a counselor, medical social worker, clergy member or cancer support group also may be helpful.

Ask your doctor about support groups in your area or contact a cancer organization, such as the National Cancer Institute or the American Cancer Society.

Preparing for your appointment

If your doctor suspects you may have colon cancer, you'll likely be referred to specialists who treat colon cancer. You may meet with a number of specialists, including a:

Doctor who treats digestive diseases (gastroenterologist)

Doctor who uses medications to treat cancer (oncologist)

Doctor who removes colon cancer using surgery (surgeon)

Doctor who uses radiation to treat cancer (radiation oncologist)

Because appointments can be brief, and because there's often a lot of ground to cover, it's a good idea to be well-prepared. Here's some information to help you get ready, and know what to expect from your doctor.

What you can do

Be aware of any pre-appointment restrictions. At the time you make the appointment, be sure to ask if there's anything you need to do in advance, such as restrict your diet.

Write down any symptoms you're experiencing, including any that may seem unrelated to the reason for which you scheduled the appointment.

Write down key personal information, including any major stresses or recent life changes.

Make a list of all medications, vitamins or supplements that you're taking.

Consider taking a family member or friend along. Sometimes it can be difficult to take in all the information provided during an appointment. Someone who accompanies you may remember something that you missed or forgot.

Write down questions to ask your doctor.

Some basic questions to ask your doctor include:

Where is my colon cancer located in my colon?

What is the stage of my colon cancer?

Can you explain my pathology report to me?

Can I have a copy of my pathology report?

Has my colon cancer spread to other parts of my body?

Will I need more tests?

What are the treatment options for my colon cancer?

Will any of the treatments cure my colon cancer?

What is the chance that my colon cancer will be cured?

How much does each treatment increase my chances that my colon cancer will be cured?

What are the potential side effects of each treatment?

How will each treatment affect my daily life?

Is there one treatment you feel is best for me?

What would you recommend to a family member or friend in my same situation?

How much time can I take to make my decision about treatment?

Should I seek a second opinion?

Should I see a specialist? What will that cost, and will my insurance cover it?

Are there any brochures or other printed material that I can take with me? What websites do you recommend?

Do my siblings or my children have an increased risk of colon cancer?

In addition to the questions that you've prepared to ask your doctor, don't hesitate to ask questions during your appointment.

What to expect from your doctor

Your doctor is likely to ask you a number of questions. Being ready to answer them may allow time to cover other points you want to address. Your doctor may ask:

When did you first begin experiencing symptoms?

Have your symptoms been continuous or occasional?

How severe are your symptoms?

What, if anything, seems to improve your symptoms?

What, if anything, appears to worsen your symptoms?

Do you have a family history of colon cancer or other cancers?

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Doctors recommend certain screening tests for healthy people with no signs or symptoms in order to look for signs of colon cancer or noncancerous colon polyps. Finding colon cancer at its earliest stage provides the greatest chance for a cure. Screening has been shown to reduce your risk of dying of colon cancer.

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Colorectal cancer symptoms and screening guidelines

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Adults who are at average risk for colorectal cancer used to start having regular colonoscopies when they turned 50. Now the timeline has changed. The American Cancer Society's newest guidelines recommend that colorectal cancer screenings begin at age 45.

The recommended age was lowered from 50 to 45 because colorectal cancer cases are on the rise among young and middle-age people. Deaths of people under age 55 increased 1% per year from 2008 to 2017, even though overall colorectal cancer rates have dropped.

Colorectal cancer is most treatable when found early. Colonoscopies not only detect the disease, but prevent cancer because precancerous polyps can be removed during the procedure.

Colonoscopies not only detect the disease, but prevent cancer because precancerous polyps can be removed during the procedure.

In May 2021, the U.S. Preventive Services Task Force issued new recommendations for colorectal cancer stating that people at average risk should start screening at age 45, which will allow health insurance companies to cover the cost of the test at a younger age.

