Etiology

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Colorectal cancer is a multifactorial disease process, and both non-modifiable and modifiable risk factors can play a role in the development of CRC.  Current research indicates that genetic factors and family history have the greatest correlation to colorectal cancer.  The progression from an adenoma (premalignant lesion) to an invasive adenocarcinoma is often associated with genetic alterations. Those with a first-degree relative (parent, sibling, or offspring) who have had CRC have 2 to 3 times the risk of developing the disease compared to those with no family history.  About 5% of patients with CRC have a well-defined genetic syndrome.  The most common of these is Lynch Syndrome (also known as hereditary nonpolyposis colorectal cancer).  Lynch Syndrome is part of a subset of genetic diseases that causes colorectal cancer due to deficient DNA mismatch repair.  Lifetime risks of CRC development in individuals with Lynch Syndrome is approximately 66% in men and 43% in women.  Familial adenomatous polyposis (FAP) is the second most common genetic syndrome that predisposes an individual to CRC.  FAP is caused by the hereditary mutation of the APC gene (adenomatous polyposis gene).  The lifetime risk of developing CRC in a person with FAP approaches 100% by age 40.  Additionally, individuals who suffer from inflammatory bowel disease, such as ulcerative colitis and Crohn’s disease, have a higher risk of developing colorectal cancer.  Modifiable risk factors include sedentary lifestyle, obesity, high consumption of red and/or processed meats, tobacco smoking, and alcohol consumption.