Ovarian cancer is the sixth most common cancer and the fifth leading cause of cancer-related death among women in developed countries. Approximately 90% of human ovarian cancer arises within the ovarian surface epithelium (OSE), with the rest originating from granulosa cells or, rarely, stroma or germ cells. Ovarian epithelial tumors are divided into mucinous, serous, endometrioid, and clear cell subtypes. Approximately 10% of ovarian cancers arise in women who have inherited mutations in cancer susceptibility genes (BRCA1 or BRCA2). The vast majority of ovarian cancers are sporadic, resulting from the accumulation of genetic damage over a lifetime. Several specific genes involved in ovarian carcinogenesis have been identified, including the p53 tumor suppressor gene and ERBB2 and PIK3CA oncogenes.
McKie AB, Vaughan S, Zanini E, Okon IS, Louis L, de Sousa C, Greene MI, Wang Q, Agarwal R, Shaposhnikov D, Wong JL, Gungor H, Janczar S, El-Bahrawy M, Lam EW, Chayen NE, Gabra H
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The OPCML tumor suppressor functions as a cell surface repressor-adaptor, negatively regulating receptor tyrosine kinases in epithelial ovarian cancer.
Carpten JD, Faber AL, Horn C, Donoho GP, Briggs SL, Robbins CM, Hostetter G, Boguslawski S, Moses TY, Savage S, Uhlik M, Lin A, Du J, Qian YW, Zeckner DJ, Tucker-Kellogg G, Touchman J, Patel K, Mousses S, Bittner M, Schevitz R, Lai MH, Blanchard KL, Thomas JE
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A transforming mutation in the pleckstrin homology domain of AKT1 in cancer.