How and when should a person get screened for this potentially deadly disease? Here are some specific recommendations:

Starting at age 45, individuals with an average risk of colorectal cancer should undergo regular screening with one of six different tests, depending on patient preference and test availability. These tests include a FIT (fecal immunochemical test) or gFOBT (guaiac-based fecal occult blood test) every year, stool DNA test every three years, a CT colonography or flexible sigmoidoscopy every five years, or colonoscopy every 10 years. The recommendations do not prioritize any one test over another.

Following a positive result from a non-colonoscopy screening test, a timely follow-up colonoscopy must be performed to prevent cancer.

Average-risk adults in good health should continue colorectal cancer screening through age 75.

For patients between 76 and 85, screening decisions should be made jointly with clinicians based on patient preferences, life expectancy, health status, and prior screening history.

Individuals over age 85 should be discouraged from continuing screening.

People with a higher risk of colorectal cancer, such as a family history, should ask their physician to determine the best age to start screening.

Colorectal cancer is expected to cause about 53,000 deaths in 2021, according to the American Cancer Society.

The University of Chicago Medicine is working to lower that number through a number of initiatives. The Illinois Colon CARES web portal is used by Chicago area clinics and hospitals to help vulnerable underserved populations have access to colonoscopies. Staff members from federally qualified health centers help people schedule colonoscopies while they're at the doctor's office, rather than asking them to call a number when they get home, closing the gap in scheduling and communication.

UChicago Medicine gastroenterologist Karen Kim, MD and her team initiated this push in 2015 after receiving a five-year, $4.5 million grant from the Centers for Disease Control and Prevention. The grant was given to the Center for Asian Health Equity - a collaboration between UChicago Medicine and the Asian Health Coalition. It marked the first time an organization in Illinois ever received CDC funding for colorectal cancer screening and prevention.

The grant was used to launch Cook County CARES (Colon Cancer Alliance to Reignite and Enhance Screening), which improved screening rates up to 30% among low-income Asian American, Hispanic and African American residents in Cook County. African Americans, in particular, are disproportionately affected by colorectal cancer.

After another round of federal funding, a $4.25 million grant in 2020, the program evolved into Illinois Colon CARES.

"Not only do we need to ensure our screening recommendations evolve along with our scientific knowledge, but we also need to ensure those individuals who need screening are getting it," Kim said.

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New guidelines lower colorectal screening age from 50 to 45

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Adults who are at average risk for colorectal cancer used to start having regular colonoscopies when they turned 50. Now the timeline has changed. The American Cancer Society's newest guidelines recommend that colorectal cancer screenings begin at age 45. The recommended age was lowered from 50 to 45 because colorectal cancer cases are on the rise among young and middle-age people.

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Lynch syndrome is the most common hereditary colorectal cancer syndrome. It accounts for about 2% to 4% of all colorectal cancers. In most cases, this disorder is caused by an inherited defect in either the MLH1, MSH2 or MSH6 gene, but changes in other genes can also cause Lynch syndrome.

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Lynch syndrome is the most common hereditary colorectal cancer syndrome. It accounts for about 2% to 4% of all colorectal cancers. In most cases, this disorder is caused by an inherited defect in either the MLH1, MSH2 or MSH6 gene, but changes in other genes can also cause Lynch syndrome.

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What Diet Is Best for Prevention of Colon Cancer?

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Quick Profiles

Choose a Different State:

Notes:
Created by statecancerprofiles.cancer.gov on 07/21/2021 12:30 pm.
For more explicit data source and footnote information please see the tables, graphs and maps that are linked to each row.

† Incidence rates (cases per 100,000 population per year) are age-adjusted to the 2000 US standard population (19 age groups: <1, 1-4, 5-9, ... , 80-84, 85+). Rates are for invasive cancer only (except for bladder cancer which is invasive and in situ) or unless otherwise specified. Rates calculated using SEER*Stat. Population counts for denominators are based on Census populations as modified by NCI. The 1969-2017 US Population Data File is used for SEER and NPCR incidence rates.
Interpret Rankings provides insight into interpreting cancer incidence statistics. When the population size for a denominator is small, the rates may be unstable. A rate is unstable when a small change in the numerator (e.g., only one or two additional cases) has a dramatic effect on the calculated rate.
Data not available for some combinations of geography, cancer site, age, and race/ethnicity.
Suppression is used to avoid misinterpretation when rates are unstable.

