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Listening to a radio-add the other day they claimed that Obesity is the second highest risk factor for getting cancer . Doing a little digging I found some interesting papers and stats on this. There are many observational study out there, often seeing the same thing. Obese people have a higher risk of getting certain types of cancer. The exact science behind it still remains elusive, but there are multiple factors involved that it will be a difficult and long journey to piece all the puzzles together.
https://www.cancer.gov/about-cancer/causes-prevention/risk/obesity/obesity-fact-sheet
https://jamanetwork.com/journals/jamaoncology/article-abstract/2705608

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This highly controversial advance in medical research provides a change for parents to eradicate a deadly disease, even before the baby is born. The maternal nucleus is transferred to a donor oocyte, whose nucleus has been removed. so that the baby receives their genetic material from 3 parents (Mitochondria from donor, sperm and egg form "original parents") Read more here: https://www.britannica.com/science/three-parent-baby

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Researchers found that brain development in children carrying the mutation leading to the fatal Huntington disease is already impaired, however diagnosis does not happen until patient are usually in their 20's. This also shows how plastic and well designed our brain is - even in development it can outperform diseased cells
for further read: https://www.technologynetworks.com/neuroscience/news/huntingtons-disease-starts-in-childhood-309142

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The Nobel prize for medicine goes to immunologist who discovered the power of our body to fight cancer!

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Two scientists who pioneered an entirely new way to treat cancer have won the 2018 Nobel Prize in Physiology or Medicine.

James Allison of the University of Texas MD Anderson Cancer Center in Houston, Texas and Tasuku Honjo from Kyoto University in Japan will share the 9 million Swedish kronor (US$1 million) prize.

The pair showed how proteins on immune cells can be used to manipulate the immune system so that it attacks cancer cells. The approach has since led to therapies that have been hailed for extending survival in some cancer patients by years, and even sending some advanced cancers into complete remission. Researchers have flocked to the approach, and immunotherapy is now one of the hottest areas in cancer research.

In the 1990s, Allison, then at the University of California, Berkeley, was one of several scientists who studied a 'checkpoint' protein, CTLA-4, that acts as a brake on immune cells called T cells. Allison and colleagues went on, in 1997, to engineer an antibody that could bind to CTLA-4, removing the brakes on T-cell activity and unleashing them to attack cancer cells in mice. A clinical study in 2010 found that the antibody had a striking effect on people with advanced melanoma skin cancer.

W﻿orking independently of Allison, in 1992, Honjo discovered a different T-cell protein, PD-1, which also acts as a brake on the immune system but via a different mechanism. PD-1 went on to become a target in the treatment of cancer. In 2012, research in people revealed that the protein was effective against several different types of cancer. The results were dramatic - some patients with metastatic cancer went into long-term remission, raising the possibility of a cure. Until that point metastatic cancer had been considered by most as incurable.

"Allison's and Honjo's discoveries have added a new pillar in cancer therapy. It represents a completely new principle, because unlike previous strategies, it is not based on targeting the cancer cells, but rather the brakes - the checkpoints - of the host immune system", said Klas Kärre, a member of the Nobel Committee and an immunologist at the Karolinska Institute in Stockholm who described the work of the prizewinners during the Nobel announcement. "The seminal discoveries by the two laureates constitutes a paradigmatic shift and a landmark in the fight against cancer."

Since these studies, clinical work on the CTLA-4 and PD-1 mechanisms -known as 'immune checkpoint therapy' - has developed apace. Treatments that block PD-1 have been shown to be effective in lung and renal cancer, lymphoma and melanoma. Recent clinical work in patients with melanoma that combined therapies targeting CTLA-4 and PD-1 showed that this can be even more effective than CTLA-4 alone. Many trials utilising checkpoint therapy against most cancer types are now underway and scientists are testing numerous other checkpoint proteins to see if they could act as targets.

But others also contributed important early discoveries about checkpoint inhibitors, notes Gordon Freeman, an immunologist at the Dana-Farber Cancer Institute in Boston, Massachusetts, who was disappointed not to be recognised for his contributions. Freeman, along with immunologists Arlene Sharpe of Harvard Medical School in Boston, and Lieping Chen of Yale University in New Haven, Connecticut, studied PD-1 and a molecule that binds to it called PD-L1.

