Abstract
Changes in DNA damage response markers with treatment in advanced ovarian cancer
Highlights
Ovarian cancer (OC) is the most lethal gynecological malignancy and the fifth leading cause of cancer-related death in women, with a five-year survival in advanced cases of 29% [1]
Patients received a median of four cycles of platinum-based neoadjuvant chemotherapy (NACT), aiming for complete cytoreduction at interval debulking surgery (IDS);
Among the clinical variables that influenced survival, in univariate analysis, only completeness of surgery had a significant impact on both progression-free survival (PFS, homologous recombination (HR) 2.94, 95%CI 1.96–4.35, p < 0.001) and overall survival (OS, HR 2.22, 95%CI 1.43–3.45, p < 0.001) for resection with no residual macroscopic disease vs. incomplete surgery or no surgery
Summary
Ovarian cancer (OC) is the most lethal gynecological malignancy and the fifth leading cause of cancer-related death in women, with a five-year survival in advanced cases of 29% [1]. 60% of patients present with advanced-stage disease, whose standard treatment consists of platinum chemotherapy and cytoreductive surgery [2]. Platinum agents cause extensive DNA damage mainly by the formation of crosslinks that elicit a variety of repair mechanisms. The initial responsiveness to platinum agents in ovarian cancer is probably linked to frequent defects in the homologous recombination (HR) pathway present in approximately 50% of cases, which make tumor cells incapable of repairing platinum-induced DNA breaks and lead to the subsequent accumulation of a fatal DNA damage burden [5,6]. The expression of DNA damage repair (DDR) proteins may provide an alternative read-out for DNA repair competency
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