Notes:
Created by statecancerprofiles.cancer.gov on 07/21/2021 12:30 pm.
For more explicit data source and footnote information please see the tables, graphs and maps that are linked to each row.

Source: Death data provided by the National Vital Statistics System public use data file. Death rates calculated by the National Cancer Institute using SEER*Stat. Death rates are age-adjusted to the 2000 US standard population (19 age groups: <1, 1-4, 5-9, ... , 80-84, 85+). The Healthy People 2020 goals are based on rates adjusted using different methods but the differences should be minimal. Population counts for denominators are based on Census populations as modified by NCI. The 1969-2017 US Population Data File is used with mortality data.

Notes:
Created by statecancerprofiles.cancer.gov on 07/21/2021 12:30 pm.
For more explicit data source and footnote information please see the tables, graphs and maps that are linked to each row.

Data statistics on this page come from the following data sources: CDC, Modeled Estimates Combining BRFSS & NHIS, Tobacco Use Supplement to the Current Population Survey, and American Nonsmokers' Rights Foundation. Please see the link on each row for the table/graph map for the specific footnote information.

Notes:
Created by statecancerprofiles.cancer.gov on 07/21/2021 12:30 pm.
For more explicit data source and footnote information please see the tables, graphs and maps that are linked to each row.

Methodology: Cancer prevalence estimates are derived from state specific cancer mortality and survival data using a statistical package called MIAMOD (Mortality-Incidence Analysis MODEL). Cancer survival models are derived from the Surveillance, Epidemiology, and End Results (SEER) Program data and adjusted to represent state specific survival.

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Quick Profiles Choose a Different State: Notes: Created by statecancerprofiles.cancer.gov on 07/21/2021 12:30 pm.For more explicit data source and footnote information please see the tables, graphs and maps that are linked to each row. † Incidence rates (cases per 100,000 population per year) are age-adjusted to the 2000 US standard population (19 age groups: <1, 1-4, 5-9, ...

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When to request genetic testing for colorectal cancer

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When to request genetic testing for colorectal cancer

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Body Image Concerns With a Stoma

Your body is different after stoma surgery, so you may experience body image issues. Explore your feelings about your body after stoma surgery and learn how to deal with new emotions.

Get body image tips after stoma surgery.

Stoma formation imposes significant changes to body image, both physically and emotionally. The process of adjustment and acceptance often takes time. After stoma surgery, give yourself the time you need to adapt. Be patient, stay positive, and seek help if you need it.
Dealing with initial body image feelings
Regardless of the reason for your stoma, or whether your stoma is temporary or permanent, coming to terms with your changed body can be overwhelming. Being open and honest with people you care about is one key to dealing with those initial feelings.

Try to explain how you feel about your body with a stoma to your partner or a supportive friend. You might have strong negative feelings that could lead to depression or anxiety, affect your sense of identity, result in reduced participation in social activities, and impact the way you behave towards those around you. Be sure to give your loved ones the best chance to understand and be there for you.

Remember that your stoma care nurse is available to you as well. He or she is well trained to support you while you adjust and recover. You are not alone. Everyone with a stoma has had to deal with these emotions, and your stoma care nurse is most likely skilled at listening, understands how you are feeling, and may be able to help guide you to other professional help if needed.
Tips for managing feelings about body image

Don't avoid going to new places or seeing new people. Avoidance can reinforce a feeling that you're being stared at in social situations, which is almost never the case.

Rather than worry about someone being too curious, change the conversation. Practice responses or one-line statements that take the focus off you and redirect the conversation. For example, smile, and say something like "Enough about me - let's talk about you."

Remember what originally attracted your partner to you. It's not likely that your tummy had much to do with the initial attraction, so focus on your strengths. Consider what is positive about you and your appearance. Say it out loud so that you hear it and believe it.

Reframe your stoma into a positive. Perhaps your stoma can come to represent well-being and being rid of illness. Nurture that feeling and share it with others to make it stronger.

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Tackling Body Image Concerns with a Stoma | Dansac UK

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Your body image changes after stoma surgery. Learn how to deal with new emotions and feelings about your appearance after stoma surgery.

