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Methylation status of the MGMT gene promoter fails to predict the clinical outcome of glioblastoma patients treated with ACNU plus cisplatin
Author(s) -
Park ChulKee,
Park SungHye,
Lee SeHoon,
Kim ChaeYong,
Kim DongWan,
Paek Sun Ha,
Kim Dong Gyu,
Heo Dae Seog,
Kim Il Han,
Jung HeeWon
Publication year - 2009
Publication title -
neuropathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 61
eISSN - 1440-1789
pISSN - 0919-6544
DOI - 10.1111/j.1440-1789.2008.00998.x
Subject(s) - cisplatin , methyltransferase , methylation , cancer research , medicine , temozolomide , oncology , gene , glioblastoma , chemotherapy , biology , genetics
We analyzed the methylation status of the O6‐methylguanine‐DNA methyltransferase (MGMT) promoter using a methylation‐specific polymerase chain reaction (MSP) in glioblastoma patients treated with 1‐(4‐amino‐2‐methyl‐5‐pyrimidinyl)methyl‐3‐(2‐chloroethyl)‐3‐nitrosourea (ACNU) plus cisplatin followed by radiation therapy. Forty‐eight patients with interpretable MSP results were included in this study. The MGMT promoter was methylated in 26 patients (54.2%, methylated group) and unmethylated in 22 patients (45.8%, unmethylated group). Comparison of clinical outcomes between the two groups revealed that the methylation status of the MGMT gene promoter was not a prognostic factor for overall survival ( P = 0.516) or a predictive factor for radiological response to ACNU plus cisplatin treatment ( P = 0.529). The most noteworthy explanation for the result is that the synergistic antitumor effects of ACNU and cisplatin resulting from inactivation of MGMT by cisplatin in MGMT active tumors offset the drug resistance.