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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 02 Oct 2014.

O-6-methylguanine-DNA methyltransferase

Methylguanine-DNA Methyltransferase, MGMT, O6-methylguanine-DNA methyltransferase
This gene is expressed only in the liver and the encoded protein is localized mostly in the peroxisomes, where it is involved in glyoxylate detoxification. Mutations in this gene, some of which alter subcellular targetting, have been associated with type I primary hyperoxaluria. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HAD, AGE, p53, CAN, POLYMERASE
Papers on Methylguanine-DNA Methyltransferase
Phase II trial of 7 days on/7 days off temozolmide for recurrent high-grade glioma.
Butowski et al., San Francisco, United States. In Neuro Oncol, 30 Sep 2014
A further exploratory objective included the investigation of whether methylation status of the O(6)-methylguanine-DNA methyltransferase (MGMT) promoter within tumor tissue predicted outcomes.
Profound prevention of experimental brain metastases of breast cancer by temozolomide in an MGMT-dependent manner.
Steeg et al., Gdańsk, Poland. In Clin Cancer Res, Jun 2014
EXPERIMENTAL DESIGN: Temozolomide was administered in mice following earlier injection of brain-tropic HER2-positive JIMT-1-BR3 and triple-negative 231-BR-EGFP sublines, the latter with and without expression of O(6)-methylguanine-DNA methyltransferase (MGMT).
Cantharidin induces DNA damage and inhibits DNA repair-associated protein levels in NCI-H460 human lung cancer cells.
Chung et al., Taiwan. In Environ Toxicol, Apr 2014
Cantharidin (5, 10, and 15 μM) treatment of NCI-H460 cells reduced protein levels of ataxia telangiectasia mutated (ATM), breast cancer 1, early onset (BRCA-1), 14-3-3 proteins sigma (14-3-3σ), DNA-dependent serine/threonine protein kinase (DNA-PK), O(6) -methylguanine-DNA methyltransferase (MGMT), and mediator of DNA damage checkpoint protein 1 (MDC1).
BCNU/PLGA microspheres: a promising strategy for the treatment of gliomas in mice.
Zhu et al., Shanghai, China. In Chin J Cancer Res, Feb 2014
Specimens were harvested, and immunohistochemical staining was used to check the expression of Bax, Bcl-2, and O(6)-methylguanine-DNA methyltransferase (MGMT).
Dose-dense temozolomide for newly diagnosed glioblastoma: a randomized phase III clinical trial.
Mehta et al., Houston, United States. In J Clin Oncol, Dec 2013
O(6)-methylguanine-DNA methyltransferase (MGMT) methylation status may be an important determinant of treatment response.
O6-methylguanine-DNA methyltransferase in the defense against N-nitroso compounds and colorectal cancer.
Kaina et al., Mainz, Germany. In Carcinogenesis, Nov 2013
Methylated DNA bases are removed by base excision repair initiated by the alkyladenine-DNA glycosylase, the family of AlkB homologs proteins, and the suicide enzyme O(6)-methylguanine-DNA methyltransferase (MGMT), which is the main focus of this review.
The somatic genomic landscape of glioblastoma.
TCGA Research Network et al., New York City, United States. In Cell, Nov 2013
Correlative analyses confirm that the survival advantage of the proneural subtype is conferred by the G-CIMP phenotype, and MGMT DNA methylation may be a predictive biomarker for treatment response only in classical subtype GBM.
Adenovirus-mediated gene therapy with sitimagene ceradenovec followed by intravenous ganciclovir for patients with operable high-grade glioma (ASPECT): a randomised, open-label, phase 3 trial.
ASPECT Study Group et al., Hamburg, Germany. In Lancet Oncol, Aug 2013
In a subgroup of patients with non-methylated MGMT, the HR was 1·72 (95% CI 1·15-2·56; p=0·008).
Performance characteristics of bisulfite conversion and SYBR green based quantitative PCR for DNA methylation analysis.
Goel et al., In J Environ Biol, Jul 2013
Currently, the experiments were undertaken using oral cancer tissue, with varying incubation time of bisulfite treatment and 2 representative genes viz MGMT and p16 were selected for the quantitative assessment of methylation by real time PCR.