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"I've been screened twice. I made everybody I love get screened," says actress Meryl Streep in this video. "People that are screened early and find cancer and are treated early-they're alive because of that early detection."

Overall, the most effective way to reduce your risk of colorectal cancer is to get screened for colorectal cancer routinely, beginning at age 45.
Almost all colorectal cancers begin as precancerous polyps (abnormal growths) in the colon or rectum. Such polyps can be present in the colon for years before invasive cancer develops. They may not cause any symptoms, especially early on. Colorectal cancer screening can find precancerous polyps so they can be removed before they turn into cancer. In this way, colorectal cancer is prevented. Screening can also find colorectal cancer early, when treatment works best.

Diet

Research is underway to find out if changes to your diet can reduce your colorectal cancer risk. Medical experts often recommend a diet low in animal fats and high in fruits, vegetables, and whole grains to reduce the risk of other chronic diseases, such as coronary artery disease and diabetes. This diet also may reduce the risk of colorectal cancer.

Aspirin

Researchers are looking at the role of some medicines and supplements in preventing colorectal cancer. The U.S. Preventive Services Task Force found that taking low-dose aspirin can help prevent cardiovascular disease and colorectal cancer in some adults, depending on age and risk factors. For more information, download Aspirin Use to Prevent Cardiovascular Disease and Colorectal Cancer: Preventive Medication.external icon

Healthy Choices

Some studies suggest that people may reduce their risk of developing colorectal cancer by increasing physical activity, limiting alcohol consumption, and avoiding tobacco.

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What Can I Do to Reduce My Risk of Colorectal Cancer?

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"I've been screened twice. I made everybody I love get screened," says actress Meryl Streep in this video. "People that are screened early and find cancer and are treated early-they're alive because of that early detection." Overall, the most effective way to reduce your risk of colorectal cancer is to get screened for colorectal cancer routinely, beginning at age 45.

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We have already talked about ways genes, gene mutations, and gene variations can affect cancer risk and even lead to cancer. In this section, we are going to talk about how finding certain genes or gene mutations can be helpful in diagnosing cancer, monitoring the effects of treatment, learning about prognosis (outlook), and in treating cancer. In each case, only one or two examples are given. To learn about how genes are important to other kinds of cancer, see our document about that kind of cancer.

Cancer diagnosis and monitoring treatment

Certain mutations are commonly found in the cells of some types of cancers. Finding certain mutations in cells can confirm the diagnosis of that cancer. Testing cells for the mutation can also be used after diagnosis to see how the cancer is responding to treatment.

For example, the leukemia cells of patients with chronic myeloid leukemia (CML) contain a mutated gene called BCR-ABL. In order to be diagnosed with CML, this mutation must be present, so testing for this mutation is used to confirm the diagnosis. Very sensitive tests can tell how many copies of this mutation are present in a blood sample (which indicates how many CML cells are present). These tests can find even tiny amounts, representing small numbers of CML cells among millions of normal cells. The number of copies is determined when treatment is started, and then again sometime later to see how well the treatment is working. If treatment has put the leukemia into remission, this test can be used to see if it is coming back and new treatment is needed.

Genes and cancer prognosis

In some cancers, specific gene changes can be used to predict which patients are likely to have a better or worse outcome. This can help guide the intensity of treatment.

For example, patients with acute myeloid leukemia (AML) whose leukemia cells have a mutation in the FLT3 gene have a poorer prognosis than patients whose leukemia cells do not contain that mutation. Doctors may recommend more intense treatment, including stem cell transplant for someone whose leukemia cells have this mutation. On the other hand, people whose leukemia cells have mutations in the NPM1 gene (and no other abnormalities) seem to have a better prognosis than people without this mutation. As a result, doctors may not feel that a stem cell transplant is needed in someone whose leukemia cells only have a NPM1 mutation.

For some cancers, tests that look at the activity (expression) of many genes at once can be useful in predicting prognosis. These tests, called gene expression panels, are performed on samples of the cancer. They are available for a number of cancers, including breast, colon, and prostate cancers. These tests can help predict which patients are more likely to have their cancers come back after treatment. So far, though, only one, the Oncotype Dx ® breast cancer assay, has been shown to help predict which patients benefit the most from certain treatments.

