Abstract 2766: DNA methylation status of MLH1, p16 and SOCS1 in Puerto Rican patients with acute myeloid leukemia

2011 
Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL Background: DNA methylation of gene promoters have been show to play a role in the pathogenesis of acute myeloid leukemia. We present in this study a preliminary report of the methylation status of MLH1, p16 and SOCS1 in Puertorrican patients with acute myeloid leukemia Methods: Peripheral blood was obtained from 24 patients with diagnosis of acute myeloid leukemia before their induction treatments. DNA was isolated and further modified with sodium bisulfite. Methylation-specific polymerase (MSP) chain reaction was performed to detect aberrant promoter methylation of MLH1, p16 and SOCS1. Results: A total of 24 samples were analyzed. The mean age was 49 years (range 22-71) with 17/24 patients younger than 60 years (71%). Most of the patients were female (13/24, 54%). Six patients had diploid cytogenetics (25%), 6 had low risk cytogenetics (25%) and 12 had high risk cytogenetics (50%). Fifteen patients were de Novo AML (63%). Nine patients (38%) presented with WBC counts higher than 10 × 109/L. Thirteen patients (54%) achieved a complete response at the end of the induction therapy. Methylation of MLH1 was detected in 3/24 patients (13%). Methylation of p16 was detected in 5/24 patients (21%). Methylation of SOCS1 was detected in 2/24 patients (8%). Conclusions: A tendency toward an association of methylated p16 with treatment resistance was noted. Also, methylation of SOCS1 was more common among relapsed AML patients. No correlation between methylated MLH1 gene and clinicopathological characteristics was noted. Collection of more patient's samples and correlation with clinical data and patient's ultimate outcome is ongoing. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2766. doi:10.1158/1538-7445.AM2011-2766
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