Preserved global histone H4 acetylation linked to ETV6-RUNX1 fusion and PAX5 deletions is associated with favorable outcome in pediatric B-cell progenitor acute lymphoblastic leukemia.
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Authors
Janczar, KarolinaJanczar, Szymon
Pastorczak, Agata
Mycko, K.
Paige, Adam J.W.
Zalewska-Szewczyk, Beata
Wagrowska-Danilewicz, M.
Danilewicz, Marian
Mlynarski, Wojciech
Issue Date
2015-10-20
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Epigenetic dysregulation is a hallmark of cancer executed by a number of complex processes the most important of which converge on DNA methylation and histone protein modifications. Epigenetic marks are potentially reversible and thus promising drug targets. In the setting of acute lymphoblastic leukemia (ALL) they have been associated with clinicopathological features including risk of relapse or molecular subgroups of the disease. Here, using immunocytochemistry of bone marrow smears from diagnosis, we studied global histone H4 acetylation, whose loss was previously linked to treatment failure in adults with ALL, in pediatric patients. We demonstrate that preserved global histone H4 acetylation is significantly associated with favorable outcome (RFS, EFS, OS) in children with B cell progenitor (BCP) ALL, recapitulating the findings from adult populations. Further, for the first time we demonstrate differential histone H4 acetylation in molecular subclasses of BCP-ALL including cases with ETV6-RUNX1 fusion gene or PAX5 deletion or deletions in genes linked to B cell development. We conclude global histone H4 acetylation is a prognostic marker and a potential therapeutic target in ALL.Citation
Janczar, K., Janczar, S., Pastorczak, K., Mycko, K., Paige, A.J.W., Zalewska-Szewczyk, Wagrowska-Danilewicz, M., Mlynarski, W. (2015) ' Preserved global histone H4 acetylation linked to ETV6-RUNX1 fusion and PAX5 deletions is associated with favorable outcome in pediatric B-cell progenitor acute lymphoblastic leukemia' Leukemia Research 39 (12) 1455-1461Publisher
ElsevierJournal
Leukemia researchPubMed ID
26520622Additional Links
http://www.sciencedirect.com/science/article/pii/S0145212615305312http://www.ncbi.nlm.nih.gov/pubmed/26520622
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ArticleLanguage
enISSN
1873-5835ae974a485f413a2113503eed53cd6c53
10.1016/j.leukres.2015.10.006
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