Genes and cancer treatment

Drugs targeting genes or gene mutations

Drugs have been developed that target some of the gene changes in certain cancers. Actually these drugs often target the protein made by the abnormal gene (and not the gene itself).

For example, HER2/neu is a proto-oncogene in normal cells that helps them grow. It becomes an oncogene when a cell has too many copies of this gene. When this happens, the cells make too much HER2/neu protein and the cancer is said to be HER2 positive. Patients with breast cancer with cells that are HER2 positive do not respond as well to certain chemotherapy drugs. But newer drugs such as trastuzumab (Herceptin ®), lapatinib (Tykerb ®), and several others, have been designed to specifically attack cells that are HER2 positive. These drugs can slow cancer cell growth and improve outcomes in patients with HER2 positive cancers. Breast cancers are now routinely tested to see if they are or the HER2 positive to identify which patients will benefit from these drugs. Other cancers also can be HER2 positive. Anti-HER2 therapy has also helped people with stomach cancer that is HER2-positive.

In chronic myeloid leukemia (CML), the cancer cells have a gene change called BCR-ABL that makes a type of protein called a tyrosine kinase. Drugs that target the BCR-ABL protein, such as imatinib (Gleevec ®), are often very effective against CML. They lead to remission of the leukemia in most patients treated in the early stages of their disease.

Drugs targeting certain mutations are useful in a number of other cancers including acute lymphocytic leukemia, gastrointestinal stromal tumors, non-small cell lung cancer, a certain kind of non-Hodgkin lymphoma, and melanoma.

Drugs that activate genes

DNA methylation is one way to turn-off genes. Drugs called hypomethylating agents can reverse methylation. This can be helpful in treating some cancers in which some genes are abnormally methylated. For example, in myelodysplastic syndrome, certain genes that are often methylated in the cancer cells when they aren't supposed to be. The hypomethylating agents decitabine (Dacogen ®) and azacytidine (Vidaza ®) can decrease this abnormal methylation, which can be useful in treating this disease.

Other drugs that help fight cancer by activating genes are the histone deacetylase inhibitors, such as vorinostat (Zolinza ®) and romidepsin (Istodax ®).

Gene testing to help predict if a drug will work

Some drugs don't help patients if the cancer cells have certain gene mutations. For example, cetuximab (Erbitux ®) and panitumumab (Vectibix ®) are drugs used to treat advanced colorectal cancers. However, these drugs don't help patients with cancers that have mutations in the KRAS gene, so doctors check the cancer cells for these mutations before they give either of these drugs.

Some drugs work better in people with certain mutations. For example, the drug erlotinib (Tarceva ®), which can be used to treat non-small cell lung cancer, works better in patients whose cancer cells have a certain mutation in the EGFR gene.

Future directions

Many researchers are very hopeful about the future of cancer treatments based on the specific gene changes found in cancer cells, and this remains a very active area of research. There are many clinical trials under way today that could lead to better treatments for many types of cancer.

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How genes can help in the diagnosis and treatment of cancer | American Cancer Society

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We have already talked about ways genes, gene mutations, and gene variations can affect cancer risk and even lead to cancer. In this section, we are going to talk about how finding certain genes or gene mutations can be helpful in diagnosing cancer, monitoring the effects of treatment, learning about prognosis (outlook), and in treating cancer.

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Regular screening, beginning at age 45, is the key to preventing colorectal cancer and finding it early. The U.S. Preventive Services Task Force (USPSTF) recommends

external icon

that adults age 45 to 75 be screened for colorectal cancer. The Task Force recommends that adults age 76 to 85 ask their doctor if they should be screened.
https://www.cdc.gov/cancer/colorectal/basic_info/screening/index.htm

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The NHQDR quality measures specific to Cancer are compared to achievable benchmarks, which are derived from the top-performing States. Better performance of a State can mean higher or lower values of a measure, depending on the desired outcome. For example, low values are desirable for measures such as infant mortality, whereas high values are desirable for measures such as preventative screening. The categories of achievement have been standardized across the measure definitions so that:

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NHQDR Web Site - National Cancer Benchmark Details

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The NHQDR quality measures specific to Cancer are compared to achievable benchmarks, which are derived from the top-performing States. Better performance of a State can mean higher or lower values of a measure, depending on the desired outcome. For example, low values are desirable for measures such as infant mortality, whereas high values are desirable for measures such as preventative screening.

