الفهرس 
Fallopian tubal carcinomaOnly 14 pages are availabe for public view
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Abstract
Epithelial ovarian cancer (EOC) remains the most lethal gynecologic cancer. Five-year survival rates are 5–30% for patients with advanced disease, despite aggressive surgical cytoreduction combined with platinum/taxane-based chemotherapy (Jemal et al. 2010) Both BRCA1 and BRCA2 tumor suppressor genes are involved in DNA repair via homologous recombination. Cells with alterations in homologous recombination pathway genes are unable to repair DNA double-strand breaks, this can result in genomic instability and a predisposition to malignant transformation. (Tutt and Ashworth 2002) Conversely, because homologous recombination pathway deficiencies can also impair tumor cells’ ability to repair DNA crosslinks introduced by chemotherapy agents such as cisplatin, it has been hypothesized that BRCA-deficient patients will likely have higher survival rates because of an improved response to platinum-based chemotherapy (Tan et al. 2008) Inhibitors of poly(ADP-ribose) polymerase (PARP) have emerged as one of the most exciting new therapies for the treatment of EOC. The greatest efficacy of PARP inhibitors has been shown in patients with cancers harboring BRCA mutations either germline or somatic/tumor mutations. Largely, PARP inhibitors exhibit their antitumor effect through inhibition of single-strand DNA break repair ultimately having a damaging impact on cells defective in homologous recombination [Murai et al. 2012].