Although the antibody that inhibits CTLA-4 was the first checkpoint inhibitor to reach patients, CTLA-4 inhibitors have so far only been shown to work in melanoma, he notes. And the US Food and Drug Administration (FDA) has approved drugs that target PD-1 and PD-L1 to treat 13 different cancers. "PD-1 and PDL-1 are what works in a really wide variety of people," he says. "And our discoveries were foundational there."

But Freeman also notes that CTLA-4 paved the way, and that Allison played a key role in pushing the field. "Jim Allison has been a real advocate and champion of the idea of immunotherapy," he says. "And CTLA-4 was a first success."

Immunologist Jerome Galon of INSERM, a biomedical research agency in Paris, was not surprised by the committee's decision to award the prize to Honjo and Allison. "I think they really deserve it," he says. "You can always multiply and have many other people, but these are the obvious two first choices."

In 2015, Allison won a prestigious Lasker prize for his work on cancer immunotherapy. In 2016, Honjo won the Kyoto Prize in basic sciences, a global prize awarded by the Inamori Foundation.

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Cancer immunologists scoop medicine Nobel Prize

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Two scientists who pioneered an entirely new way to treat cancer have won the 2018 Nobel Prize in Physiology or Medicine. James Allison of the University of Texas MD Anderson Cancer Center in Houston, Texas and Tasuku Honjo from Kyoto University in Japan will share the 9 million Swedish kronor (US$1 million) prize.

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Tweets by Katjetz

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First human trial in the US?

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Gene-editing has been attempted on cells inside a patient, in a world first by doctors in California.

Brian Madeux, 44 from Arizona, was given the experimental treatment to try to correct a defect in his DNA that causes Hunter's syndrome.

Mr Madeux says he was prepared to take part in the trial as he is "in pain every second of the day".

It is too soon to know whether or not the gene-editing has worked in Mr Madeux's case.

Hunter's syndrome is rare. Patients are born without the genetic instructions for an enzyme that breaks down long sugary molecules called mucopolysaccharides.

Instead, they build up in the body and damage the brain and other organs. Severe cases are often fatal.

"I actually thought I wouldn't live past my early 20s," said Mr Madeux.

Patients need regular enzyme replacement therapy to break down the mucopolysaccharides.

But Mr Madeux has been given an experimental treatment to rewrite his DNA to give him the instructions for making the enzyme.

The therapy was infused into his bloodstream on Monday at Oakland's UCSF Benioff Children's Hospital.

The therapy contains two molecular scissors - called zinc finger nucleases - that cut the DNA at a precise spot.

This creates an opening for a new piece of DNA, containing the desired instructions, to be inserted into the patient's genetic code.

The genetic therapy has been designed so it becomes active only once it gets inside Mr Madeux's liver cells.

Dr Chester Whitley, one of the doctors working on the trial, told the BBC: "If works as well as it does in mice, this has huge ramifications.

"I'm very optimistic we have a both safe and efficacious way of providing gene therapy."

His long-term hope is to perform gene-editing shortly after birth, because an "untreated baby loses 20 IQ points per year".

Gene editing has been tried in people before, but cells have been taken out of the body, edited, checked for errors and then placed back in.

That works for tissues that can be temporally removed and returned at a later date like a sample of bone marrow.

However, such an approach is impossible for organs like the liver, heart or brain. It is why doctors have attempted the gene editing inside the patient's body.

The trial is testing only the safety of performing the gene editing and it will require more research to know if it could be a valid therapy.

So far there have been no side effects in Mr Madeux and if everything continues to go well, then up to nine patients will receive the experimental procedure as part of the study.

'New frontier'

Dr Sandy Macrae, from Sangamo Therapeutics, which designed the therapy, said: "For the first time, a patient has received a therapy intended to precisely edit the DNA of cells directly inside the body.

"We are at the start of a new frontier of genomic medicine."

Further safety trials using the same technology to treat haemophilia B and Hurler syndrome are also planned.

Mr Madeux says he is prepared to have his DNA altered "if it will prolong my life and help scientists find cures for humankind".

Follow James on Twitter.

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First gene-editing in human body attempt

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Gene-editing has been attempted on cells inside a patient, in a world first by doctors in California. Brian Madeux, 44 from Arizona, was given the experimental treatment to try to correct a defect in his DNA that causes Hunter's syndrome.

