Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy

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Recent advances in the development of protein–protein interactions modulators: mechanisms and clinical trials (2020, background): “4a).(94) The BIR3 domain of the XIAP binds to and inhibits pro-apoptotic caspase-9, thus suspends the apoptosis.”
Targeting mitochondria for cancer therapy (2010, background): “ANT, adenine nucleotide translocase; ATN-224, tetrathiomolybdate; BCL-2, B-cell lymphoma protein 2; BCL-W, also known as BCL2-like protein 2 (BCL2L2); BCL-X L , also known as BCL2-like protein 1 (BCL2L1); CD437, 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2naphthalene carboxylic acid; DMAPT, dimethylamino-p”
The E-Cadherin and N-Cadherin Switch in Epithelial-to-Mesenchymal Transition: Signaling, Therapeutic Implications, and Challenges (2019, background): “Several stimuli such as DNA damage, ischemia and oxidative stress lead to perturbation of mitochondrial membrane and release of cytochrome C into cytosol, where it initiates intrinsic apoptosis by inducing caspase activation [72,74].”
Combination therapy in combating cancer (2017, background): “com/oncotarget preventing the normal apoptotic response [165].”