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Cell survival and apoptosis pathways encompass the intricate biochemical signaling networks that regulate the life-and-death decisions of a cell. In cancer cell lines, these pathways are frequently hijacked to promote uncontrolled proliferation and resistance to therapy, often through the upregulation of anti-apoptotic BCL-2 family proteins or the constitutive activation of the PI3K/AKT/mTOR survival axis (Hanahan & Weinberg, 2011). The apoptotic process itself is divided into the intrinsic pathway, which involves mitochondrial outer membrane permeabilization, and the extrinsic pathway, which is triggered by extracellular death ligands (Fuchs & Steller, 2011). Many modern oncology drugs are designed to intervene in these pathways, such as Venetoclax, which inhibits BCL-2 to induce apoptosis in chronic lymphocytic leukemia (Roberts et al., 2016). However, the high degree of crosstalk and redundancy between survival and death signals often allows cancer cells to develop resistance, making these pathways a primary focus for combination therapy research (Thorpe et al., 2015). Targeting these mechanisms requires a precise understanding of the specific molecular dependencies within a given tumor type to avoid systemic toxicity.
Induction of programmed cell death through the inhibition of anti-apoptotic proteins or the blockade of pro-survival signaling cascades.
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