ReviewCell cycle (Georgetown, Tex.)2012
BRCA1-directed, enhanced and aberrant homologous recombination: mechanism and potential treatment strategies.
Review in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- BKM120 sensitizes BRCA-proficient triple negative breast cancer cells to olaparib through regulating FOXM1 and Exo1 expression.Scientific reports · 2021Article
- Vorinostat enhances the anticancer effect of oxaliplatin on hepatocellular carcinoma cells.Cancer medicine · 2018Article
- DNA repair pathways to regulate response to chemoradiotherapy in patients with locally advanced head and neck cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- BRCA1-hapoinsufficiency: Unraveling the molecular and cellular basis for tissue-specific cancer.Cell cycle (Georgetown, Tex.) · 2016Review
- Peptide library approach to uncover phosphomimetic inhibitors of the BRCA1 C-terminal domain.ACS chemical biology · 2015Article
- Deregulation of the EGFR/PI3K/PTEN/Akt/mTORC1 pathway in breast cancer: possibilities for therapeutic intervention.Oncotarget · 2014Review
- Revisiting p53 for cancer-specific chemo- and radiotherapy: ten years after.Cell cycle (Georgetown, Tex.) · 2014Review
- Article
- Structural mechanisms underlying signaling in the cellular response to DNA double strand breaks.Mutation research · 2013Review
- BRCA1 downregulates the kinase activity of Polo-like kinase 1 in response to replication stress.Cell cycle (Georgetown, Tex.) · 2013Article
- DNA double-strand break repair as determinant of cellular radiosensitivity to killing and target in radiation therapy.Frontiers in oncology · 2013Article
- BRCA1 in the DNA damage response and at telomeres.Frontiers in genetics · 2013Article
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 2 institutions in 1 country.
Funding
Abstract
Despite intense studies, questions still remain regarding the molecular mechanisms leading to the development of hereditary breast and ovarian cancers. Research focused on elucidating the role of the breast cancer susceptibility gene 1 (BRCA1) in the DNA damage response may be of the most critical importance to understanding these processes. The BRCA1 protein has an N-terminal RING domain possessing E3 ubiquitinligase activity and a C-terminal BRCT domain involved in binding specific phosphoproteins. These domains are involved directly or indirectly in DNA double-strand break (DSB) repair. As the two terminal domains of BRCA1 represent two separate entities, understanding how these domains communicate and are functionally altered in regards to DSB repair is critical for understanding the development of BRCA1-related breast and ovarian cancers and for developing novel therapeutics. Herein, we review recent findings of how altered functions of these domains might lead to cancer through a mechanism of increased aberrant homologous recombination and possible implications for the development of BRCA1 inhibitors.
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.