ArticleCancer research2009
A role for BRCA1 in uterine leiomyosarcoma.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 55 citations in OpenAlex.
- High-level tumour methylation ofNAR cancer · 2024Article
- Epigenetic Features in Uterine Leiomyosarcoma and Endometrial Stromal Sarcomas: An Overview of the Literature.Biomedicines · 2022Review
- Drivers of genomic loss of heterozygosity in leiomyosarcoma are distinct from carcinomas.NPJ precision oncology · 2022Article
- Interrogating the Genomic Landscape of Uterine Leiomyosarcoma: A Potential for Patient Benefit.Cancers · 2022Review
- Genomic Landscape of Uterine Sarcomas Defined Through Prospective Clinical Sequencing.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Observational
- Modelling Epithelial Ovarian Cancer in Mice: Classical and Emerging Approaches.International journal of molecular sciences · 2020Review
- Pharmacogenomics Biomarkers of Soft Tissue Sarcoma Therapies.Frontiers in oncology · 2020Review
- Liquid Biopsy as a Tool for Differentiation of Leiomyomas and Sarcomas of Corpus Uteri.International journal of molecular sciences · 2019Review
- Article
- Molecular biomarkers for uterine leiomyosarcoma and endometrial stromal sarcoma.Cancer science · 2018Review
- Activity of trabectedin and the PARP inhibitor rucaparib in soft-tissue sarcomas.Journal of hematology & oncology · 2017Article
- Association of the germline BRCA2 missense variation Glu2663Lys with high sensitivity to trabectedin-based treatment in soft tissue sarcoma.Cancer biology & therapy · 2016Article
- Follicle Depletion Provides a Permissive Environment for Ovarian Carcinogenesis.Molecular and cellular biology · 2016Article
- Development and potential applications of CRISPR-Cas9 genome editing technology in sarcoma.Cancer letters · 2016Review
- Deletion of Arid1a in Reproductive Tract Mesenchymal Cells Reduces Fertility in Female Mice.Biology of reproduction · 2016Article
- Article
- Do hereditary syndrome-related gynecologic cancers have any specific features?Insights into imaging · 2015Article
- A Mouse Model That Reproduces the Developmental Pathways and Site Specificity of the Cancers Associated With the Human BRCA1 Mutation Carrier State.EBioMedicine · 2015Article
- Malignant tumors of the uterine corpus: molecular background of their origin.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
- Epigenetic regulation of DNA repair machinery in Helicobacter pylori-induced gastric carcinogenesis.World journal of gastroenterology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 1 country.
Funding
Abstract
Uterine leiomyosarcoma (ULMS) is a rare gynecologic malignancy with a low survival rate. Currently, there is no effective treatment for ULMS. Infrequent occurrences of human ULMS hamper the understanding of the initiation and progression of the disease, thereby limiting the ability to develop efficient therapies. To elucidate the roles of the p53 and BRCA1 tumor suppressor genes in gynecologic malignancies, we generated mice in which p53 and/or BRCA1 can be conditionally deleted using anti-Müllerian hormone type II receptor (Amhr2)-driven Cre recombinase. We showed that conditional deletion of p53 in mice results in the development of uterine tumors that resemble human ULMS and that concurrent deletion of p53 and BRCA1 significantly accelerates the progression of these tumors. This finding led to our hypothesis that BRCA1 may play a role in human ULMS development. Consistent with this hypothesis, we showed that the BRCA1 protein is absent in 29% of human ULMS and that BRCA1 promoter methylation is the likely mechanism of BRCA1 downregulation. These data indicate that the loss of BRCA1 function may be an important step in the progression of ULMS. Our findings provide a rationale for investigating therapies that target BRCA1 deficiency in ULMS.
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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.