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

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

doi:10.1016/j.leukres.2004.11.002

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

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

Hematology

Research output: Contribution to journal › Article › peer-review

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 (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.

Original language	English (US)
Pages (from-to)	511-515
Number of pages	5
Journal	Leukemia Research
Volume	29
Issue number	5
DOIs	https://doi.org/10.1016/j.leukres.2004.11.002
State	Published - May 2005

Keywords

Cell cycle
Methylation
Myelofibrosis with myeloid metaplasia

ASJC Scopus subject areas

Hematology
Oncology
Cancer Research

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10.1016/j.leukres.2004.11.002

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title = "Methylation analysis of the cell cycle control genes in myelofibrosis with myeloid metaplasia",

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.",

keywords = "Cell cycle, Methylation, Myelofibrosis with myeloid metaplasia",

author = "Takashi Kumagai and Ayalew Tefferi and Letetia Jones and Koeffler, {H. Phillip}",

note = "Funding Information: This work was supported by the Phyllis and Brian Harvey Foundation and NIH grants. H. Phillip Koeffler holds the Mark Goodson Endowed Chair of Oncology Research at Cedars Sinai Medical Center and is a member of the Molecular Biology Institute and Jonsson Cancer Center, UCLA. ",

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AU - Jones, Letetia

AU - Koeffler, H. Phillip

N1 - Funding Information: This work was supported by the Phyllis and Brian Harvey Foundation and NIH grants. H. Phillip Koeffler holds the Mark Goodson Endowed Chair of Oncology Research at Cedars Sinai Medical Center and is a member of the Molecular Biology Institute and Jonsson Cancer Center, UCLA.

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N2 - 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.

AB - 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.

KW - Cell cycle

KW - Methylation

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

Abstract

Keywords

ASJC Scopus subject areas

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