Molecular biology of human ovarian cancer.

Abstract

It has been proposed that epithelial ovarian cancers are of unifocal origin and arise from a single cell. Many alterations occur during the multistep carcinogenesis including interaction of peptide growth factors, activation of protooncogenes, and loss of tumor-suppressor genes. Increased activity of TGF-alpha and decreased activity of TGF-beta may contribute to the development of many ovarian cancers. Loss of TGF-beta responsiveness has been associated with the downregulation of c-myc expression in the development of ovarian cancer. Alternative expression of many oncogenes including ras, erbB2 and c-myc, were detected in many studies. p53 mutation was detected in 50% of advanced ovarian cancer, suggesting that loss of tumor-suppressor gene function facilitates transformation. Serum parameters like AFP, CEA, CA-125, IAP, LDH, SA, TGF-alpha, and M-CSF have been used as ovarian tumor markers. None of these biochemical markers is presently consistent and specific enough to be an early detection for ovarian cancers.

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@article{Chow1996MolecularBO, title={Molecular biology of human ovarian cancer.}, author={S N Chow and C H Chien and Chien-Hong Chen}, journal={International surgery}, year={1996}, volume={81 2}, pages={152-7} }