Gastrointestinal toxicity of targeted cancer therapies in the United States: Clinicopathologic patterns, FDA safety frameworks, and implications for national patient protection (IMAGE)
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Figure 1: Mechanisms of Gastrointestinal Toxicity from Targeted Cancer Therapies.
This schematic illustrates the major mechanistic pathways by which targeted therapies cause gastrointestinal toxicity. TKIs primarily act through vascular compromise, ADCs through direct epithelial injury, and CAR-T cells via cytokine-mediated inflammation. Other classes, including mTOR and PARP inhibitors, contribute apoptotic and DNA-repair–linked injury patterns. Abbreviations: ADC: Antibody–Drug Conjugate; CAR-T: Chimeric Antigen Receptor T-cell; CLDN18.2: Claudin 18.2; CRS: Cytokine Release Syndrome; GI: Gastrointestinal; mTOR: Mammalian Target of Rapamycin; PARP: Poly (ADP-ribose) Polymerase; TKI: Tyrosine Kinase Inhibitor; VEGF/VEGFR: Vascular Endothelial Growth Factor/(Receptor).
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