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Most people should begin screening for colorectal cancer soon after turning 45, then continue getting screened at regular intervals. However, you may need to be tested earlier than 45, or more often than other people, if—

You or a close relative have had colorectal polyps or colorectal cancer.

You have an inflammatory bowel disease such as Crohn’s disease or ulcerative colitis.

You have a genetic syndrome such as familial adenomatous polyposis (FAP)
external icon or hereditary non-polyposis colorectal cancer (Lynch syndrome).

If you think you are at increased risk for colorectal cancer, speak with your doctor about—

When to begin screening.

Which test is right for you.

How often to get tested.https://www.cdc.gov/cancer/colorectal/basic_info/screening/index.htm

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Attempt to maintain a diet that maintains BM's about soft-serve consistency

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Attempt to maintain a diet that maintains BM's about soft-serve consistency

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This Unicorn Changed the Way I Poop - #SquattyPotty

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What is palliative care at home?

The main goal of palliative care in the home is to improve the quality of life for patients. At Crossroads Hospice & Palliative Care, we believe that receiving care in the patient's own home is comforting, convenient and reduces stress.

Following are the palliative services that can come to your home :

Medical evaluations, including monitoring for common symptoms like nausea, vomiting, pain, and anxiety

Prescribing medications to ease these symptoms

Additional medical applications like treating wounds and other medical needs

Physical therapy and other rehabilitation needs

Providing emotional and spiritual support in addition to physical

Providing social interaction

Providing guidance on navigating the healthcare system and understanding individual healthcare needs

If you'd like to learn more about what palliative care at-home is and entails, please contact us via one of the private options in the blue Help Bar above.

What are the benefits of receiving palliative care in the home ?

Maximum convenience - we come to your home based on your schedule

Remain as comfortable as possible in your own familiar surroundings

Avoid additional costs for hospital stays, medical fees, travel, etc.

Receive help for medical, emotional and spiritual support needs

When we say we come to you, it doesn't literally mean you have to receive palliative care at home. If the person needing care lives in a nursing home or is even in the hospital during the time of need, we will come to wherever the patient is. We truly want to make things as simple and comfortable for you as possible during this difficult time.

We have administrative offices in 14 locations throughout seven states. View our locations here.

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The main goal of palliative care in the home is to improve the quality of life for patients. At Crossroads Hospice & Palliative Care, we believe that receiving care in the patient's own home is comforting, convenient and reduces stress.

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Colorectal Cancer Screening - ACG Clinical Guidelines: 2021

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how does it work?

relearn the first thing you learned

Your body relies on a bend in the colon (where your poop lives) and the anus (where your poop says hi) to keep everything stored until showtime.

Your Puborectalis Muscle helps keep your poop in place by kinking your colon (like a garden hose) while you're standing or sitting. This is helpful when you are sitting and don't want to poop but unhelpful when you do want to poop. If only there was a way to tell your body to unkink that hose...

Your colon's sweet spot comes with the squat. This is the only position in which the Puborectalis Muscle fully relaxes which straightens the kink and allows for complete elimination without straining. Bombs away!

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Official Site Of The Original Squatty Potty® Toilet Stool

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relearn the first thing you learned Your body relies on a bend in the colon (where your poop lives) and the anus (where your poop says hi) to keep everything stored until showtime. Your Puborectalis Muscle helps keep your poop in place by kinking your colon (like a garden hose) while you're standing or sitting.

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Understanding and dealing with your own or family members' colorectal cancer can be challenging. Genetic counseling can help by providing information, resources, and support for you and your family. Genetic counseling can help you better understand your likelihood of getting cancer and make an informed decision about what genetic testing option is best for you.

