© Springer Science+Business Media New York 2013. All rights are reserved. In the Western world, endometrial carcinoma is the most common malignant tumor of the female genital tract. The annual incidence has been estimated at 10-20 per 100,000 women. Two clinicopathological variants are recognized: the estrogen-related (type I, endometrioid) and the nonestrogen-related (type II, nonendometrioid). The clinicopathological differences are paralleled by specific genetic alterations, with type I showing microsatellite instability and mutations in PTEN, PIK3CA, K-RAS, andCTNNB1 (b-catenin), and type II exhibiting p53 mutations and chromosomal instability. Women with hereditary nonpolyposis colorectal carcinoma (HNPCC) have germline mutations in one of the DNA mismatch repair genes and frequently develop endometrioid endometrial carcinomas. Some nonendometrioid carcinomas probably arise from preexisting endometrioid carcinomas as a result of tumor progression and, not surprisingly, some tumors exhibit combined or mixed features at the clinical, pathological, and molecular levels. In endometrial carcinomas, apoptosis-resistance may play a role in tumor progression. Understanding pathogenesis at the molecular level is essential in identifying biomarkers for successful targeted therapies. This chapter reviews the genetic changes of endometrial carcinogenesis in the light of morphological features of the tumors and their precursors.
|Title of host publication||Molecular Surgical Pathology|
|Number of pages||19|
|Publication status||Published - 1 May 2013|