The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
BRCA1 Mutation Analysis of 41 Human Breast Cancer Cell Lines Reveals Three New Deleterious Mutants
Abstract
Germ line mutations of the BRCA1 gene confer a high risk of breast cancer and ovarian cancer to female mutation carriers. The BRCA1 protein is involved in the regulation of DNA repair. How specific tumor-associated mutations affect the molecular function of BRCA1, however, awaits further elucidation. Cell lines that harbor BRCA1 gene mutations are invaluable tools for such functional studies. Up to now, the HCC1937 cell line was the only human breast cancer cell line with an identified BRCA1 mutation. In this study, we identified three other BRCA1 mutants from among 41 human breast cancer cell lines by sequencing of the complete coding sequence of BRCA1. Cell line MDA-MB-436 had the 5396 + 1G>A mutation in the splice donor site of exon 20. Cell line SUM149PT carried the 2288delT mutation and SUM1315MO2 carried the 185delAG mutation. All three mutations were accompanied by loss of the other BRCA1 allele. The 185delAG and 5396 + 1G>A mutations are both classified as pathogenic mutations. In contrast with wild-type cell lines, none of the BRCA1 mutants expressed nuclear BRCA1 proteins as detected with Ab-1 and Ab-2 anti-BRCA1 monoclonal antibodies. These three new human BRCA1 mutant cell lines thus seem to be representative breast cancer models that could aid in further unraveling of the function of BRCA1. (Cancer Res 2006; 66(1): 41-5)
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Genetic instabilities in human cancers
Lengauer, C., Kinzler, K. W., & Vogelstein, B. (1998) · Nature · doi:10.1038/25292 · Cited by 4,168 · cited 1×
“Allelic losses at 17q are therefore often underestimated, as karyotype-based methods do not detect loss when the retained allele is amplified or reduplicated (6, 12).”
BackgroundCancer Susceptibility and the Functions of BRCA1 and BRCA2
Venkitaraman, A. R. (2002) · Cell · doi:10.1016/s0092-8674(02)00615-3 · Cited by 1,713
Promoter Hypermethylation and BRCA1 Inactivation in Sporadic Breast and Ovarian Tumors
Esteller, M. (2000) · Journal of the National Cancer Institute · doi:10.1093/jnci/92.7.564 · Cited by 1,233
In search of the tumour-suppressor functions of BRCA1 and BRCA2
Scully, R., & Livingston, D. M. (2000) · Nature · doi:10.1038/35044000 · Cited by 643
The relationship between the roles of BRCA genes in DNA repair and cancer predisposition
Tutt, A., & Ashworth, A. (2002) · Trends in Molecular Medicine · doi:10.1016/s1471-4914(02)02434-6 · Cited by 345
Characterization of a breast cancer cell line derived from a germ-line BRCA1 mutation carrier.
Tomlinson, G. E., Chen, T. T., Stastny, V., Virmani, A. K., Spillman, M. A., Tonk, V. S., Blum, J. L., Schneider, N. R., Wistuba, I. I., Shay, J. W., et al. (1998) · PubMed · Cited by 294
The multiple nuclear functions of BRCA1: transcription, ubiquitination and DNA repair
Starita, L. (2003) · Current Opinion in Cell Biology · doi:10.1016/s0955-0674(03)00042-5 · Cited by 235
Shen, C., Yu, J.-C., Lo, Y.-L., Kuo, C. H., Yue, C. T., Jou, Y., Huang, C., Lung, J. C., & Wu, C.-H. (2000) · PubMed · Cited by 157
(1980) · PubMed · Cited by 154
Mutant E-cadherin breast cancer cells do not display constitutive Wnt signaling.
van de Wetering, M., Barker, N., Harkes, I. C., van der Heyden, M. A. G., Dijk, N. J., Hollestelle, A., Klijn, J. G. M., Clevers, H. C., & Schutte, M. E. M. (2001) · PubMed · Cited by 151
Self-citation
Cited by
Sieuwerts, A. M., Kraan, J., Bolt, J., van der Spoel, P., Elstrodt, F., Schutte, M., Martens, J. W. M., Gratama, J.-W., Sleijfer, S., & Foekens, J. A. (2009) · JNCI: Journal of the National Cancer Institute · doi:10.1093/jnci/djn419 · Cited by 435
Self-citationCRISPR screens identify genomic ribonucleotides as a source of PARP-trapping lesions
Zimmermann, M., Murina, O., Reijns, M. A. M., Agathanggelou, A., Challis, R., Tarnauskaitė, Ž., Muir, M., Fluteau, A., Aregger, M., McEwan, A., et al. (2018) · Nature · doi:10.1038/s41586-018-0291-z · Cited by 401
Polθ inhibitors elicit BRCA-gene synthetic lethality and target PARP inhibitor resistance
Zatreanu, D., Robinson, H. M. R., Alkhatib, O., Boursier, M., Finch, H., Geo, L., Grande, D., Grinkevich, V., Heald, R. A., Langdon, S., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-23463-8 · Cited by 357
Saal, L. H., Gruvberger-Saal, S. K., Persson, C., Lövgren, K., Jumppanen, M., Staaf, J., Jönsson, G., Pires, M. M., Maurer, M., Holm, K., et al. (2008) · Nature Genetics · doi:10.1038/ng.2007.39 · Cited by 355
Self-citationGarcia, A. I., Buisson, M., Bertrand, P., Rimokh, R., Rouleau, E., Lopez, B. S., Lidereau, R., Mikaélian, I., & Mazoyer, S. (2011) · EMBO Molecular Medicine · doi:10.1002/emmm.201100136 · Cited by 265
Metadata
- Authors
- Elstrodt, F., Hollestelle, A., Nagel, J. H. A., Gorin, M., Wasielewski, M., van den Ouweland, A., Merajver, S. D., Ethier, S. P., & Schutte, M.
- Venue
- Cancer Research
- Published
- 2006-01-01
- Volume
- 66
- Issue
- 1
- Pages
- 41-45
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2074446011
- Cited by
- 305
- References
- 13
- FWCI
- 7.60
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: BRCA1 Mutation Analysis of 41 Human Breast Cancer Cell Lines Reveals Three New Deleterious Mutants. https://app.cochat.ai/papers/10.1158/0008-5472.can-05-2853
- The paper
- Elstrodt, F., Hollestelle, A., Nagel, J. H. A., Gorin, M., Wasielewski, M., van den Ouweland, A., Merajver, S. D., Ethier, S. P., & Schutte, M. (2006). BRCA1 Mutation Analysis of 41 Human Breast Cancer Cell Lines Reveals Three New Deleterious Mutants. Cancer Research. https://doi.org/10.1158/0008-5472.can-05-2853
Data sources
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.
