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      <title>My exquisite stream by </title>
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      <description>Made with no regrets, whatsoever</description>
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      <pubDate>2019-03-01 14:52:18 UTC</pubDate>
      <lastBuildDate>2019-03-01 15:38:03 UTC</lastBuildDate>
      <webMaster>hello@padlet.com</webMaster>
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         <author>jmtforvalue1</author>
         <link>https://padlet.com/jmtforvalue1/kxmn6cngpoa8/wish/336867427</link>
         <description><![CDATA[Hereditary non-polyposis colorectal cancer (HNPCC)]]></description>
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         <pubDate>2019-03-01 14:58:44 UTC</pubDate>
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         <description><![CDATA[o answer the following questions:

What effect do these defects have in terms of the frequency of mutations in their cells?
What effect do these defects have on the risk of cancer developing in these patients?]]></description>
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         <pubDate>2019-03-01 14:59:15 UTC</pubDate>
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         <description><![CDATA[<div>Genetics<br>Hereditary non-polyposis colorectal cancer accounts for two to seven per cent of cases of colorectal cancer.<br>The risk of an individual developing hereditary non-polyposis colorectal cancer is increased by mutations in a set of genes normally responsible for repairing DNA.<br>Only one inherited copy of a mutated gene is sufficient to raise an individual’s risk of cancer?.<br>Mutations in the MLH1, MSH2, MSH6 or PMS2 genes all increase an individual's risk of developing hereditary non-polyposis colorectal cancer.<br>Mutations in the MSH2 and MLH1 genes are most common (90 per cent of cases).<br>Mutations in the EPCAM gene can also indirectly increase an individual’s risk of developing the disorder. The EPCAM gene lies next to the gene MSH2 on chromosome? 2 and some mutations in the EPCAM gene can switch the MSH2 gene off.<br>Hereditary non-polyposis colorectal cancer also increases the risk of other cancer types including cancers of the ovary, stomach, small intestine, brain and skin.<br>Biology<br>The genes MLH1, MSH2, MSH6 and PMS2 are all involved in repairing the mistakes that occur when DNA is copied in preparation for cell division?.<br>Mutations in these genes mean that mistakes made during DNA replication? are not properly repaired and the cells continue to divide, copying the mistakes over and over.<br>This can then lead to uncontrolled cell growth and possibly cancer.<br>However, not all individuals with these mutations will develop cancerous tumours.</div>]]></description>
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         <pubDate>2019-03-01 15:17:57 UTC</pubDate>
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         <author>jmtforvalue1</author>
         <link>https://padlet.com/jmtforvalue1/kxmn6cngpoa8/wish/336879665</link>
         <description><![CDATA[Genetics
Hereditary non-polyposis colorectal cancer accounts for two to seven per cent of cases of colorectal cancer.
The risk of an individual developing hereditary non-polyposis colorectal cancer? is increased by mutations? in a set of genes? normally responsible for repairing DNA?.
Only one inherited copy of a mutated gene is sufficient to raise an individual’s risk of cancer?.
Mutations in the MLH1, MSH2, MSH6 or PMS2 genes all increase an individual's risk of developing hereditary non-polyposis colorectal cancer.
Mutations in the MSH2 and MLH1 genes are most common (90 per cent of cases).
Mutations in the EPCAM gene can also indirectly increase an individual’s risk of developing the disorder. The EPCAM gene lies next to the gene MSH2 on chromosome? 2 and some mutations in the EPCAM gene can switch the MSH2 gene off.
Hereditary non-polyposis colorectal cancer also increases the risk of other cancer types including cancers of the ovary, stomach, small intestine, brain and skin.
Biology
The genes MLH1, MSH2, MSH6 and PMS2 are all involved in repairing the mistakes that occur when DNA is copied in preparation for cell division?.
Mutations in these genes mean that mistakes made during DNA replication? are not properly repaired and the cells continue to divide, copying the mistakes over and over.
This can then lead to uncontrolled cell growth and possibly cancer.
However, not all individuals with these mutations will develop cancerous tumours.]]></description>
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         <pubDate>2019-03-01 15:23:04 UTC</pubDate>
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         <author>jmtforvalue1</author>
         <link>https://padlet.com/jmtforvalue1/kxmn6cngpoa8/wish/336882075</link>
         <description><![CDATA[Q1 If the DNA repair mechanism is broken more mutations will be processed – just like if you do not proof read then more spelling errors are likely to occur.
Q2 The chance of dedveloping cancer increases as the number of mutations increase.
]]></description>
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         <pubDate>2019-03-01 15:27:17 UTC</pubDate>
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