Methylation analysis of the cell cycle control genes in myelofibrosis with myeloid metaplasia

Leuk Res. 2005 May;29(5):511-5. doi: 10.1016/j.leukres.2004.11.002. Epub 2005 Jan 15.

Abstract

Promoter hypermethylation represents a primary mechanism in the inactivation of tumor suppressor genes during tumorigenesis. We analyzed the promoter methylation status of eight tumor-associated genes (p14 ARF, p15 INK4B, p16 INK4A, Rb, hMLH1, hMSH2, APC, and DAPK) in 30 patients with myelofibrosis with myeloid metaplasia (MMM) by methylation specific PCR. The study showed no hypermethylation of the promoters of p16(INK4A), Rb, hMLH1, hMSH2, APC, and DAPK genes. The p14 ARF, p15 INK4B promoters were hypermethylated in only one patient each. This study indicates that, although methylation of these genes is important in other cancers, it is rare in MMM and causation of this disease should be focused elsewhere.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Aged
  • Cell Cycle Proteins / genetics*
  • DNA Methylation*
  • Female
  • Genes, Tumor Suppressor / physiology*
  • Humans
  • Male
  • Middle Aged
  • Primary Myelofibrosis / genetics*
  • Promoter Regions, Genetic / genetics*

Substances

  • Cell Cycle Proteins