The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
Apoptosis in cancer
Abstract
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.
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Citations
Cites
Apoptosis in the Pathogenesis and Treatment of Disease
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Death Receptors: Signaling and Modulation
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Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
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p53 is required for radiation-induced apoptosis in mouse thymocytes
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Self-citationHypoxia-mediated selection of cells with diminished apoptotic potential in solid tumours
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Self-citationSunburn and p53 in the onset of skin cancer
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A Chemical Inhibitor of p53 That Protects Mice from the Side Effects of Cancer Therapy
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Cited by
Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607
PUMA, a Novel Proapoptotic Gene, Is Induced by p53
Nakano, K., & Vousden, K. H. (2001) · Molecular Cell · doi:10.1016/s1097-2765(01)00214-3 · Cited by 2,315
Johnstone (2002) · doi:10.1016/s0092-8674(02)00625-6 · Cited by 1,876
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Self-citationThe cGAS–cGAMP–STING pathway connects DNA damage to inflammation, senescence, and cancer
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Metadata
- Authors
- Lowe, S. W., & Lin, A. W.
- Venue
- Carcinogenesis
- Publisher
- Oxford University Press (OUP)
- Published
- 2000-03
- Volume
- 21
- Issue
- 3
- Pages
- 485-495
- ISSN
- 0143-3334 (ISSN-L)
- 1460-2180
- OpenAlex
- W2170507464
- Cited by
- 1,876
- References
- 16
- FWCI
- 20.16
- Type
- journal article
- Language
- en
- Open access
- closed
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
