ArticleBritish journal of cancer2012
Mismatch repair deficiency: a temozolomide resistance factor in medulloblastoma cell lines that is uncommon in primary medulloblastoma tumours.
Article in British journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 45 citations in OpenAlex.
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- Article
- Predictive capacity of mismatch repair status in the use of immune checkpoint inhibitors for the treatment of aggressive pituitary tumors and pituitary carcinomas: An illustrative case report and literature review.Surgical neurology international · 2026Article
- Unveiling divergent treatment prognoses in IDHwt-GBM subtypes through multiomics clustering: a swift dual MRI-mRNA model for precise subtype prediction.Journal of translational medicine · 2024Article
- A Review of Approaches to Potentiate the Activity of Temozolomide against Glioblastoma to Overcome Resistance.International journal of molecular sciences · 2024Review
- Triple combination of lomustine, temozolomide and irradiation reduces canine glioma cell survival in vitro.Veterinary medicine and science · 2023Article
- Pan-cancer association of DNA repair deficiencies with whole-genome mutational patterns.eLife · 2023Article
- Role of DNMTs in the Brain.Advances in experimental medicine and biology · 2022Review
- Prognostic and Predictive Biomarkers in Gliomas.International journal of molecular sciences · 2021Review
- DNA direct reversal repair and alkylating agent drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- Medulloblastoma epigenetics and the path to clinical innovation.Journal of neuro-oncology · 2020Review
- The humanin analogue (HNG) prevents temozolomide-induced male germ cell apoptosis and other adverse effects in severe combined immuno-deficiency (SCID) mice bearing human medulloblastoma.Experimental and molecular pathology · 2019Article
- Effect of OMolecular and clinical oncology · 2017Article
- The germline variants in DNA repair genes in pediatric medulloblastoma: a challenge for current therapeutic strategies.BMC cancer · 2017Article
- Wnt/β-catenin pathway regulates MGMT gene expression in cancer and inhibition of Wnt signalling prevents chemoresistance.Nature communications · 2015Article
- Targeting the parasite's DNA with methyltriazenyl purine analogs is a safe, selective, and efficacious antitrypanosomal strategy.Antimicrobial agents and chemotherapy · 2015Article
- Temozolomide Resistance in Glioblastoma Cell Lines: Implication of MGMT, MMR, P-Glycoprotein and CD133 Expression.PloS one · 2015Article
- Overcoming multiple drug resistance mechanisms in medulloblastoma.Acta neuropathologica communications · 2014Article
- Asparagine depletion potentiates the cytotoxic effect of chemotherapy against brain tumors.Molecular cancer research : MCR · 2014Article
- Multiplex mapping of chromatin accessibility and DNA methylation within targeted single molecules identifies epigenetic heterogeneity in neural stem cells and glioblastoma.Genome research · 2014Article
Corrections and comments
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Authors and funding
13 authors at 11 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTumours are responsive to temozolomide (TMZ) if they are deficient in O(6)-methylguanine-DNA methyltransferase (MGMT), and mismatch repair (MMR) proficient.
methodsThe effect of TMZ on medulloblastoma (MB) cell killing was analysed with clonogenic survival assays. Expression of DNA repair genes and enzymes was investigated using microarrays, western blot, and immunohistochemistry. DNA sequencing and promoter methylation analysis were employed to investigate the cause of loss of the expression of MMR gene MLH1.
resultsTemozolomide exhibited potent cytotoxic activity in D425Med (MGMT deficient, MLH1 proficient; IC(50)=1.7 μM), moderate activity against D341Med (MGMT proficient, MLH1 deficient), and DAOY MB cells (MGMT proficient, MLH1 proficient). MGMT inhibitor O(6)-benzylguanine sensitised DAOY, but not D341Med cells to TMZ. Of 12 MB cell lines, D341Med, D283Med, and 1580WÜ cells exhibited MMR deficiency due to MLH1 promoter hypermethylation. DNA sequencing of these cells provided no evidence for somatic genetic alterations in MLH1. Expression analyses of MMR and MGMT in MB revealed that all patient specimens (n=74; expression array, n=61; immunostaining, n=13) are most likely MMR proficient, whereas some tumours had low MGMT expression levels (according to expression array) or were totally MGMT deficient (3 out of 13 according to immunohistochemistry).
conclusionA subset of MB may respond to TMZ as some patient specimens are MGMT deficient, and tumours appear to be MMR proficient.
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