| Literatürler Hematoloji Uzmanlık Derneği
Literatür Detay Bilgisi
Classical Hodgkin lymphoma shows epigenetic features of an abortive plasma cellular differentiation.

Yazarlar : Seitz V, Thomas PE, Zimmermann K, Paul U, Ehlers A, Joosten M, Dimitrova L, Lenze D, Sommerfeld A, Oker E, Leser U, Stein H, Hummel M.

Yayın : Haematologica.

Yayın Yılı : 2011

Pubmed Linki : http://www.ncbi.nlm.nih.gov/pubmed/21393330

Konu : Lenfoma

Literatür İçeriği :  

Abstract

Background. Epigenetic changes are involved in the extinction of the B-cell gene expression program of classical Hodgkin lymphoma. However, little is known regarding epigenetic similarities between classical Hodgkin lymphoma and plasma cell myeloma cells both of which share an extinction of the gene expression program of mature B-cells. Design and methods. Global histone H3 acetylation patterns were determined in cell lines derived from classical Hodgkin lymphoma, plasma cell myeloma and B-cell lymphoma by chromatin immunoprecipitation and subsequent hybridization onto promoter tiling arrays. H3K27 trimethylation was analyzed by chromatin immunoprecipitation and real-time DNA-PCR for selected genes. Epigenetic modifications were compared to gene expression data. Results. B-cell characteristic genes were hypoacetylated in classical Hodgkin lymphoma and plasma cell myeloma cell lines as demonstrated by comparison of their histone H3 acetylation patterns to those of B-cell lines. However, the number of genes jointly hyperacetylated and expressed in classical Hodgkin lymphoma and plasma cell myeloma cell lines such as IFR4/MUM1 and RYBP is limited. Moreover, H3K27 trimethylation for selected B-cell characteristic genes revealed that this additional epigenetic silencing is much more prevalent in classical Hodgkin lymphoma as compared to plasma cell myeloma. Conclusion. Our epigenetic data support the view that classical Hodgkin lymphoma is characterised by an abortive plasma cell differentiation with a down-regulation of B-cell characteristic genes but without activation of most plasma cell typical genes.


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