Journal
EUROPEAN JOURNAL OF CANCER
Volume 39, Issue 16, Pages 2298-2305Publisher
ELSEVIER SCI LTD
DOI: 10.1016/S0959-8049(03)00552-5
Keywords
chronic myeloid leukaemia; acceleration; p16(INK4A); p14(ARF); promoter methylation
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The frequency and mechanism of p16(INK4A) and p(14ARF) gene alterations were Studied in cell samples from 30 patients with Philadelphia (Ph) chromosome-positive chronic myeloid leukaemia (CML), both at diagnosis and at the onset of the accelerated phase (AP) of the disease. No alterations in the p16(INK4A) or p(14ARF) genes were found in any of the chronic phase (CP) samples. DNA sequencing analyses detected p16(INK4A) or p(14ARF) mutations in 17 AP samples. All mutations were heterozygous without loss of the other allele. Aberrant methylation of the p16(INK4A) or p14(ARF) promoters was found in 14 of 30 AP samples. The most common situation was the simultaneous methylation of both promoters. Our data indicate that p16(INK4A) and p14(ARF) are primary targets for inactivation by promoter methylation in the acceleration of CML. Transcriptional silencing of the p16(INK4A) and p14(ARF) genes may be important in the conversion of CML from the CP to the AP. (C) 2003 Elsevier Ltd. All rights reserved.
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