How Genetics Affects Colon Cancer Disease

colon-cancer-diseaseStudies have shown that the third most frequently occurring cancer in both sexes is colon cancer. It is a disorder mainly caused by improper lifestyle choices but genetics also play a great role in its development. Colon cancer disease is an abnormal, disorderly, and uncontrollable growth of cells in the large intestine, where the body’s waste material is stored.

Abnormal mushroom growths tend to start in the inner surface of the colon or rectum and some eventually become malignant tumors while others remain benign polyps. Once a polyp develops into a tumor, it grows very fast and it can immediately block, invade, break through the colon walls then spread through other parts of the body. Colon cancer disease commonly presents with rectal bleeding, marked decrease in diameter of stools, constipation or diarrhea, unexplained weight loss, abdominal pain, and on extreme cases, it manifests with anemia and total prevention of excretion.

There are major risk factors that predispose a person to developing colon cancer and these are age, polyps in the colon, diet and lifestyle, chronic inflammatory bowel disease, and familial or genetic history. Among these, research show that thirty percent of cases are associated to genetic factors. Finding out the genetic changes in colon cancer makes a person more aware of how much risk he or she has in developing cancer of the colon.

Does having a relative who suffered from colon cancer disease immediately translate to developing the disease? Cancer of the colon cannot be inherited but having genes related to it can increase one’s risk of having the disease. Learn about the genetic changes in colon cancer as evidenced by hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome), familial adenomatous polyposis (FAP), juvenile polyposis (JP), and Peutz-Jeghers syndrome (PJS).

Hereditary Nonpolyposis Colorectal Cancer disease is responsible for up to seven percent of colorectal diseases. The genetic changes in colon cancer accountable for this condition are in MLH1, MSH2, MSH6, and PMS2. Parents carrying these genes may pass on the risk to their children.

If one parent has the mutation in one or more gene, he/she can give it to his/her child thereby increasing the risk for colorectal cancer. If the child is autosomal recessive then he/she will not have the increased risk for the disease while if the child is autosomal dominant then he/she will have the higher predisposition to the disease. It should be noted that it is not the cancer that is passed on but only the increased risk for having colorectal cancer.

colon cancer diseaseFamilial Adenomatous Polyposis is an inherited disease in which thousands of polyps form in the large intestine of the body. Gene mutations in MUTYH and APC are responsible for this disease. Because polyps usually develop into tumors, having several polyps increase the chances of developing colorectal cancer disease.

Juvenile Polyposis is a condition where polyps develop in the colon of young adults below the age of twenty. When these polyps are not removed by the age of thirty five, there is twenty percent chance that they will develop into colon cancer disease. The genetic changes in colon cancer responsible for Juvenile Polyposis are SMAD4 and BMPR1A.

Peutz-Jeghers syndrome is a disease characterized by development of growths called Hamartomatous polyps in the gastrointestinal tract particular in the stomach and intestines. These polyps increase the risk for developing colorectal cancer. The gene mutations in STK11 is the main cause this condition.

These are the different gene mutations which are responsible for developing certain diseases that when gone unmanaged may develop into colorectal cancer disease. Remember that having these mutated genes does not necessarily dictate that a person will have colon cancer disease but rather increases one’s risk for it. Being aware of the risk allows an individual to do all the necessary measures to completely prevent developing the dreadful disease.