Colorectal Cancer Essay

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Colorectal cancer refers to colon or rectal cancer. Most colorectal cancers are of glandular origin and hence can be classified as adenocarcinomas. It can also be called bowel cancer and is the third most common type of cancer in the world with 45 out of 100,000 people suffering from the same according to The National Institute of Cancer statistics as of 2013. These two types of cancers are significantly similar in their genomic mutations and also bear symptomatic semblance [1]. Colorectal cancer is characterized by tumors that form in the tissues of the colon or the rectum. Like tumors in general, these too are a formed as a result of abnormal and uncontrolled division of cells. The causes of colorectal cancer are mostly unknown although it may be inherited or genetically unrelated [2].
Cancer occurs when mutations in the DNA cause uncontrolled cell proliferation and hence tumor formation. Cancer causing genes can be divided into two classes: 1.) Tumor suppressor genes 2.) Oncogenes. Tumor suppressors if underexpressed are unable to check cell proliferation, resulting in tumor formation. On the other hand, the same results if proto-oncogenes (the precursors of oncogenes) are overexpressed or activated. Isolating the causal genes in colorectal cancer, we identified 54 genes that in various capacities play an important role in the same. On screening on the basis of target site mutations we narrowed this down to 34 major genes. Around 40% of these genes show tumor suppressor properties and apart from them, others point to a number of biological processes and molecular functions such as phosphorylation, regulation and modification of proteins, binding and signaling.
With disease genetics becoming an increasingly investigated field, ...

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...e proved to meddle with immunotherapy by lowering responsiveness to it[13,14]. Another very important gene, TP53 has also been found to be overexpressed due to TS mutations. This gene plays a pivotal role in cell cycle arrest due to its function of binding to DNA to form the p21 protein that ultimately acts as a stop signal in the cell cycle [15].
Thus with the help of a systematic computational protocol of analysis and filtering we were able to isolate certain genes that can considerably alter correct genetic functioning due to predicted mutations in their nucleotide sequences. Given the functions of the above described genes, it can be said that their under or overexpression is crucial to the manifestation of cancer. The analysis of microRNA Target Site SNPs corroborating these facts say that they also might have a determining role to play in the cause of disease.

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