ArticleMolecular cancer therapeutics2014
Glioblastoma cells containing mutations in the cohesin component STAG2 are sensitive to PARP inhibition.
Article in Molecular cancer therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
What it found
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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
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Systematic identification of mutations and copy number alterations associated with cancer patient prognosis.eLife · 2018Pooled it
- Phase 1/2 trial of talazoparib in combination with temozolomide in children and adolescents with refractory/recurrent solid tumors including Ewing sarcoma: A Children's Oncology Group Phase 1 Consortium study (ADVL1411).Pediatric blood & cancer · 2020Trial
- Trial
- 3D chromatin architecture in cancer: mechanisms of dysregulation and emerging therapeutic strategies.Experimental & molecular medicine · 2026Review
- Cohesin mutations and chromatin changes in cancer.International journal of cancer · 2026Review
- Tumor-suppressive activities of SA1/STAG2 and effects of PARP impairment during brain development.Disease models & mechanisms · 2026Article
- A coregulatory influence map of glioblastoma heterogeneity and plasticity.NPJ precision oncology · 2025Article
- STAG2 expression imparts distinct therapeutic vulnerabilities in muscle-invasive bladder cancer cells.Oncogenesis · 2025Article
- Emerging roles of cohesin-STAG2 in cancer.Oncogene · 2025Review
- A STAG2-PAXIP1/PAGR1 axis suppresses lung tumorigenesis.The Journal of experimental medicine · 2025Article
- Biologic and Clinical Analysis of Childhood Gamma Delta T-ALL Identifies LMO2/STAG2 Rearrangements as Extremely High Risk.Cancer discovery · 2024Article
- Synthetic Lethality between Cohesin and WNT Signaling Pathways in Diverse Cancer Contexts.Cells · 2024Article
- The synergism of SMC1A cohesin gene silencing and bevacizumab against colorectal cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- Article
- STAG2 Regulates Homologous Recombination Repair and Sensitivity to ATM Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Cohesin maintains replication timing to suppress DNA damage on cancer genes.Nature genetics · 2023Article
- Article
- Alterations of cohesin complex genes in acute myeloid leukemia: differential co-mutations, clinical presentation and impact on outcome.Blood cancer journal · 2023Article
- Glioblastoma-derived extracellular vesicle subpopulations following 5-aminolevulinic acid treatment bear diagnostic implications.Journal of extracellular vesicles · 2022Article
- STAG2 expression is associated with adverse survival outcomes and regulates cell phenotype in muscle-invasive bladder cancer.Cancer research communications · 2022Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Recent data have identified STAG2, a core subunit of the multifunctional cohesin complex, as a highly recurrently mutated gene in several types of cancer. We sought to identify a therapeutic strategy to selectively target cancer cells harboring inactivating mutations of STAG2 using two independent pairs of isogenic glioblastoma cell lines containing either an endogenous mutant STAG2 allele or a wild-type STAG2 allele restored by homologous recombination. We find that mutations in STAG2 are associated with significantly increased sensitivity to inhibitors of the DNA repair enzyme PARP. STAG2-mutated, PARP-inhibited cells accumulated in G2 phase and had a higher percentage of micronuclei, fragmented nuclei, and chromatin bridges compared with wild-type STAG2 cells. We also observed more 53BP1 foci in STAG2-mutated glioblastoma cells, suggesting that these cells have defects in DNA repair. Furthermore, cells with mutations in STAG2 were more sensitive than cells with wild-type STAG2 when PARP inhibitors were used in combination with DNA-damaging agents. These data suggest that PARP is a potential target for tumors harboring inactivating mutations in STAG2, and strongly recommend that STAG2 status be determined and correlated with therapeutic response to PARP inhibitors, both prospectively and retrospectively, in clinical trials.
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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.