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Abstract Background and Objective: Mismatch repair plays a role in the DNA damage response pathway that eliminates severely damaged cells and prevents both mutagenesis in the short term and tumorgenesis in the long term. Loss of expression of MMR proteins can occur by two mechanisms: One is promotor hypermethylation, which silences gene expression and occurs in sporadic CRC (10-15% of CRC) Second is germline mutation which occurs in hereditary cases (Lynch Syndrome/hereditary non polyposis colorectal cancer (HNPCC) (1-5 % of CRC). Lynch syndrome (HNPCC) is an autosomal dominant genetic condition that has a high risk of colon canceras well as other cancers including endometrial cancer (second most common), ovary, stomach, small intestine, hepatobiliary, upper urinary tract, brain, and skin. The objective of our study is to assess expression of MMR genes (MLH1, MSH2, MSH6, and PMS2) by immunohistochemical technique, assess mismatch repair status in CRC and in precancerous lesions, also to identify patients with possibility to have Lynch syndrome, and to analyze association between mismatch repair status and different clinicopathological parameters |