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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 28 Aug 2015.

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, Id1
Papers on Methylguanine-DNA Methyltransferase
Investigating a signature of temozolomide resistance in GBM cell lines using metabolomics.
Morin et al., Moncton, Canada. In J Neurooncol, 28 Sep 2015
This approach was also utilized to explore the metabolic changes modulated upon cell treatment with temozolomide and lomeguatrib, an MGMT inhibitor with temozolomide-sensitizing potential.
Genetic and epigenetic characterization of low-grade gliomas reveals frequent methylation of the MLH3 gene.
Michalova et al., Praha, Czech Republic. In Genes Chromosomes Cancer, 25 Sep 2015
The O-6-methylguanine-DNA-methyltransferase (MGMT) promoter was methylated in 83% of LGO and 59% of LGA.
Temozolomide treatment for pediatric refractory anaplastic ependymoma with low MGMT protein expression.
Shigeta et al., Nagano, Japan. In Pediatr Blood Cancer, 25 Sep 2015
We did not detect O(6) -methylguanine-DNA methyltransferase (MGMT) promoter methylation in tumor samples; however, MGMT protein expression was low.
Outcome and toxicity profile of salvage low-dose-rate iodine-125 stereotactic brachytherapy in recurrent high-grade gliomas.
Nachbichler et al., München, Germany. In Acta Neurochir (wien), 23 Sep 2015
Favorable factors for TTF and PRS were age ≤ 50 years and a methylated O(6)-methylguanine-DNA methyltransferase (MGMT)-promoter.
Glioblastoma multiforme: Pathogenesis and treatment.
Trafalis et al., Athens, Greece. In Pharmacol Ther, 31 Aug 2015
Lately, efforts have been made to investigate tumor resistance, which results from complex alternate signaling pathways, the existence of glioma stem-cells, the influence of the blood-brain barrier as well as the expression of 0(6)-methylguanine-DNA methyltransferase.
The role of temozolomide in the treatment of aggressive pituitary tumors.
Eloy et al., Newark, United States. In J Clin Neurosci, Jun 2015
In this article, the authors review the development of temozolomide, its biochemistry and interaction with O(6)-methylguanine-DNA methyltransferase (MGMT), its role in adjuvant treatment of aggressive pituitary neoplasms, and future works that could influence the efficacy of temozolomide therapy.
Treatment of elderly patients with glioblastoma: a systematic evidence-based analysis.
Das et al., Toronto, Canada. In Jama Neurol, May 2015
EVIDENCE REVIEW: We performed a systematic review to identify articles from the temozolomide era (2005-present) that reported survival data related to treatment of elderly patients with GBM using either temozolomide alone or radiotherapy alone, with consideration of O6-methylguanine-DNA-methyltransferase gene (MGMT) promoter methylation status.
Chemoresistance and chemotherapy targeting stem-like cells in malignant glioma.
Beier et al., Odense, Denmark. In Adv Exp Med Biol, Dec 2014
O6-methyl-guanidine methyltransferase (MGMT) remains the most potent mediator of chemoresistance, but disturbed mismatch repair system and multidrug resistance proteins contribute substantially.
Aberrant methylation patterns in cancer: a clinical view.
Hudler et al., Ljubljana, Slovenia. In Biochem Med (zagreb), Dec 2014
Even more, promoter methylation patterns of some genes, such as MGMT, SHOX2, and SEPT9, have already been translated into commercial clinical assays aiding in patient assessment as adjunct diagnostic tools.
The Role of Chemotherapy in Well-Differentiated Gastroenteropancreatic Neuroendocrine Tumors.
Pavel et al., Tampa, United States. In Front Horm Res, Dec 2014
Methyl-guanine-methyl-transferase (MGMT) deficiency is likely to be a positive predictive factor for alkylating agents, but needs to be evaluated prospectively.
Cilengitide combined with standard treatment for patients with newly diagnosed glioblastoma with methylated MGMT promoter (CENTRIC EORTC 26071-22072 study): a multicentre, randomised, open-label, phase 3 trial.
CENTRIC study team et al., Zürich, Switzerland. In Lancet Oncol, Sep 2014
Data from phase 2 trials suggest that it has antitumour activity as a single agent in recurrent glioblastoma and in combination with standard temozolomide chemoradiotherapy in newly diagnosed glioblastoma (particularly in tumours with methylated MGMT promoter).
Dose-dense temozolomide for newly diagnosed glioblastoma: a randomized phase III clinical trial.
Mehta et al., Houston, United States. In J Clin Oncol, 2013
O(6)-methylguanine-DNA methyltransferase (MGMT) methylation status may be an important determinant of treatment response.
The somatic genomic landscape of glioblastoma.
TCGA Research Network et al., New York City, United States. In Cell, 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, 2013
In a subgroup of patients with non-methylated MGMT, the HR was 1·72 (95% CI 1·15-2·56; p=0·008).
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, 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.
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
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