The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Apoptosis in the development and treatment of cancer
Abstract
Our somatic cells are born by mitosis and almost all will die by apoptosis, a physiological process of cellular suicide. Cancers can occur when this balance is disturbed, either by an increase in cell proliferation or a decrease in cell death. The goal of cancer therapy is to promote the death of cancer cells without causing too much damage to normal cells. Our knowledge of the mechanisms of apoptosis has enhanced our understanding of how some cancers originate and progress. It has also revealed that existing cancer therapies can work in two ways, by induction of apoptosis as well as by direct toxicity. In some cases resistance to apoptosis may explain why cancer therapies fail. Novel treatments designed to exploit our knowledge of apoptotic mechanisms are under development to promote apoptosis of cancer cells and limit concurrent death of normal cells.
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Cites
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Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
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Mice Lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control
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Genetic control of programmed cell death in the nematode C. elegans
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IAP proteins: blocking the road to death's door
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Lindsten, T., Ross, A. J., King, A., Zong, W.-X., Rathmell, J. C., Shiels, H. A., Ulrich, E., Waymire, K. G., Mahar, P., Frauwirth, K., et al. (2000) · Molecular Cell · doi:10.1016/s1097-2765(00)00136-2 · Cited by 1,489
p53- and Drug-Induced Apoptotic Responses Mediated by BH3-Only Proteins Puma and Noxa
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A Chemical Inhibitor of p53 That Protects Mice from the Side Effects of Cancer Therapy
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Metadata
- Authors
- Gerl, R.
- Venue
- Carcinogenesis
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-09-16
- Volume
- 26
- Issue
- 2
- Pages
- 263-270
- ISSN
- 0143-3334 (ISSN-L)
- 1460-2180
- OpenAlex
- W2162916643
- Cited by
- 385
- References
- 9
- FWCI
- 2.84
- Type
- journal article
- Language
- en
- Open access
- closed
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