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A small trial on dogs in the UK showed a 92% recovery of dystrophin, a protein mutated and degraded in Duchenne muscular dystrophy.

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Scientists have for the first time used gene-editing to treat Duchenne muscular dystrophy in a large mammal, a significant step towards effective treatment for people with the disorder.

The condition, which has no cure, leads to loss of muscle function and strength and ultimately an early death.

But in a study on dogs, scientists were able to partially restore the key protein people with DMD cannot make.

They hope in the future to test the technique in people.

Duchenne muscular dystrophy (DMD) is the most common fatal genetic disease in children and almost entirely affects boys and young men - about 2,500 of them in the UK have the condition.

Children born with the degenerative disease have a genetic mutation that stops them producing dystrophin, a protein that is vital for muscle strength and function.

The same disorder also occurs in many dog breeds.

Using the Crispr gene-editing tool, scientists were able to restore dystrophin in four dogs that had the most common genetic mutation seen in DMD patients, by making a single strategic cut in the faulty DNA.

This was done by injecting the dogs, who were one month old, with two harmless viruses that edited the genome of the dog in the cells of the muscles and heart.

Within several weeks of the edit made in the dogs, the missing protein was restored in muscle tissue throughout the body, including a 92% correction in the heart and 58% in the diaphragm, the main muscle needed for breathing, according to the study in the journal Science.

Scientists have estimated that a 15% or greater improvement is needed to significantly help patients.

The study was a collaboration between the Royal Veterinary College, in London, and the UT Southwestern Medical Center, in the US.

Dr Eric Olson, one of the authors, from UT Southwestern, said: "Children with DMD often die either because their heart loses the strength to pump or their diaphragm becomes too weak to breathe.

"This encouraging level of dystrophin expression would hopefully prevent that from happening."

Richard Piercy, professor of comparative neuromuscular disease at the Royal Veterinary College, said: "The ambition is to show that this is safe and effective in dogs and then move into humans trials.

"If that works, then the treatment could also apply to pet dogs that we see in our clinics - and that's what we hope for here at the college, as it's our goal to make animals better."

Corrections of DMD mutations have been done in mice and human cells before. But this was the first time the technique was carried out in a large mammal.

The proof-of-concept study raises hopes that Crispr can ultimately lead to more effective treatments for DMD.

At the moment, few treatments are available for the condition, which causes a progressive loss of function in the body and eventually an early death, usually by patients' 20s or early 30s.

The technique used in the study was for a genetic fault that affects about 13% of people with DMD. But experts say it could potentially be applied to the many other mutations those with the condition have.

The lab will next conduct longer-term studies to measure whether the dystrophin levels remain stable and to ensure there are no adverse side-effects.

Dr Olson hopes the next step beyond dogs is a clinical trial in humans.

"Our strategy is different from other therapeutic approaches for DMD because it edits the mutation that causes the disease and restores normal expression of the repaired dystrophin," said Dr Leonela Amoasii, lead author of the study.

"But we have more to do before we can use this clinically."

'Key step forward'

Independent experts said the study was "promising" and might one day be seen as "ground-breaking" but pointed out that there were some limitations, including the small group of dogs used.

And while dystrophin production was increased, what impact this might have had on improvements in muscle function was not measured.

Nevertheless, experts said the findings were an important step towards the use of gene editing for DMD.

Darren Griffin, professor of genetics at the University of Kent, said: "This work represents a small, but very significant step towards the use of gene editing for DMD.

"Any steps towards significant treatment regimes can only be good news. In the fullness of time, this paper may well be seen as one of the ground-breaking studies that led the way to effective treatment."

Dr Kate Adcock, director of research and innovation at the charity Muscular Dystrophy UK, said: "The next step will be to conduct larger, longer-term studies to see if the gene editing approach does help to slow the progression of the condition and improve muscle strength.

"This won't be a cure - but that shouldn't obscure that this is a key step forward in proving the Crispr technology could work for Duchenne."

Follow Alex on Twitter.

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Gene-editing hope for muscular dystrophy

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Scientists have for the first time used gene-editing to treat Duchenne muscular dystrophy in a large mammal, a significant step towards effective treatment for people with the disorder. The condition, which has no cure, leads to loss of muscle function and strength and ultimately an early death.