What is mgmt gene

Nucleoplasm 4 See all subcellular structures. DNA Damage Reversal. DNA Damage. Busulfan Pathway, Pharmacodynamics. Cyclophosphamide Pathway, Pharmacodynamics. This gene is overexpressed in Liver x5.

This gene is overexpressed in Lymph node Show more. Liver 4. This gene was present in the common ancestor of animals and fungi. All consequence types are included: molecular consequences e. Gene Damage Index Score : 6. Quality Products:. DNA Damage Reversal -. DNA Damage -.

Busulfan Pathway, Pharmacodynamics -. Cyclophosphamide Pathway, Pharmacodynamics -. ENSP 19 P Induction of MGMT expression is associated with temozolomide resistance in glioblastoma xenografts. Cankovic, M. A simplified laboratory validated assay for MGMT promoter hypermethylation analysis of glioma specimens from formalin-fixed paraffin-embedded tissue.

Schold, S. Jr et al. O 6 -benzylguanine suppression of O 6 -alkylguanine-DNA alkyltransferase in anaplastic gliomas. Quinn, J. Phase II trial of temozolomide plus O 6 -benzylguanine in adults with recurrent, temozolomide-resistant malignant glioma.

Koch, D. Local intracerebral administration of O 6 -benzylguanine combined with systemic chemotherapy with temozolomide of a patient suffering from a recurrent glioblastoma.

Larochelle, A. In vivo selection of hematopoietic progenitor cells and temozolomide dose intensification in rhesus macaques through lentiviral transduction with a drug resistance gene. Glas, M. Long-term survival of patients with glioblastoma treated with radiotherapy and lomustine plus temozolomide.

Weiler, M. Chemoradiotherapy of newly diagnosed glioblastoma with intensified temozolomide. Yung, W. Multicenter phase II trial of temozolomide in patients with anaplastic astrocytoma or anaplastic oligoastrocytoma at first relapse. Temodal Brain Tumor Group. MGMT prognostic impact on glioblastoma is dependent on therapeutic modalities. Zawlik, I. Promoter methylation and polymorphisms of the MGMT gene in glioblastomas: a population-based study.

Neuroepidemiology 32 , 21—29 Prados, M. Phase II study of erlotinib plus temozolomide during and after radiation therapy in patients with newly diagnosed glioblastoma multiforme or gliosarcoma. Clarke, J. Randomized phase II trial of chemoradiotherapy followed by either dose-dense or metronomic temozolomide for newly diagnosed glioblastoma.

Correlations between O6-methylguanine DNA methyltransferase promoter methylation status, 1p and 19q deletions, and response to temozolomide in anaplastic and recurrent oligodendroglioma: a prospective GICNO study. Yu, J. Methylation profiles of thirty four promoter-CpG islands and concordant methylation behaviours of sixteen genes that may contribute to carcinogenesis of astrocytoma. BMC Cancer 4 , 65 Bello, M. Nakamura, M. Carcinogenesis 22 , — Watanabe, T.

Phenotype versus genotype correlation in oligodendrogliomas and low-grade diffuse astrocytomas. Acta Neuropathol. Brell, M. Prognostic significance of O 6 -methylguanine-DNA methyltransferase determined by promoter hypermethylation and immunohistochemical expression in anaplastic gliomas.

Kamiryo, T. Correlation between promoter hypermethylation of the O6-methylguanine-deoxyribonucleic acid methyltransferase gene and prognosis in patients with high-grade astrocytic tumors treated with surgery, radiotherapy, and 1- 4-aminomethylpyrimidinyl methyl 2-chloroethyl nitrosourea-based chemotherapy. Neurosurgery 54 , — Dong, S. Concurrent hypermethylation of multiple genes is associated with grade of oligodendroglial tumors. Blanc, J. Correlation of clinical features and methylation status of MGMT gene promoter in glioblastomas.

O 6 -methyl-guanine -DNA methyltransferase methylation in serum and tumor DNA predicts response to 1, 3-bis 2-chloroethyl nitrosourea but not to temozolamide plus cisplatin in glioblastoma multiforme. PubMed Google Scholar. O 6 -methylguanine -DNA methyltransferase methylation and TP53 mutation in malignant astrocytomas and their relationships with clinical course. Download references. You can also search for this author in PubMed Google Scholar.

Correspondence to Michael Weller. Stupp has acted as a consultant for and received honoraria from Merck Serono and Schering-Plough, and has acted as a consultant for Oncomethylome Sciences. Wick has acted as a consultant for and received honoraria from Merck Serono and Schering-Plough.

Hegi has acted as a consultant for and received research support from OncoMethylome Sciences and Merck Serono, and has received honoraria from OncoMethylome Sciences and Schering-Plough. Reprints and Permissions. MGMT promoter methylation in malignant gliomas: ready for personalized medicine?.

Nat Rev Neurol 6, 39—51 Download citation. Published : 08 December Issue Date : January Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Clinical Epigenetics Wiener klinisches Magazin Der Pathologe BMC Cancer Advanced search. Skip to main content Thank you for visiting nature.

Key Points MGMT O 6 -methylguanine-DNA methyltransferase promoter methylation has become the most powerful molecular prognosticator in malignant gliomas MGMT promoter methylation is predictive for response to alkylating agent chemotherapy in glioblastoma Methylation-specific PCR is the only validated technique to derive prognostic information from determination of the MGMT status The MGMT status has become a parameter for stratification of patients with glioma within clinical trials.

Access through your institution. Buy or subscribe. Rent or Buy article Get time limited or full article access on ReadCube. Figure 4: Bisulfite conversion of tumor DNA. The characterisation is mainly qualitative, in fact the PCR products are separated by electrophoresis and visualised by transilluminator as bands. However, based on intensity of bands, it is also possible to carry out a semi-quantitative analysis.

MS-PCR is a highly standardised technique; the results are solid, reliable and are obtained in a few hours. For this reason, it is possible that small cellular clones with methylated MGMT gene promoter are missed.

MS-qLNAPCR analysis requires a proven and solid technical experience of the operators as well as specific instruments and reagents, which increases the costs for each patient. This system increases the sensitivity of the analysis, which allows the identification of small tumoural cellular clones, and reduces the number of false negative cases.

For each sample a double reaction must be set up in order to reduce the analytic bias and guarantee reproducible results. The presence of a cytosine residue after bisulfite treatment indicates that the cytosine residue is protected by methylation from bisulfite modification. Relative quantification of the methylated and unmethylated allele ratio is calculated according to DDCt method using an equal amount of SssI-treated wild-type DNA fully methylated mixed with the same amount of untreated DNA as a calibrator [13,14].

The major concerns with the evaluation of MGMT gene promoter methylation are based on the absence of validation studies of available assays for its technical reproducibility. Strict quality control studies, both in processing and assessment of data, would need the collaborative effort of neuro-oncological surgeons, neuropathologists, and molecular pathologists.