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"Tumor cell apoptosis" is the process of programmed cell death occurring within neoplastic (cancerous) cells. It is a vital homeostatic mechanism to eliminate dangerous or superfluous cells. In cancer, resistance to apoptosis—commonly through dysregulation of Bcl-2 family proteins, p53 mutations, or impaired death receptor signaling—enables malignant cells to survive and proliferate. Therapeutic approaches in oncology often target the molecular machinery regulating apoptosis to restore this cell death process in tumor cells. However, "tumor cell apoptosis" designates the desired outcome (cell death in tumors) rather than a specific molecular entity, receptor, or canonical target.
Drugs can stimulate tumor cell apoptosis through: Inhibiting anti-apoptotic proteins (e.g., Bcl-2); Activating death receptors (e.g., TRAIL-R1/DR4, TRAIL-R2/DR5); Promoting pro-apoptotic gene transcription (e.g., via p53); Direct caspase activation.
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