Hypermethylation of the p15 Gene in Myelodysplastic Syndromes

Previous studies have shown that the cyclin-dependent kiterestingly, the p15 gene was frequently methylated in patients with high-risk MDS (refractory anemia with excess nase inhibitor (CDKI) genes p15 and p16 are frequently inactivated by genetic alterations in many malignant blasts [RAEB], RAEB in transformation [RAEB-t], and overt leukemia evolved from MDS; 14/18 [78%]) compared with tumors and that they are candidate tumor-suppressor genes. Although genetic alterations in these genes may be patients with low-risk MDS (refractory anemia [RA] and refractory anemia with ring sideroblast [RARS]; 1/12 [8%]). limited to lymphoid malignancies, it has been reported that their inactivation by aberrant methylation of 5* CpG islands Furthermore, methylation status of the p15 gene was progressed with the development of MDS in most patients may be involved in various hematologic malignancies. In this study, we investigated the p15 and p16 genes to examined. In contrast, none of the MDS patients showed apparent hypermethylation of the p16 gene. These reclarify their roles in the pathogenesis of myelodysplastic syndrome (MDS). Southern blotting analysis showed no sults suggest that hypermethylation of the p15 gene is involved in the pathogenesis of MDS and is one of the imgross genetic alterations in either of these genes. However, hypermethylation of the 5* CpG island of the p15 gene portant late events during the development of MDS.