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The term **"Cancer cell apoptosis pathways"** refers to a set of molecular and cellular processes that regulate programmed cell death in cancer. There are two central apoptosis signaling routes: the **extrinsic pathway** (triggered by activation of cell-surface death receptors like Fas, TNFR1, and DR4/5 by their ligands) and the **intrinsic pathway** (regulated by mitochondrial membrane permeabilization, primarily controlled by BCL-2 family proteins such as BAX, BAK, and BH3-only proteins). Both converge on the activation of a caspase cascade resulting in characteristic morphological and biochemical features of apoptosis. Disruption of these pathways is fundamental to oncogenesis, tumor progression, and drug resistance, making components of these pathways attractive—but challenging—therapeutic targets[3][4][5][6][7]. Targeting individual molecular components within these pathways (as in BCL-2 family proteins or death receptors) offers therapeutic opportunities, but the broad term itself is not a single druggable target.
Induction of apoptosis via extrinsic (death receptor) or intrinsic (mitochondrial) pathways Activation of caspases (particularly caspase-8, caspase-9, and downstream executioners like caspase-3) Blockade of anti-apoptotic proteins (such as BCL-2, BCL-xL, MCL-1)
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