A genetic counselor or other health care provider with specialty training in cancer genetics can provide genetic counseling. Often getting counseling for Lynch syndrome is covered by insurance companies, but not always. Risk information obtained through genetic testing could potentially impact your insurance eligibility. A law called the Genetic Information Nondiscrimination Act prevents employers and health insurers for discriminating against people based on genetic test results. However, life insurance, disability insurance, and long term care insurance are not included under this law.
Your doctor may refer you for genetic counseling if you have

Already had colorectal cancer

After surgery to remove colorectal cancer, tumor tissue samples are often screened to see if the tumor could have been caused by Lynch syndrome.

In some cases, additional testing is needed to know for sure if the cancer was caused by Lynch syndrome.

A family member diagnosed with Lynch syndrome
Genetic counseling is recommended to see if testing for the Lynch syndrome mutation that runs in your family is right for you.

A family history of colorectal cancer

Your doctor may recommend genetic counseling to see if the cancers in your family are caused by Lynch syndrome, especially if members of your family were diagnosed with colorectal cancer before age 50.

The first person tested in your family should be someone who has had colorectal cancer, if possible.

Do you have an increased risk for colorectal cancer because of your family health history?

What is the chance you have a Lynch syndrome gene mutation?

Could the colorectal, or other cancers that runs in your family be due to mutations in genes other than the Lynch syndrome genes?

If you have Lynch syndrome, or another hereditary cancer syndrome, how likely are you to get cancer?

How will the results of genetic testing for colorectal cancer affect your family members?

Who in your family should be the first to have genetic testing for Lynch syndrome?

What are the possible results of genetic testing for Lynch syndrome and what do the results mean?

What are the potential risks and limitations of genetic testing for Lynch syndrome?

How will knowing you have Lynch syndrome help you lower your risks for cancer?

If you have already had colorectal or other cancers, how will knowing if you have Lynch syndrome affect your treatment plan?

If you have previously been treated for colorectal cancer, what are the chances you will get cancer again?

Following genetic counseling, you can decide whether you would like to have genetic testing done. If you decide to have genetic testing, additional genetic counseling following the testing can help you better understand your test results. The genetic counselor will be available to answer any questions you have regarding your results and your medical options.

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Understanding and dealing with your own or family members' colorectal cancer can be challenging. Genetic counseling can help by providing information, resources, and support for you and your family. Genetic counseling can help you better understand your likelihood of getting cancer and make an informed decision about what genetic testing option is best for you.

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Genetics, gene mutations, and cancer risk

Genetics is the field of science that looks at how traits (such as eye color) are passed down from parents to their children through genes.

Genes are pieces of DNA (deoxyribonucleic acid) inside our cells that tell the cell how to make the proteins the body needs to function. DNA is the genetic "blueprint" in each cell. Genes affect inherited traits passed on from a parent to a child, such as hair color, eye color, and height. They can also affect whether a person is likely to develop certain diseases, such as cancer.

Changes in genes, called mutations, play an important role in the development of cancer. Mutations can cause a cell to make (or not make) proteins that affect how the cell grows and divides into new cells. Certain mutations can cause cells to grow out of control, which can lead to cancer. Still, only about 5% to 10% of all cancers are thought to be strongly related to an inherited gene mutation.

Usually several gene changes or mutations are needed before a cell becomes cancer.

Most cancers start because of acquired gene mutations that happen during a person's lifetime. Sometimes these gene changes have an outside cause, such as exposure to sunlight or tobacco. But gene mutations can also be random events that sometimes happen inside a cell, without a clear cause.

Acquired mutations only affect the cells that grow from the mutated cell. They do not affect all the cells in the person's body. This means all the cancer cells will have the mutations, but normal cells in the body will not. Because of this, the mutations are not passed on to a person's children. This is very different from inherited mutations, which are in every cell in the body - even the cells without cancer.

What is genetic testing?

Genetic testing is the use of medical tests to look for certain mutations in a person's genes. Many types of genetic tests are used today, and more are being developed.

Genetic testing can be used in many ways, but here we'll focus on its use in looking for gene changes linked to cancer.

