Methylation of histones in myeloid leukemias as a potential marker of granulocyte abnormalities
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
15507473
DOI
10.1189/jlb.0704388
PII: jlb.0704388
Knihovny.cz E-zdroje
- MeSH
- akutní nemoc MeSH
- antitumorózní látky farmakologie MeSH
- buněčná diferenciace účinky léků MeSH
- chromatin metabolismus MeSH
- chronická myeloidní leukemie diagnóza genetika metabolismus MeSH
- dospělí MeSH
- granulocyty metabolismus patologie MeSH
- histony genetika metabolismus MeSH
- HL-60 buňky MeSH
- homolog proteinu s chromoboxem 5 MeSH
- lidé středního věku MeSH
- lidé MeSH
- metylace * MeSH
- myeloidní leukemie diagnóza genetika metabolismus MeSH
- nádorové biomarkery metabolismus MeSH
- progrese nemoci MeSH
- proliferace buněk MeSH
- senioři MeSH
- tretinoin farmakologie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- senioři MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antitumorózní látky MeSH
- CBX5 protein, human MeSH Prohlížeč
- chromatin MeSH
- histony MeSH
- homolog proteinu s chromoboxem 5 MeSH
- nádorové biomarkery 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.
Citace poskytuje Crossref.org
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