The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
G2 checkpoint abrogation and checkpoint kinase-1 targeting in the treatment of cancer
Open accessAbstract
Rigorous quality control steps, termed checkpoints, tightly regulate progression through the cell cycle. DNA-damaging chemotherapy and radiation activate functional cellular checkpoints. These checkpoints can facilitate DNA repair and promote cell death in unrepaired cells. There are at least three DNA damage checkpoints - at G1/S, S, and G2/M - as well as a mitotic spindle checkpoint. Most cancer cells harbour mutations in tumour suppressors and/or oncogenes, which impair certain cell checkpoints. Inhibiting the remaining cell checkpoints - particularly after exposure of cancer cells to chemotherapy and/or radiation - allows cell death, a strategy now being employed in cancer therapeutics. With our increasing knowledge of cell cycle regulation, many compounds have been developed to inhibit specific checkpoint components, particularly at the G2/M transition. One such target is checkpoint kinase-1 (Chk1). We review here the molecular framework of the cell cycle, the rationale for targeting Chk1, the preclinical concepts related to the development of Chk1 inhibitors, and the efficacy and safety results from Chk1 inhibitors now in phase I/II trials.
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Cites
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Cited by
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Mitotic catastrophe: a mechanism for avoiding genomic instability
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Integrated Proteogenomic Characterization of Clear Cell Renal Cell Carcinoma
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BackgroundIonizing Radiation-Induced DNA Damage, Response, and Repair
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Metadata
- Authors
- Bucher, N., & Britten, C. D.
- Venue
- British Journal of Cancer
- Published
- 2008-01-29
- Volume
- 98
- Issue
- 3
- Pages
- 523-528
- ISSN
- 0007-0920 (ISSN-L)
- 1532-1827
- OpenAlex
- W2023942118
- Cited by
- 349
- References
- 45
- FWCI
- 13.40
- Type
- journal article
- Language
- en
- Open access
- hybrid
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