ReviewOncogene2000
Lessons learned from BRCA1 and BRCA2.
Review in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 187 citations in OpenAlex.
- Article
- Exploring the causal role and mechanism of galanin in glioblastoma: integration of mendelian randomization, network analysis, molecular docking and experimental validation.Frontiers in pharmacology · 2026Article
- Druggable Molecular Networks inBiology · 2025Review
- Preliminary insights on the mutational spectrum of BRCA1 and BRCA2 genes in Pakhtun ethnicity breast cancer patients from Khyber Pakhtunkhwa (KP), Pakistan.Neoplasia (New York, N.Y.) · 2024Article
- R-Loops and R-Loop-Binding Proteins in Cancer Progression and Drug Resistance.International journal of molecular sciences · 2023Review
- Review
- Review
- Screening and identification of phytochemical drug molecules against mutant BRCA1 receptor of breast cancer using computational approaches.Molecular and cellular biochemistry · 2022Article
- Article
- The Effect of Prophylactic Adnexectomy on the Quality of Life and Psychosocial Functioning of Women with theInternational journal of environmental research and public health · 2019Article
- Identification of Mutation in Exon11 of BRCA1 Gene in Bangladeshi Patients with Breast Cancer.Asian Pacific journal of cancer prevention : APJCP · 2019Article
- Genetic Association between ERCC2, NBN, RAD51 Gene Variants and Osteosarcoma Risk: a Systematic Review and Meta-AnalysisAsian Pacific journal of cancer prevention : APJCP · 2017Article
- BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity.Nature communications · 2016Article
- Biallelic BRCA2 Mutations Shape the Somatic Mutational Landscape of Aggressive Prostate Tumors.American journal of human genetics · 2016Article
- Pathogenesis of serous, extra-uterine Müllerian epithelial cancer and therapeutic implications.Translational cancer research · 2015Article
- Targeting tumor suppressor networks for cancer therapeutics.Current drug targets · 2014Article
- The yin-yang of DNA damage response: roles in tumorigenesis and cellular senescence.International journal of molecular sciences · 2013Article
- From systems to structure: bridging networks and mechanism.Molecular cell · 2013Review
- Article
- Unbalanced replication as a major source of genetic instability in cancer cells.American journal of blood research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BRCA1 and BRCA2 are breast cancer susceptibility genes. Mutations within BRCA1 and BRCA1 are responsible for most familial breast cancer cases. Targeted deletion of Brca1 or Brca2 in mice has revealed an essential function for their encoded products, BRCA1 and BRCA2, in cell proliferation during embryogenesis. Mouse models established from conditional expression of mutant Brca1 alleles develop mammary gland tumors, providing compelling evidence that BRCA1 functions as a breast cancer suppressor. Human cancer cells and mouse cells deficient in BRCA1 or BRCA2 exhibit radiation hypersensitivity and chromosomal abnormalities, thus revealing a potential role for both BRCA1 and BRCA2 in the maintenance of genetic stability through participation in the cellular response to DNA damage. Functional analyses of the BRCA1 and BRCA2 gene products have established their dual participation in transcription regulation and DNA damage repair. Potential insight into the molecular basis for these functions of BRCA1 and BRCA2 has been provided by studies that implicate these two tumor suppressors in both the maintenance of genetic stability and the regulation of cell growth and differentiation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.