ArticleTranslational oncology2012
The Changes in MGMT Promoter Methylation Status in Initial and Recurrent Glioblastomas.
Article in Translational oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Correlation Between RASSF1A Gene Promoter Hypermethylation in Serum or Sputum and Non-Small Cell Lung Cancer (NSCLC): A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2019Pooled it
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- Mechanisms, Microenvironments, and Models: Understanding Therapeutic Resistance in Glioblastoma.International journal of radiation oncology, biology, physics · 2026Review
- MGMT promoter methylation across glioma subtypes: biological relevance, treatment response, and survival outcomes.Molecular biology reports · 2026Review
- Synthesis and Biological Evaluation of a Novel Dual-Targeting Small Molecule Drug Conjugate Modulating the Crosstalk between α5β1 Integrin and MDM2 in Glioblastoma.ACS medicinal chemistry letters · 2026Article
- MGMT promoter methylation modulates the effect of residual tumor on survival after re-resection of recurrent glioblastoma.Acta neuropathologica communications · 2026Article
- MGMT protein expression is a reliable predictive biomarker for temozolomide-containing chemotherapy in osteosarcoma.Cancer science · 2024Article
- AHR, a novel inhibitory immune checkpoint receptor, is a potential therapeutic target for chemoresistant glioblastoma.Journal of cancer research and clinical oncology · 2023Article
- Glioblastoma, from disease understanding towards optimal cell-based in vitro models.Cellular oncology (Dordrecht, Netherlands) · 2022Review
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- DNA damage repair in glioblastoma: current perspectives on its role in tumour progression, treatment resistance and PIKKing potential therapeutic targets.Cellular oncology (Dordrecht, Netherlands) · 2021Review
- Article
- Temozolomide treatment outcomes and immunotherapy efficacy in brain tumor.Journal of neuro-oncology · 2021Review
- Mechanisms of temozolomide resistance in glioblastoma - a comprehensive review.Cancer drug resistance (Alhambra, Calif.) · 2021Article
- Implication of Lactucopicrin in Autophagy, Cell Cycle Arrest and Oxidative Stress to Inhibit U87Mg Glioblastoma Cell Growth.Molecules (Basel, Switzerland) · 2020Article
- Phenotypic selection through cell death: stochastic modelling of O-6-methylguanine-DNA methyltransferase dynamics.Royal Society open science · 2020Article
- Is There an Independent Role of TERT and NF1 in High Grade Gliomas?Translational oncology · 2020Article
- Changes of OCancers · 2019Review
- Temozolomide Induced Hypermutation in Glioma: Evolutionary Mechanisms and Therapeutic Opportunities.Frontiers in oncology · 2019Review
- Stereotactic image-based histological analysis reveals a correlation betweenOncology letters · 2018Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To evaluate the mechanism of the development of therapeutic resistance after temozolomide treatment, we focused on changes in O(6)-methylguanine DNA methyltransferase (MGMT) and mismatch repair (MMR) between initial and recurrent glioblastomas. Tissue samples obtained from 24 paired histologically confirmed initial and recurrent adult glioblastoma patients who were initially treated with temozolomide were used for MGMT and MMR gene promoter methylation status and protein expression analysis using methylation-specific multiplex ligation probe amplification (MS-MLPA), methylation-specific polymerase chain reaction (MSP), and immunohistochemical staining. There was a significant decrease in the methylation ratio of the MGMT promoter determined by MS-MLPA, which was not detectable with MSP, and MGMT protein expression changes were not remarkable. However, there was no epigenetic variability in MMR genes, and a relatively homogeneous expression of MMR proteins was observed in initial and recurrent tumors. We conclude that the development of reduced methylation in the MGMT promoter is one of the mechanisms for acquiring therapeutic resistance after temozolomide treatment in glioblastomas.
Identifiers
What OpenQuestion holds
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.