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 Blood, 15 August 2008, Vol. 112, No. 4, pp. 1366-1373.
Prepublished online as a Blood First Edition Paper on June 3, 2008; DOI 10.1182/blood-2007-11-126227.

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NEOPLASIA

Aberrant CpG island methylation in acute myeloid leukemia is accentuated at relapse

Heike Kroeger1,*, Jaroslav Jelinek1,*, Marcos R. H. Estécio1, Rong He1, Kimie Kondo1, Woonbok Chung1, Li Zhang2, Lanlan Shen1, Hagop M. Kantarjian1, Carlos E. Bueso-Ramos3, and Jean-Pierre J. Issa1

Departments of1 Leukemia, 2 Bioinformatics and Computational Biology, and 3 Hematopathology, University of Texas M. D. Anderson Cancer Center, Houston

DNA methylation of CpG islands around gene transcription start sites results in gene silencing and plays a role in leukemia pathophysiology. Its impact in leukemia progression is not fully understood. We performed genomewide screening for methylated CpG islands and identified 8 genes frequently methylated in leukemia cell lines and in patients with acute myeloid leukemia (AML): NOR1, CDH13, p15, NPM2, OLIG2, PGR, HIN1, and SLC26A4. We assessed the methylation status of these genes and of the repetitive element LINE-1 in 30 patients with AML, both at diagnosis and relapse. Abnormal methylation was found in 23% to 83% of patients at diagnosis and in 47% to 93% at relapse, with CDH13 being the most frequently methylated. We observed concordance in methylation of several genes, confirming the presence of a hypermethylator pathway in AML. DNA methylation levels increased at relapse in 25 of 30 (83%) patients with AML. These changes represent much larger epigenetic dysregulation, since methylation microarray analysis of 9008 autosomal genes in 4 patients showed hypermethylation ranging from 5.9% to 13.6% (median 8.3%) genes at diagnosis and 8.0% to 15.2% (median 10.6%) genes in relapse (P < .001). Our data suggest that DNA methylation is involved in AML progression and provide a rationale for the use of epigenetic agents in remission maintenance.


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