ArticleClinical cancer research : an official journal of the American Association for Cancer Research2020
Restoration of Temozolomide Sensitivity by PARP Inhibitors in Mismatch Repair Deficient Glioblastoma is Independent of Base Excision Repair.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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The trial behind it
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Who cites it
85 citing papers in PubMed, 112 citations in OpenAlex.
- Phase Ib/II Study of Pamiparib Plus Radiation Therapy and/or Temozolomide in Adult Patients with Treatment-Naïve or Recurrent/Refractory Glioblastoma.Current oncology (Toronto, Ont.) · 2025Trial
- Article
- Divergent Roles of Canonical and Non-Canonical Mismatch Repair in Regulating Temozolomide Sensitivity in Glioblastoma.International journal of molecular sciences · 2026Review
- ARGLU1 in Glioma: A Novel Potential Regulator of Splicing, DNA Repair, and Therapeutic Resistance.Cells · 2026Review
- Folic Acid-Guided PLGA-Zein Core-Shell Nanoparticles for Co-Delivery of Temozolomide and Ellagic Acid to Overcome PARP-Mediated Chemoresistance in Glioblastoma.Pharmaceutics · 2026Article
- Rethinking the role of synergy calculations in the next century of drug combination discovery.Med (New York, N.Y.) · 2026Review
- Modeling glioblastoma relapse in vitro: a critical journey from 2D models to organ-on-chip alternatives.NPJ precision oncology · 2026Review
- miR-181d coordinates homologous recombination and anti-tumor immune responses in glioblastoma.iScience · 2026Article
- Polymorphisms of mismatch repair pathway genes predict clinical outcomes in acute myeloid leukemia patients.Genes & diseases · 2026Article
- Future of PARP inhibitors in cancer treatment: overcoming resistance and enhancing efficacy with combination therapies.Journal of Zhejiang University. Science. B · 2025Review
- The PIK3CA/AKT pathway drives therapy resistance in rhabdomyosarcoma.Nature communications · 2025Article
- Shared and non-overlapping functions of RECQL4 and BLM helicases in chemotherapeutics-induced glioma cell responses.BMC cancer · 2025Article
- Inhibition of anti-apoptotic Bcl-2 family members promotes synergistic cell death with ER stress inducers by disrupting autophagy in glioblastoma.Cell death discovery · 2025Article
- Identification and Characterization of Novel Inhibitors of Human Poly(ADP-Ribose) Polymerase-1.Molecules (Basel, Switzerland) · 2025Article
- Overcoming temozolomide resistance in glioma: recent advances and mechanistic insights.Acta neuropathologica communications · 2025Review
- Glioblastoma multiforme: an updated overview of temozolomide resistance mechanisms and strategies to overcome resistance.Discover oncology · 2025Review
- Diffuse glioneuronal tumor in Lynch syndrome: illustrative case.Journal of neurosurgery. Case lessons · 2025Article
- The CYLD-PARP1 feedback loop regulates DNA damage repair and chemosensitivity in breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mutations in theBiomedicines · 2024Article
- The landscape of circRNAs in gliomas temozolomide resistance: Insights into molecular pathways.Non-coding RNA research · 2024Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
purposeEmergence of mismatch repair (MMR) deficiency is a frequent mechanism of acquired resistance to the alkylating chemotherapeutic temozolomide (TMZ) in gliomas. Poly(ADP-ribose) polymerase inhibitors (PARPi) have been shown to potentiate TMZ cytotoxicity in several cancer types, including gliomas. We tested whether PARP inhibition could re-sensitize MSH6-null MMR-deficient gliomas to TMZ, and assessed the role of the base excision repair (BER) DNA damage repair pathway in PARPi-mediated effects. EXPERIMENTAL
designIsogenic pairs of MSH6 wild-type and MSH6-inactivated human glioblastoma (GBM) cells (including both
resultsWhile having no detectable effect in MSH6 wild-type GBMs, PARPi selectively restored TMZ sensitivity in MSH6-deficient GBM cells. This genotype-specific restoration of activity translated
conclusionsPARPi restoration of TMZ chemosensitivity in MSH6-inactivated glioma represents a promising strategy to overcome acquired chemoresistance caused by MMR deficiency. Mechanistically, this PARPi-mediated synthetic phenotype was independent of BER blockage and was not recapitulated by loss of PARP1.
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