Genetic testing for cancer risk

Predictive genetic testing is the type of testing used to look for inherited gene mutations that might put a person at higher risk of getting certain kinds of cancer. This type of testing might be advised:

For a person with a strong family history of certain types of cancer, to see if they carry a gene mutation that increases their risk. If they do have an inherited mutation, they might want to have tests to look for cancer early, or even take steps to lower their risk. An example is testing for changes in the BRCA1 and BRCA2 genes (which are known to increase the risk of breast cancer and some other cancers) in a woman whose mother and sister had breast cancer.

For a person already diagnosed with cancer, especially if there are other factors to suggest the cancer might have been caused by an inherited mutation (such as a strong family history or if the cancer was diagnosed at a young age). Testing might show if the person has a higher risk of some other cancers. It can also help other family members decide if they want to be tested for the mutation.

For family members of a person known to have an inherited gene mutation that increases cancer risk. Testing can help them know if they need tests to look for cancer early, or if they should take steps to try to lower their risk.

Most people (even people with cancer) do not need this type of genetic testing. It's usually done when family history suggests there's a cancer that may be inherited (see below).

Testing cancer cells for genetic changes

Sometimes after a person has been diagnosed with cancer, the doctor will do tests on a sample of cancer cells to look for certain gene changes. These tests can sometimes give information on a person's outlook (prognosis) and help tell whether certain types of treatment might be useful.

These types of tests look for acquired gene changes only in the cancer cells that are taken from the patient. These tests are not the same as the tests used to find out about inherited cancer risk.

For more about this kind of testing and its use in cancer treatment, see our information on specific types of cancer.

Who should have genetic testing?

Genetic counseling and testing may be recommended for people who have had certain cancers or certain patterns of cancer

in their family. If you have any of the following, you might consider genetic testing:

Several first-degree relatives (mother, father, sisters, brothers, children) with cancer

Many relatives on one side of the family who have had the same type of cancer

A cluster of cancers in your family that are known to be linked to a single gene mutation ( such as breast, ovarian, and pancreatic cancers in your family).

A family member with more than 1 type of cancer

Family members who had cancer at a younger age than normal for that type of cancer

Close relatives with cancers that are linked to rare hereditary cancer syndromes

A family member with a rare cancer, such as breast cancer in a male or retinoblastoma

Ethnicity (for example, Jewish ancestry is linked to ovarian and breast cancers)

A physical finding that's linked to an inherited cancer (such as having many colon polyps)

A known genetic mutation in one or more family members who have already had genetic testing

If you are concerned about a pattern of cancer in your family, cancer you've had in the past, or other cancer risk factors, you may want to talk to a health care provider about whether genetic counseling and testing might be a good option for you.

You need to know your family history and what kinds of tests are available. For some types of cancer, no known mutations have been linked to an increased risk. Other cancer types may have known mutations, but there's no way to test for them yet.

Family Cancer Syndromes gives you more information on the types of cancers that may be linked to inherited genes.

Next steps

It's important to find out how useful testing may be for you before you do it. Talk to your health care provider and plan to meet with a genetic counselor before the actual test. This will help you know what to expect. The counselor can tell you about the pros and cons of the test, what the results might mean, and what your options are.

If you are considering taking a home-based genetic test, you need to know what it's testing for. Home-based tests do not provide information on a person's overall risk of developing any type of cancer. A home-based genetic test should not be used as a substitute for cancer screening or genetic counseling that may be recommended by a medical professional based on your risk for cancer.

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Understanding Genetic Testing for Cancer

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Genetics is the field of science that looks at how traits (such as eye color) are passed down from parents to their children through genes. Genes are pieces of DNA (deoxyribonucleic acid) inside our cells that tell the cell how to make the proteins the body needs to function.

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Lynch syndrome is the most common hereditary colorectal cancer syndrome. It accounts for about 2% to 4% of all colorectal cancers. In most cases, this disorder is caused by an inherited defect in either the MLH1, MSH2 or MSH6 gene, but changes in other genes can also cause Lynch syndrome.

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Lynch syndrome is the most common hereditary colorectal cancer syndrome. It accounts for about 2% to 4% of all colorectal cancers. In most cases, this disorder is caused by an inherited defect in either the MLH1, MSH2 or MSH6 gene, but changes in other genes can also cause Lynch syndrome.

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Colonoscopy: A Journey Though the Colon and Removal of Polyps