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A correction has been published: N Engl J Med 2001;344(9):686.

Volume 343:1350-1354 November 9, 2000 Number 19 Next

	Full Text PDF Editorial by Weinstein, J. N. Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited Related Article Related Article by Buckner, J. C. PubMed Citation

ABSTRACT

Background The DNA-repair enzyme O ⁶-methylguanine-DNA methyltransferase (MGMT) inhibits the killing of tumor cells by alkylating agents. MGMT activity is controlled by a promoter; methylation of the promoter silences the gene in cancer, and the cells no longer produce MGMT. We examined gliomas to determine whether methylation of the MGMT promoter is related to the responsiveness of the tumor to alkylating agents.

Methods We analyzed the MGMT promoter in tumor DNA by a methylation-specific polymerase-chain-reaction assay. The gliomas were obtained from patients who had been treated with carmustine (1,3-bis(2-chloroethyl)-1-nitrosourea, or BCNU). The molecular data were correlated with the clinical outcome.

Results The MGMT promoter was methylated in gliomas from 19 of 47 patients (40 percent). This finding was associated with regression of the tumor and prolonged overall and disease-free survival. It was an independent and stronger prognostic factor than age, stage, tumor grade, or performance status.

Conclusions Methylation of the MGMT promoter in gliomas is a useful predictor of the responsiveness of the tumors to alkylating agents.

Source Information

From the Divisions of Cancer Biology (M.E., S.B.B., J.G.H.) and Biostatistics (S.N.G.), Johns Hopkins Oncology Center, Baltimore; and the Biotechnology Laboratory, Cell Therapy Area, Department of Oncology, Clinica Universitaria, Pamplona, Spain (J.G.-F., E.A., O.F.H., V.V.).

Address reprint requests to Dr. Herman at the Johns Hopkins Oncology Center, 1650 Orleans, Baltimore, MD 21231, or at hermanji{at}jhmi.edu.

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