ArticleMolecular and cellular biology2006
Hyperplasia and spontaneous tumor development in the gynecologic system in mice lacking the BRCA1-Delta11 isoform.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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Who cites it
23 citing papers in PubMed, 52 citations in OpenAlex.
- DNA end-resection is stimulated by an interaction between BRCA1 exon 11 and TOPBP1.EMBO reports · 2026Article
- Insights from three decades of BRCA1/2 modeling in mice.Nature genetics · 2026Review
- Reduced penetrance BRCA1 and BRCA2 pathogenic variants in clinical germline genetic testing.NPJ precision oncology · 2024Article
- Hyperplastic ovarian stromal cells express genes associated to tumor progression: a case study.BMC veterinary research · 2024Article
- BRCA1 the Versatile Defender: Molecular to Environmental Perspectives.International journal of molecular sciences · 2023Review
- Genetically engineered mouse models for hereditary cancer syndromes.Cancer science · 2023Review
- Consistency of variant interpretations among bioinformaticians and clinical geneticists in hereditary cancer panels.European journal of human genetics : EJHG · 2022Article
- Article
- Review
- BRCA1 and homologous recombination: implications from mouse embryonic development.Cell & bioscience · 2020Review
- Alternative Splicing in Breast Cancer and the Potential Development of Therapeutic Tools.Genes · 2017Review
- Stochastic principles governing alternative splicing of RNA.PLoS computational biology · 2017Article
- MicroRNA-206 is differentially expressed in Brca1-deficient mice and regulates epithelial and stromal cell compartments of the mouse mammary gland.Oncogenesis · 2016Article
- A Mouse Model That Reproduces the Developmental Pathways and Site Specificity of the Cancers Associated With the Human BRCA1 Mutation Carrier State.EBioMedicine · 2015Article
- BRCA1 EXON 11, a CERES (composite regulatory element of splicing) element involved in splice regulation.International journal of molecular sciences · 2014Article
- BRCA1 and estrogen/estrogen receptor in breast cancer: where they interact?International journal of biological sciences · 2014Review
- SOCS5 and SOCS6 have similar expression patterns in normal and cancer tissues.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012Article
- Wild-type BRCA1, but not mutated BRCA1, regulates the expression of the nuclear form of beta-catenin.Molecular cancer research : MCR · 2010Article
- Impaired skin and mammary gland development and increased gamma-irradiation-induced tumorigenesis in mice carrying a mutation of S1152-ATM phosphorylation site in Brca1.Cancer research · 2009Article
- Preclinical mouse models for BRCA1-associated breast cancer.British journal of cancer · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Alternative splicing in the BRCA1 locus generates multiple protein products including BRCA1-Delta11, which is identical to the BRCA1 full-length isoform (BRCA1-FL) except for the absence of exon 11. Mutation analysis using gene targeting to create null mutations or disrupt BRCA-FL has provided much of our understanding of BRCA1 functions; however, targeted mutation of specific short forms of BRCA1 has not been reported. To understand the physiologic functions of BRCA1-Delta11, we used a knock-in approach that blocks alternative splicing between exons 10 and 12 to prevent the formation of this form of BRCA1. We showed that homozygous mutant mice (Brca1(FL/FL)) were born at a Mendelian ratio without obvious developmental defects. However, the majority of Brca1(FL/FL) female mice showed mammary gland abnormalities and uterine hyperplasia after one year of age with spontaneous tumor formation. Cultured Brca1(FL/FL) cells exhibited abnormal centrosome amplification and reduction of G(1) population that was accompanied by accumulation of cyclin E and cyclin A. Accumulation of cyclin E was also found in epithelial layers of dilated ducts and hyperproliferative lobular regions in the mammary glands of Brca1(FL/FL) mice. These observations provide evidence that BRCA1 splicing variants are involved in BRCA1 functions in modulating G(1)/S transition, centrosome duplication, and repressing tumor formation.
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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.