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• W2736183265 abstract "1599 5-aza-2′-deoxycytidine (decitabine) is a cytosine analog that has the unique ability to inhibit DNA methylation. Decitabine has been used in numerous clinical trials and has shown consistent activity in myeloid leukemias. We wished to investigate whether decitabine has activity in leukemia via its ability to inhibit DNA methylation. We therefore studied samples from leukemia patients who were treated in two clinical trials using decitabine. The first trial used a “high” dose of decitabine at 50-90mg/m 2 twice daily for 5 days. A second clinical trial used a “low” dose strategy of 5-20mg/m 2 once daily for 10 days in order to take advantage of the demethylating properties of decitabine. We analyzed DNA methylation of p15, H19, HoxA5 and Alu repetitive elements in peripheral blood samples of patients before, during and after treatment to examine methylation changes induced by decitabine. The p15 gene is a tumor suppressor gene that is normally unmethylated, but becomes aberrantly methylated in cancer. H19 is an imprinted locus that is only methylated on the paternal allele, and HoxA5 is a gene that is normally heavily methylated. Alu elements were studied as a surrogate marker for global genome methylation. We found that decitabine treatment could decrease DNA methylation in all the genes studied, but Alu methylation gave the most consistent results probably because Alu elements are more abundant and heavily methylated in the genome. Overall most patients (88%) showed a decrease in Alu methylation with decitabine treatment. However, the mean decrease in Alu methylation was only 7.7% with a range of –10.3 to 31.5% (SD=8.2%). We found a dose dependent decrease in methylation after decitabine treatment with a plateau at high doses. We examined patients treated at six doses (5, 10, 15, 20, 100 and 180mg/m 2 /day). Demethylation averaged 2.8%, 1.1%, 7.3%, 11.6%, 10.9%, and 8.5% at these six doses, respectively. Thus there did not appear to be a significant increase in demethylation beyond 20mg/m 2 /day. However, the number of patients studied at some doses was limited. There was a statistically significant correlation between inhibition of methylation and response to decitabine in the “low” dose strategy. Low dose study patients whose leukemia did not respond showed a mean decrease of only 3.3%, while those patients whose leukemia responded to decitabine showed a mean decrease of 11.5% (p=0.02). Remarkably, this dose-response relationship was not seen at high doses of decitabine, which in vitro induces primarily cytotoxic cell death. These data are consistent with previous in vitro studies that show that low doses of decitabine are optimal for inducing differentiation, and suggest that hypomethylation rather than cytotoxicity is critical for response to this agent." @default.
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• W2736183265 date "2004-04-01" @default.
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• W2736183265 title "DNA methylation changes in leukemia patients treated with 5-aza-2′-deoxycytidine (decitabine)" @default.
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