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

Takashi Kumagai, Ayalew Tefferi, Letetia Jones, H. Phillip Koeffler

Research output: Contribution to journalArticle

23 Scopus citations

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 (p14ARF, p15INK4B, p16INK4A, 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 p14ARF, p15INK4B 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.

Original languageEnglish (US)
Pages (from-to)511-515
Number of pages5
JournalLeukemia Research
Volume29
Issue number5
DOIs
StatePublished - May 2005

Keywords

  • Cell cycle
  • Methylation
  • Myelofibrosis with myeloid metaplasia

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

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