Ask about this productRelated genes to: MGMT protein
- Gene:
- MGMT NIH gene
- Name:
- O-6-methylguanine-DNA methyltransferase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 10q26.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-10-16
- Date modifiied:
- 2016-10-05
Related products to: MGMT protein
Related articles to: MGMT protein
- Cellular senescence (CS) is defined as a condition of permanent cessation of growth, accompanied by distinct morphological and physiological alterations. This phenomenon is closely associated with DNA damage. Recently, our department identified that inhibition of the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) by O-6-benzylguanine (O6-BG) induces CS in vascular smooth muscle cells (VSMCs). Consequently, we have resolved to validate these findings in an animal model. The objective of this study was to examine the impact of O6-BG on CS in vascular smooth muscle and to assess its influence on the relaxation response. - Source: PubMed
Publication date: 2025/11/01
Nasim Alinejad KasbakhiMgr Peter Vavrinec - The EF-14 trial established the survival benefit of adding Tumor Treating Fields (TTFields) to maintenance temozolomide (TMZ) following standard radiochemotherapy in glioblastoma (GBM). Whether this benefit is reproducible in Chinese grade 4 glioma patients in real-world practice-and what biomarkers predict response-remains unknown. This study evaluates TTFields efficacy in a Chinese cohort and explores predictive biomarkers. - Source: PubMed
Publication date: 2026/07/23
Zhu WenjunRao JieHu GuangyuanWang RunkunLuo XiaoxiaoLi Qianxia - Glioblastoma (GBM) is the most common and most aggressive primary malignant tumor of the central nervous system in adults. Although GBM is characterized by highly infiltrative growth within the brain parenchyma, spontaneous transdural extension with direct invasion of the calvarium and skull base at initial presentation is exceptionally rare. Such cases may radiologically mimic metastatic skull tumors or other extra-axial lesions, creating diagnostic and therapeutic challenges. - Source: PubMed
Publication date: 2026/08/07
Yang ZhijieAi LingShen JunZhou AibinZhang Shaolin - Mutations in isocitrate dehydrogenase 1 or 2 (IDH1/2) define a major subgroup of adult-type diffuse gliomas and induce accumulation of D-2-hydroxyglutarate, resulting in extensive DNA and histone methylation changes. This epigenetic reprogramming underlies the glioma CpG island methylator phenotype (G-CIMP) and contributes to tumour lineage, differentiation state and clinical behaviour. DNA methylation profiling has consequently evolved from a research tool into an important ancillary method for CNS tumour classification, molecular subclassification and copy-number analysis. This narrative review examines the biological basis, analytical platforms and clinical applications of DNA methylation profiling in IDH-mutant gliomas. Particular attention is given to the distinction between research-defined G-CIMP-high and G-CIMP-low states and classifier-defined lower-grade and high-grade methylation subclasses. High-grade signatures, including A_IDH_HG and G-CIMP-low, are associated with adverse genomic features and outcome but should not be considered interchangeable or used in isolation to assign CNS WHO grade. Their interpretation requires integration with histology and established molecular criteria, including homozygous CDKN2A/B deletion. The review also discusses array-based profiling, emerging Nanopore and long-read approaches, computational quality control, and the integration of methylation data with genomic and transcriptomic alterations. Longitudinal studies indicate that a subset of IDH-mutant astrocytomas undergoes methylation loss, copy-number accumulation and altered cell-state differentiation during progression, although these changes are not universal. The clinical relevance of MGMT promoter methylation is more context-dependent than in IDH-wildtype glioblastoma. Moreover, the INDIGO trial established the clinical activity of mutant IDH inhibition in selected Grade 2 gliomas but did not validate methylation class as a predictive biomarker or demonstrate complete epigenetic reversal. Emerging applications, including single-cell and spatial epigenomics, tumour microenvironment deconvolution and CSF methylation profiling, remain investigational. Overall, DNA methylation profiling is most valuable when used as integrated diagnostic and risk-stratification evidence within the complete histological, genomic and clinical context. - Source: PubMed
Tralongo PietroRicciardi GabrieleBallato MariagiovannaFiorentino VincenzoZuccalà ValeriaCastellani GiorgiaD'Alessandris Quintino GiorgioFadda GuidoRicci-Vitiani LuciaCaffo MariaMartini Maurizio - Glioblastoma research increasingly relies on large, well-curated imaging datasets that combine standardized MRI data, accurate tumor segmentations, and molecular profiling. We constructed a multi-center dataset of preoperative MRI scans from 337 patients with histologically confirmed primary glioblastoma collected across eight hospitals. All cases include T1-weighted (pre- and post-contrast), T2-weighted, and FLAIR sequences. Images underwent systematic quality assessment, BIDS organization, defacing, skull stripping, and linear registration to the MNI152 template. Tumor segmentation was performed using a SegResNet CNN model following the BraTS labeling convention, with all masks reviewed and manually refined by neuroradiologists. MGMT promoter methylation status was determined for all patients. This dataset provides a robust, clinically representative resource for radiomics, deep learning, and radiogenomic research in glioblastoma, supporting concrete downstream tasks including automated segmentation benchmarking (mean Dice = 0.94) and MGMT methylation prediction (baseline ACC = 0.60). Its multi-center origin, comprehensive preprocessing, expert-refined segmentations, and complete MGMT annotations address limitations of existing datasets and support the development and validation of reproducible imaging biomarkers. - Source: PubMed
Publication date: 2026/08/07
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