Pseudoprogression after glioma therapy: a comprehensive review.
Robins et al., Madison, United States. In Expert Rev Neurother, Apr 2013
The authors have summarized the literature relative to the incidence, chronological sequence, therapy-relatedness, impact of O-6-methylguanine-DNA methyltransferase methylation status and clinical features of pseudoprogression.
Intrinsic molecular subtypes of glioma are prognostic and predict benefit from adjuvant procarbazine, lomustine, and vincristine chemotherapy in combination with other prognostic factors in anaplastic oligodendroglial brain tumors: a report from EORTC study 26951.
French et al., Rotterdam, Netherlands. In J Clin Oncol, Feb 2013
They are prognostic for PFS independent of clinical (age, performance status, and tumor location), molecular (1p/19q loss of heterozygosity [LOH], IDH1 mutation, and MGMT methylation), and histologic parameters.
Toward a Molecular Classification of Colorectal Cancer: The Role of MGMT.
Minoo, Calgary, Canada. In Front Oncol, 2012
O(6)-methylguanine DNA methyltransferase (MGMT) is a DNA repair enzyme with the ability to protect cells from DNA mutations by removing alkyl groups from the O(6) position of guanine.
Personalized treatment strategies in glioblastoma: MGMT promoter methylation status.
Kreth et al., München, Germany. In Onco Targets Ther, 2012
In glioblastoma, the most malignant intrinsic brain tumor entity in adults, the promoter methylation status of the gene encoding for the repair enzyme O6-methylguanine-DNA methyltransferase (MGMT) indicates increased efficacy of current standard of care, which is concomitant and adjuvant chemoradiotherapy with the alkylating agent temozolomide.
O6-methylguanine DNA methyltransferase as a promising target for the treatment of temozolomide-resistant gliomas.
Jiang et al., Xuzhou, China. In Cell Death Dis, 2012
One of the major mechanisms of cancer drug resistance is enhanced activity of a DNA repair enzyme, O(6)-methylguanine-DNA-methyltransferase (MGMT), which counteracts chemotherapy-induced DNA alkylation and is a key component of chemoresistance.
Uncoupling of eNOS causes superoxide anion production and impairs NO signaling in the cerebral microvessels of hph-1 mice.
Katusic et al., Rochester, United States. In J Neurochem, 2012
Reduced tetrahydrobiopterin bioavailability causes endothelial NOS uncoupling, increases superoxide anion production, inhibits eNOS/cGMP signaling, and imposes significant oxidative stress in the cerebral microvasculature.
Angiotensin-II and MARCKS: a hydrogen peroxide- and RAC1-dependent signaling pathway in vascular endothelium.
Michel et al., Boston, United States. In J Biol Chem, 2012
a critical role for H(2)O(2) in angiotensin-II signaling to the endothelial cytoskeleton in a novel pathway that is critically dependent on MARCKS, Rac1, and c-Abl.
The prolyl hydroxylase PHD3 identifies proinflammatory macrophages and its expression is regulated by activin A.
Corbí et al., Madrid, Spain. In J Immunol, 2012
These results indicate that EGLN3 gene expression in macrophages is dependent on activin A
Loss of the oxygen sensor PHD3 enhances the innate immune response to abdominal sepsis.
Schneider et al., Heidelberg, Germany. In J Immunol, 2012
It is concluded that impairment of PHD3 enzyme function aggravates the clinical course of abdominal sepsis
PHD3-dependent hydroxylation of HCLK2 promotes the DNA damage response.
Patterson et al., Chapel Hill, United States. In J Clin Invest, 2012
mice lacking PHD3 were resistant to the effects of ionizing radiation and had decreased thymic apoptosis, a biomarker of genomic integrity
Genetic variations and patient-reported quality of life among patients with lung cancer.
Yang et al., Rochester, United States. In J Clin Oncol, 2012
Three SNPs in the MGMT gene (adjusted analysis, rs3858300; unadjusted analysis, rs10741191 and rs3852507) from DNA repair pathway were associated with overall quality of life in patients with lung cancer.
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