The Genetics Of Risk: Colon Cancer

A great example of how genetics can play a role in cancer risk is colon cancer. 80% of colon cancer patients, in fact, carry a mutation in the APC gene – also known as adenomatous polyposis coli. Interestingly, APC plays an important role in all cells in the body “switching off” a molecular pathway centered around another molecule known as the beta-catenin. Beta-catenin is a powerful molecule that is classified a sa “transcription factor” – which means that it can enter the nucleus where the DNA is kept and it can alter what parts of the DNA are “switched on” and “switched off”. This dramatically alters the behavior the cell: in particular, beta-catenin is capable of turning on the switch that makes cells divide.

When APC is mutated, beta-catenin is therefore permanently switched on – and cancer cells are replicating uncontrollably. As we have explored throughout this series, uncontrolled replication is the first step towards forming a new tumor. In a way, APC stands alone to block this particular form of cancer initiation. Genes that play this kind of role are known as tumor suppressor genes. Once a tumor suppressor gene is mutated, it stops functioning properly and it can no longer stop cancer from forming. The opposite of a tumor suppressor gene is known as an oncogene. Oncogenes have the power to create a tumor when permanently switched on by mutation.  One really important oncogene in colorectal cancer is known as CDK8. When CDK8 is mutated and permanently active it leads to the permanent activation of beta-catenin – which leads to the cells lining the intestine proliferating uncontrollably and eventually forming a tumor. In a way, APC and CDK8 are the “on” and “off” switches for beta-catenin – the key to cell replication and therefore to cancer.

Thankfully, over the past decade the rates of colorectal cancer have been steadily dropping owing to exceptional cancer-screening programs – and improved lifestyle changes including a balanced diet and healthy exercise.


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