Absence of p21(CIP 1), p27(KIP 1) and p 57(KIP 2) methylation in MDS and AML

Leuk Res. 2005 Nov;29(11):1357-60. doi: 10.1016/j.leukres.2005.04.012.

Abstract

Transcriptional silencing of tumour suppressor genes (TSG) due to hypermethylation is a common event in human tumours. The three members of the KIP/CIP family of cyclin dependent kinase inhibitors (CDKIs), p21(CIP 1), p27(KIP 1), and p 57(KIP 2), play key roles in cell cycle regulation, but little is known about their methylation in myeloid neoplasia. Therefore, we analysed 9 haematopoietic cell lines, 67 myelodysplastic syndrome (MDS) and 26 acute myeloid leukaemia (AML) cases as well as 11 controls. p 57(KIP 2) hypermethylation was found in 4/9 cell lines, but methylation of p21(CIP 1) and p27(KIP 1) was infrequent. All patient samples analysed were methylation-negative for these three genes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Adult
  • Aged
  • Aged, 80 and over
  • Cell Cycle / drug effects
  • Cell Line, Tumor
  • Cyclin-Dependent Kinase Inhibitor p21 / genetics*
  • Cyclin-Dependent Kinase Inhibitor p27 / genetics*
  • Cyclin-Dependent Kinase Inhibitor p57 / genetics*
  • DNA Methylation
  • Female
  • Gene Silencing
  • Humans
  • Leukemia, Myeloid / genetics*
  • Male
  • Middle Aged
  • Myelodysplastic Syndromes / genetics*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transcription, Genetic

Substances

  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclin-Dependent Kinase Inhibitor p57
  • Cyclin-Dependent Kinase Inhibitor p27