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Ovarian cancer cell survival and proliferation pathways represent a complex network of integrated signaling cascades and biological processes that drive the growth, maintenance, and chemoresistance of ovarian malignancies. Key components include the PI3K/AKT/mTOR and MAPK/ERK signaling axes, which are frequently dysregulated and promote uncontrolled cell cycle progression and evasion of apoptosis (Ghoneum et al., 2021, Cancers). Additionally, DNA damage response (DDR) pathways, particularly those involving BRCA1/2 and PARP, play a critical role in maintaining genomic stability in these cancer cells (NIH/NCI). In therapeutic contexts, these pathways are targeted by a variety of agents, including PARP inhibitors that exploit synthetic lethality and anti-angiogenic drugs like bevacizumab that disrupt the tumor microenvironment (StatPearls). Because this entry describes a broad set of cellular mechanisms rather than a single molecular entity, it is classified as a pathway or phenotypic category rather than a specific therapeutic target. Understanding the crosstalk between these survival signals is essential for developing combination therapies and overcoming the high rates of recurrence observed in advanced ovarian cancer.
Inhibition of intracellular signaling cascades (e.g., PI3K/AKT/mTOR, MAPK/ERK), disruption of DNA damage repair mechanisms, and induction of apoptosis or cell cycle arrest.
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