Abstract
Colorectal cancer (CRC) is a multifactorial disease that arises due to the accumulation of genetics as well as epigenetic alterations in a number of onco-, tumor suppressor-, mismatch repair-, and cell cycle-genes in colon mucosa cells. Epigenetic silencing of the key tumor suppressor genes has been identified as one of the new and distinct mechanisms driving the tumor initiation and progression. In this review we have explored the mechanism of hypermethylation of the CpG islands and its consequent role in colorectal carcinogenesis. We have also discussed the epigenetic view of molecular and pathological basis of colorectal neoplasia and also the role of 1-carbon metabolism in driving the methylation of key genes in CRC.
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