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Immunohistochemistry (IHC) · Gastroenterology, Women's Health
Postmeiotic segregation increased 2 (PMS2) is part of the DNA mismatch repair (MMR) pathway, which is utilized by normal proliferating cells to repair mutations that may occur during DNA replication. PMS2 deficiency or loss of function results in an increased mutation rate and contributes to the development of sporadic colorectal carcinoma as well as hereditary non-polyposis colorectal carcinoma (HNPCC, also called Lynch syndrome). HNPCC accounts for 1-5% of colorectal cancers (1, 2). Antibodies to PMS2 are useful for identifying mismatch repair deficiencies in tumors of the gastrointestinal tract, including HNPCC and associated extracolonic cancers. PMS2 deficiency has also been reported in endometrial, ovarian, breast, esophageal, and ampullary carcinomas, and melanomas. PMS2 is dependent upon MLH1 for stable expression, thus at the protein level, both sporadic and hereditary colorectal cancers deficient in MLH1 generally exhibit concomitant loss of PMS2.