ArticleCell death & disease2015
Acquisition of meiotic DNA repair regulators maintain genome stability in glioblastoma.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 28 citations in OpenAlex.
- Expression of DNA-damage response genes after exposure to high LET particles used in BNCT in glioblastoma cells with altered radiosensitivity.Scientific reports · 2025Article
- ABL1-mediated tyrosine phosphorylation of SYCP2 contributes to transcription-coupled homologous recombination and platinum resistance in ovarian cancer.NAR cancer · 2025Article
- Cellular senescence in Alzheimer's disease: from physiology to pathology.Translational neurodegeneration · 2024Review
- PPP2R1A silencing suppresses LUAD progression by sensitizing cells to nelfinavir-induced apoptosis and pyroptosis.Cancer cell international · 2024Article
- Review
- The Transcriptome and Proteome Networks of Malignant Tumours Reveal Atavistic Attractors of Polyploidy-Related Asexual Reproduction.International journal of molecular sciences · 2022Article
- The DNA Double-Strand Break Repair in Glioma: Molecular Players and Therapeutic Strategies.Molecular neurobiology · 2022Review
- Meiotic Genes and DNA Double Strand Break Repair in Cancer.Frontiers in genetics · 2022Review
- Review
- A Risk Signature with Nine Stemness Index-Associated Genes for Predicting Survival of Patients with Uterine Corpus Endometrial Carcinoma.Journal of oncology · 2021Article
- The ectopic expression of meiCT genes promotes meiomitosis and may facilitate carcinogenesis.Cell cycle (Georgetown, Tex.) · 2020Review
- Human iPSC-Derived Neuronal Cells FromFrontiers in neuroscience · 2020Article
- A 'parameiosis' drives depolyploidization and homologous recombination in Candida albicans.Nature communications · 2019Article
- The RecQ helicase Sgs1 drives ATP-dependent disruption of Rad51 filaments.Nucleic acids research · 2019Article
- CHD4 regulates the DNA damage response and RAD51 expression in glioblastoma.Scientific reports · 2019Article
- Article
- Cancer Stem Cells: Cellular Plasticity, Niche, and its Clinical Relevance.Journal of stem cell research & therapy · 2016Article
- Enhanced efficacy of combined HDAC and PARP targeting in glioblastoma.Molecular oncology · 2016Article
- Genome management and mismanagement--cell-level opportunities and challenges of whole-genome duplication.Genes & development · 2015Review
- Pharmacologic inhibition of RBBP4/p300-mediated homologous recombination activity enhances glioblastoma sensitivity to temozolomide.Neuro-oncology advancesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
Glioblastoma (GBM), the most prevalent type of primary intrinsic brain cancer in adults, remains universally fatal despite maximal therapy, including radiotherapy and chemotherapy. Cytotoxic therapy generates double-stranded DNA breaks (DSBs), most commonly repaired by homologous recombination (HR). We hypothesized that cancer cells coopt meiotic repair machinery as DSBs are generated during meiosis and repaired by molecular complexes distinct from genotoxic responses in somatic tissues. Indeed, we found that gliomas express meiotic repair genes and their expression informed poor prognosis. We interrogated the function of disrupted meiotic cDNA1 (DMC1), a homolog of RAD51, the primary recombinase used in mitotic cells to search and recombine with the homologous DNA template. DMC1, whose only known function is as an HR recombinase, was expressed by GBM cells and induced by radiation. Although targeting DMC1 in non-neoplastic cells minimally altered cell growth, DMC1 depletion in GBM cells decreased proliferation, induced activation of CHK1 and expression of p21CIP1/WAF1, and increased RPA foci, suggesting increased replication stress. Combining loss of DMC1 with ionizing radiation inhibited activation of DNA damage responses and increased radiosensitivity. Furthermore, loss of DMC1 reduced tumor growth and prolonged survival in vivo. Our results suggest that cancers coopt meiotic genes to augment survival under genotoxic stress, offering molecular targets with high therapeutic indices.
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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.