Apoptosis in cancer

• Published in: Carcinogenesis (New York) Vol. 21; no. 3; pp. 485 - 495
• Main Authors: Lowe, Scott W., Lin, Athena W.
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01-03-2000; Oxford Publishing Limited (England)
• Subjects: Apoptosis; Biological and medical sciences; Cell physiology; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes; Fundamental and applied biological sciences. Psychology; Humans; IGF; insulin-like growth factor; Molecular and cellular biology; Mutation; Neoplasms - genetics; Neoplasms - pathology; Neoplasms - therapy; NF-κB; nuclear factor κB; Oncogenes; permeability transition pore; PTP; TNF receptor-associated factor; TNF-α; TRAF-2; tumor necrosis factor α; Antineoplastic agent; Cytotoxicity; Tumor initiation; Review; Metastasis; Malignant tumor; Inductor; Prospective; Sensitivity; Treatment; Tumor progression; Disruption; Mutation; Apoptosis
• ISSN: 0143-3334; 1460-2180
• DOI: 10.1093/carcin/21.3.485

In the last decade, basic cancer research has produced remarkable advances in our understanding of cancer biology and cancer genetics. Among the most important of these advances is the realization that apoptosis and the genes that control it have a profound effect on the malignant phenotype. For example, it is now clear that some oncogenic mutations disrupt apoptosis, leading to tumor initiation, progression or metastasis. Conversely, compelling evidence indicates that other oncogenic changes promote apoptosis, thereby producing selective pressure to override apoptosis during multistage carcinogenesis. Finally, it is now well documented that most cytotoxic anticancer agents induce apoptosis, raising the intriguing possibility that defects in apoptotic programs contribute to treatment failure. Because the same mutations that suppress apoptosis during tumor development also reduce treatment sensitivity, apoptosis provides a conceptual framework to link cancer genetics with cancer therapy. An intense research effort is uncovering the underlying mechanisms of apoptosis such that, in the next decade, one envisions that this information will produce new strategies to exploit apoptosis for therapeutic benefit.