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Chemotherapy cytotoxicity pathways represent the collective biochemical and molecular processes through which antineoplastic drugs induce damage and death in cancer cells (StatPearls, 2023). These pathways are typically activated following the interaction of a drug with its primary molecular target, such as DNA, topoisomerases, or tubulin (PubMed, PMC4506279). Key mechanisms include the induction of DNA double-strand breaks, inhibition of nucleotide synthesis, and disruption of the mitotic spindle, which collectively trigger the DNA damage response (DDR) (NIH, 2021). If the damage is irreparable, the cell proceeds toward programmed cell death, primarily via the intrinsic (mitochondrial) apoptotic pathway, though necrosis, autophagy, and senescence may also occur (Wikipedia, 2023). While these pathways are the foundation of conventional cancer treatment, their activation in non-malignant cells leads to characteristic side effects like myelosuppression and gastrointestinal distress (PubChem, 2024). Understanding these pathways is crucial for identifying biomarkers of drug sensitivity and developing strategies to overcome chemoresistance (PubMed, PMC4506279).
Activation of cellular death signaling following DNA damage, microtubule disruption, or metabolic inhibition (StatPearls, 2023; PubMed, PMC4506279).
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