作者: Peter W. Schlosshauer , Liane Deligdisch , Frédérique Penault-Llorca , Delaram Fatemi , Rui Qiao
DOI: 10.1097/PGP.0B013E3181ED89B3
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摘要: According to a tumor progression model, low-grade ovarian serous carcinomas may evolve from borderline tumors or micropapillary tumors. We sought investigate the role of and associations between BRAF mutational status, extracellular signal regulated kinase activation, p16(INK4A) expression in various types analyzed 29 typical tumors, 8 4 invasive carcinomas, 24 high-grade for status at codon 600; addition, levels downstream signaling protein suppressor were assessed by immunohistochemistry. There was decline with almost complete loss carcinomas. High-grade had variable pattern. found T1799A mutation 12 (41%) 1 (12.5%). No mutations (0%). Among cases tended have stronger compared wild-type BRAF. other correlations identified proteins. Loss be pathogenetic factor The divergent molecular profiles support theory that are unrelated