The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Cell Cycle Control and Cancer
Abstract
Multiple genetic changes occur during the evolution of normal cells into cancer cells. This evolution is facilitated in cancer cells by loss of fidelity in the processes that replicate, repair, and segregate the genome. Recent advances in our understanding of the cell cycle reveal how fidelity is normally achieved by the coordinated activity of cyclin-dependent kinases, checkpoint controls, and repair pathways and how this fidelity can be abrogated by specific genetic changes. These insights suggest molecular mechanisms for cellular transformation and may help to identify potential targets for improved cancer therapies.
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Citations
Cites
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Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
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Self-citationp53 is required for radiation-induced apoptosis in mouse thymocytes
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Cited by
DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
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Self-citationCisplatin: mode of cytotoxic action and molecular basis of resistance
Siddik, Z. H. (2003) · Oncogene · doi:10.1038/sj.onc.1206933 · Cited by 3,335
Requirement for p53 and p21 to Sustain G 2 Arrest After DNA Damage
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Mice Lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control
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Cell cycle checkpoint signaling through the ATM and ATR kinases
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Metadata
- Authors
- Hartwell, L. H., & Kastan, M. B.
- Venue
- Science
- Published
- 1994-12-16
- Volume
- 266
- Issue
- 5192
- Pages
- 1821-1828
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2084147994
- Cited by
- 2,535
- References
- 15
- FWCI
- 58.64
- 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.
