The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
The Role of BRCA1 in the Cellular Response to Chemotherapy
Abstract
Germline mutations of the BRCA1 gene account for approximately 5% of breast and ovarian cancer cases, and lower than normal BRCA1 expression or function may be an important contributing factor in sporadic cancers. The major role of BRCA1 is to respond to DNA damage by participating in cellular pathways for DNA repair, mRNA transcription, cell cycle regulation, and protein ubiquitination. Because most chemotherapeutic agents function by directly or indirectly damaging DNA, the role of BRCA1 as a regulator of chemotherapy-induced DNA damage has been the subject of an increasing number of investigations. We review published preclinical and clinical evidence that the level of BRCA1 function in an individual patient's tumor can guide the choice of chemotherapeutic agents for breast and ovarian cancer. We conclude that a loss of BRCA1 function is associated with sensitivity to DNA-damaging chemotherapy and may also be associated with resistance to spindle poisons. We recommend that prospective clinical studies investigating the role of BRCA1 in the response to chemotherapy be conducted.
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Cites
Slamon, D. J., Leyland-Jones, B., Shak, S., Fuchs, H., Paton, V., Bajamonde, A., Fleming, T., Eiermann, W., Wolter, J., Pegram, M., et al. (2001) · New England Journal of Medicine · doi:10.1056/nejm200103153441101 · Cited by 11,500
Genome maintenance mechanisms for preventing cancer
Hoeijmakers, J. H. J. (2001) · Nature · doi:10.1038/35077232 · Cited by 3,939
Sensing DNA Damage Through ATRIP Recognition of RPA-ssDNA Complexes
Zou, L., & Elledge, S. J. (2003) · Science · doi:10.1126/science.1083430 · Cited by 2,693
Brca1 Controls Homology-Directed DNA Repair
Moynahan, M. E., Chiu, J. W., Koller, B. H., & Jasin, M. (1999) · Molecular Cell · doi:10.1016/s1097-2765(00)80202-6 · Cited by 1,245
Wang, Y., Cortez, D., Yazdi, P., Neff, N., Elledge, S. J., & Qin, J. (2000) · Genes & Development · doi:10.1101/gad.14.8.927 · Cited by 1,221
Biallelic Inactivation of BRCA2 in Fanconi Anemia
Howlett, N. G., Taniguchi, T., Olson, S., Cox, B., Waisfisz, Q., de Die-Smulders, C., Persky, N., Grompe, M., Joenje, H., Pals, G., et al. (2002) · Science · doi:10.1126/science.1073834 · Cited by 1,149
The Fanconi anaemia/BRCA pathway
D'Andrea, A. D., & Grompe, M. (2003) · Nature Reviews Cancer · doi:10.1038/nrc970 · Cited by 822
Bernstein, C. (2002) · Mutation Research/Reviews in Mutation Research · doi:10.1016/s1383-5742(02)00009-1 · Cited by 527
Cited by
Triple-negative breast cancer: challenges and opportunities of a heterogeneous disease
Bianchini, G., Balko, J. M., Mayer, I. A., Sanders, M. E., & Gianni, L. (2016) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2016.66 · Cited by 3,079
Natural and synthetic compounds in Ovarian Cancer: A focus on NRF2/KEAP1 pathway
Tossetta, G., & Marzioni, D. (2022) · Pharmacological Research · doi:10.1016/j.phrs.2022.106365 · Cited by 115
Hurley, J., Reis, I. M., Rodgers, S. E., Gomez-Fernandez, C., Wright, J., Leone, J. P., Larrieu, R., & Pegram, M. D. (2013) · Breast Cancer Research and Treatment · doi:10.1007/s10549-013-2497-y · Cited by 83
Hereditary breast cancer: From molecular pathology to tailored therapies
Tan, D. S. P., Marchiò, C., & Reis-Filho, J. S. (2008) · Journal of Clinical Pathology · doi:10.1136/jcp.2008.057950 · Cited by 60
Metadata
- Authors
- Kennedy, R. D., Quinn, J. E., Mullan, P. B., Johnston, P. G., & Harkin, D. P.
- Venue
- JNCI Journal of the National Cancer Institute
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-11-16
- Volume
- 96
- Issue
- 22
- Pages
- 1659-1668
- ISSN
- 0027-8874 (ISSN-L)
- 1460-2105
- OpenAlex
- W2142460765
- Cited by
- 430
- References
- 8
- FWCI
- 10.44
- Type
- journal article
- Language
- en
- Open access
- closed
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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.
