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RUNX1 repression‐independent mechanisms of leukemogenesis by fusion genes CBFB–MYH11 and AML1–ETO ( RUNX1–RUNX1T1 )
Author(s) -
Hyde R. Katherine,
Liu P. Paul
Publication year - 2010
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22596
Subject(s) - runx1 , psychological repression , fusion protein , transcription factor , biology , fusion gene , core binding factor , runx1t1 , oncogene proteins , gene , cancer research , genetics , chromosomal translocation , regulation of gene expression , gene expression , recombinant dna
The core binding factor (CBF) acute myeloid leukemias (AMLs) are a prognostically distinct subgroup that includes patients with the inv(16) and t(8:21) chromosomal rearrangements. Both of these rearrangements result in the formation of fusion proteins, CBFB–MYH11 and AML1–ETO , respectively, that involve members of the CBF family of transcription factors. It has been proposed that both of these fusion proteins function primarily by dominantly repressing normal CBF transcription. However, recent reports have indicted that additional, CBF‐repression independent activities may be equally important during leukemogenesis. This article will focus on these recent advances. J. Cell. Biochem. 110: 1039–1045, 2010. Published 2010 Wiley‐Liss, Inc.