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[Defective autophagy constitutes a hallmark of cancer cells together with: (1) provision of autonomous growth signals;, (2) insensitivity to antiproliferative stimuli; (3) disabled apoptosis; (4) limitless replication; (5) production of angiogenic factors; (6) tissue invasion with metastasis; (7) avoidance of the immune response; and (8) enhanced anabolism. p53 is the best-known human oncosuppressor protein, and its genetic/epigenetic inactivation has been observed in more than 50% of all human cancers. p53 mostly mediates tumor suppression by transactivating pro-apoptotic and cell cycle arresting genes, but also by favoring mitochondrial apoptosis in a transcription-independent fashion, by modulating metabolic circuitries and by regulating autophagy. p53 mutations (or epigenetic changes) that simultaneously abolish its pro-apoptotic and autophagy-inhibitory functions behave as 'multi-hit' events, as opposed to 'single-hit' mutations that only affect the classical (pro-apoptotic and/or cell cycle-arresting) functions of the p53 system.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
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Gene-disease associations inferred from text-mining the literature.
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