Using the population based San Francisco Adult Glioma study, we evaluated associations between XRCC1 Arg399Gln, MGMT Leu84Phe, and MGMTIle143Val polymorphisms with glioma risk among white cases (n = 441 to 453) and controls (n = 487 to 526).
A previous study using the RNA microarray technique showed that decrease of MGMT mRNA stands out among the alterations in gene expression caused by the cell growth-depressing transfection of a T98G glioma cell line with liver-type glutaminase (LGA) [Szeliga et al.(2009) Glia, 57, 1014].
MGMT promoter methylation represents a favorable prognostic factor and has been associated with a better response to alkylating agents in glioma and systemic lymphoma.
Finally, the MGMT methylation status determined in the initial glioma tumor did not correlate with the clinical response to temozolomide when this drug was administered as treatment for relapses (P = 0.729).
The objective of this study is to assess the real impact of Io MRI in O-6-methylguanine-DNA methyltransferase and non-O-6-methylguanine-DNA methyltransferase methylated glioma surgery.
The basal promoter in glioma cells with minimal MGMT expression, however, which is 75% unmethylated, was much less accessible, and the basal promoter in nonexpressing cells, which is 50% unmethylated, was entirely inaccessible to restriction enzymes.
Chemoresistance to temozolomide in human glioma cell line U251 is associated with increased activity of O6-methylguanine-DNA methyltransferase and can be overcome by metronomic temozolomide regimen.
The positive rate of MGMT autoantibody to 20 peptides in glioma groups is compared with healthy individuals, the positive rate of MGMT-02 (45%), MGMT-04 (27%), MGMT-07 (21%), MGMT-10 (13%), and MGMT-18 (24%) were significantly elevated in patients with glioma.
In addition, transferrin nanoparticles encapsulating temozolomide have the potential of a promising anti-tumor strategy against glioma of the O6-methylguanine-DNA-methyltransferase gene promoter methylation.
<i>FoxD2-AS1</i> is a prognostic factor in glioma and promotes temozolomide resistance in a O<sup>6</sup>-methylguanine-DNA methyltransferase-dependent manner.
In this study, we investigated the relationship between SWI features and glioma grades, and the expression of key molecular markers isocitrate dehydrogenase 1 (IDH1), O-6-methylguanine-DNA methyltransferase (MGMT), and 1p19q.
We found that the MGMT expression was effectively downregulated by 20(S)-Rg3 via the Wnt/β-catenin pathway in glioma cell lines, and TMZ resistance was significantly reversed by 20(S)-Rg3.
We evaluated the O(6)-methylguanine-DNA methyltransferase mRNA expression and promoter methylation status in glioma patients before and after recurrence by quantitative real-time PCR and methylation-specific PCR assay.
This meta-analysis suggests that glioma susceptibility is associated with rs1799782 and rs25487 of X-ray repair complementing defective repair in Chinese hamster cells 1 (XRCC1), rs1805377 of XRCC4, rs1800067 of excision repair cross-complementing rodent repair deficiency complementation group 4 (ERCC4) and rs3212986 of ERCC1 in Asian population, and rs12917 of O-6-methylguanine-DNA methyltransferase (MGMT) and rs1136410 of poly(ADP-ribose) polymerase 1 (PARP1) in Caucasian population.
Glioma cells rich in miR-181b were more sensitive to temozolomide. miR-181b expression was not correlated with MGMT promoter methylation status. miR-181b combined with temozolomide enhanced glioma cell sensitivity and apoptosis.
Recent practice-changing clinical trials have defined a role for routine assessment of O-6-methylguanine-DNA methyltransferase (MGMT) promoter methylation in glioblastoma patients, especially in the elderly, and 1p and 19q codeletions in patients with anaplastic glial tumors.
Although methylguanine-DNA-methyltransferase (MGMT) plays an important role in resistance to temozolomide (TMZ) in glioma, 40% of gliomas with MGMT inactivation are still resistant to TMZ.The underlying mechanism is not clear.
However, the promoter regions the methylation of which correlates best with survival in aggressive glioma and whether the promoter methylation status predictive value could be refined or improved by other MGMT-associated molecular markers are not precisely known.