ReviewTrends in genetics : TIG2013
Synthetic lethality and cancer: cohesin and PARP at the replication fork.
Review in Trends in genetics : TIG, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- S-phase PARylation of microprotein RSMC enhances the function of Sororin in sister chromatid cohesion.The EMBO journal · 2026Article
- Regulating epithelial-mesenchymal plasticity from 3D genome organization.Communications biology · 2024Review
- Article
- Genetically induced redox stress occurs in a yeast model for Roberts syndrome.G3 (Bethesda, Md.) · 2022Article
- The three-dimensional structure of Epstein-Barr virus genome varies by latency type and is regulated by PARP1 enzymatic activity.Nature communications · 2022Article
- Genetic alterations of the SUMO isopeptidase SENP6 drive lymphomagenesis and genetic instability in diffuse large B-cell lymphoma.Nature communications · 2022Article
- 3D CRISPR screen in prostate cancer cells reveals PARP inhibitor sensitization through TBL1XR1-SMC3 interaction.Frontiers in oncology · 2022Article
- Modeling DNA trapping of anticancer therapeutic targets using missense mutations identifies dominant synthetic lethal interactions.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- Genetic relationship between Hashimoto`s thyroiditis and papillary thyroid carcinoma with coexisting Hashimoto`s thyroiditis.PloS one · 2020Article
- Noise-induced bistability in the fate of cancer phenotypic quasispecies: a bit-strings approach.Scientific reports · 2018Article
- PARP inhibition causes premature loss of cohesion in cancer cells.Oncotarget · 2017Article
- Synthetic lethal interaction between the tumour suppressor STAG2 and its paralog STAG1.Oncotarget · 2017Article
- Abrupt transitions to tumor extinction: a phenotypic quasispecies model.Journal of mathematical biology · 2017Article
- Meeting Proceedings ICBS2016-Translating the Power of Chemical Biology to Clinical Advances.ACS chemical biology · 2017Article
- Dynamic cohesin-mediated chromatin architecture controls epithelial-mesenchymal plasticity in cancer.EMBO reports · 2016Article
- SGO1 is involved in the DNA damage response in MYCN-amplified neuroblastoma cells.Scientific reports · 2016Article
- Reduced cohesin destabilizes high-level gene amplification by disrupting pre-replication complex bindings in human cancers with chromosomal instability.Nucleic acids research · 2016Article
- Functional interplay between cohesin and Smc5/6 complexes.Chromosoma · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Cohesins are mutated in a significant number of tumors of various types making them attractive targets for chemotherapeutic intervention. However, cohesins have a spectrum of cellular roles including sister chromatid cohesion, transcription, replication, and repair. Which of these roles are central to cancer biology and which roles can be exploited for therapeutic intervention? Genetic interaction networks in yeast have identified synthetic lethal interactions between mutations in cohesin and replication fork mediators. These interactions are conserved in worms and in human cells suggesting that inhibition of replication fork stability mediators such as poly (ADP-ribose) polymerase (PARP) could result in the specific killing of tumors with cohesin mutations. These findings also highlight the utility of genetic interaction networks in model organisms for the identification of clinically relevant interactions. Here, we review this type of approach, emphasizing the power of synthetic lethal interactions to reveal new avenues for developing cancer therapeutics.
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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.