Methylation of histones in myeloid leukemias as a potential marker of granulocyte abnormalities
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
15507473
DOI
10.1189/jlb.0704388
PII: jlb.0704388
Knihovny.cz E-resources
- MeSH
- Acute Disease MeSH
- Antineoplastic Agents pharmacology MeSH
- Cell Differentiation drug effects MeSH
- Chromatin metabolism MeSH
- Leukemia, Myelogenous, Chronic, BCR-ABL Positive diagnosis genetics metabolism MeSH
- Adult MeSH
- Granulocytes metabolism pathology MeSH
- Histones genetics metabolism MeSH
- HL-60 Cells MeSH
- Chromobox Protein Homolog 5 MeSH
- Middle Aged MeSH
- Humans MeSH
- Methylation * MeSH
- Leukemia, Myeloid diagnosis genetics metabolism MeSH
- Biomarkers, Tumor metabolism MeSH
- Disease Progression MeSH
- Cell Proliferation MeSH
- Aged MeSH
- Tretinoin pharmacology MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Aged MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Antineoplastic Agents MeSH
- CBX5 protein, human MeSH Browser
- Chromatin MeSH
- Histones MeSH
- Chromobox Protein Homolog 5 MeSH
- Biomarkers, Tumor MeSH
- Tretinoin MeSH
We show that common heterochromatin antigenic protein markers [HP1alpha, -beta, -gamma and mono-, di-, and trimethylated histone H3 lysine 9 (H3K9)], although present in human blood progenitor CD34+ cells, differentiated lymphocytes, and monocytes, are absent in neutrophil granulocytes and to large extent, in eosinophils. Monomethylated and in particular, dimethylated H3K9 are present to variable degrees in the granulocytes of chronic myeloid leukemia (CML) patients, without being accompanied by HP1 proteins. In patients with an acute phase of CML and in acute myeloid leukemia patients, strong methylation of H3K9 and all isoforms of HP1 are detected. In chronic forms of CML, no strong correlations among the level of histone methylation, disease progression, and modality of treatment were observed. Histone methylation was found even in "cured" patients without Philadelphia chromosome (Ph) resulting from +(9;22)(q34;q11) BCR/ABL translocation, suggesting an incomplete process of developmentally regulated chromatin remodeling in the granulocytes of these patients. Similarly, reprogramming of leukemia HL-60 cells to terminal differentiation by retinoic acid does not eliminate H3K9 methylation and the presence of HP1 isoforms from differentiated granulocytes. Thus, our study shows for the first time that histone H3 methylation may be changed dramatically during normal cell differentiation. The residual histone H3 methylation in myeloid leukemia cells suggests an incomplete chromatin condensation that may be linked to the leukemia cell proliferation and may be important for the prognosis of disease treatment and relapse.
References provided by Crossref.org
Spatial-Temporal Genome Regulation in Stress-Response and Cell-Fate Change
Histone modifications and nuclear architecture: a review
