Epigenetic therapy as a novel approach for GFI136N-associated murine/human AML

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Epigenetic therapy as a novel approach for GFI136N-associated murine/human AML

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作者：Lacramioara Botezatu^a ; Lars C. Michel^a ; Anne Helness^b ; Charles Vadnais^b ; Hideki Makishima^c ; Judith M. H&ouml ; nes^a ; Franç ; ois Robert^b ; ^d ; Lothar Vassen^a ; Aniththa Thivakaran^a ; Yahya Al-Matary^a ; Robert F. Lams^a ; Judith Schü ; tte^a ; Bernd Giebel^e ; André ; G&ouml ; rgens^e ; Michael Heuser^f ; Hind Medyouf^g ; Jaroslaw Maciejewski^c ; Ulrich Dü ; hrsen^a ; Tarik M&ouml ; r&ouml ; y^b ; ^h ; ⁱ ; ^{Tarik.Moroy@ircm.qc.ca" class="auth_mail" title="E-mail the corresponding author} ; Cyrus Khandanpour^a ; ^{cyrus.khandanpour@uk-essen.de" class="auth_mail" title="E-mail the corresponding author}
刊名：Experimental Hematology
出版年：2016
出版时间：August 2016
年：2016
卷：44
期：8
页码：713-726.e14
全文大小：8395 K

文摘

•: The GFI1^36N variant accelerates development of acute myeloid leukemia in acute myeloid leukemia/myelodysplastic syndrome mouse models.
•: GFI1^36N induces genomewide epigenetic changes in murine and human acute myeloid leukemia.
•: GFI^36N human and murine leukemic cells respond specifically to histone acetyltransferase inhibitor treatment in vitro.
•: Use of histone acetyltransferase inhibitor prolongs survival of mice transplanted with GFI1^36N-expressing leukemia.

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