In acute myeloid leukemia (AML) with inv (3)(q21; q26) or t (3; 3)(q21; q26), a translocated
GATA2 enhancer drives oncogenic expression of EVI1. We generated an EVI1-GFP AML …

Chromosomal rearrangements are a frequent cause of oncogene deregulation in human
malignancies. Overexpression of EVI1 is found in a subgroup of acute myeloid leukemia …

Chromosomal rearrangements involving the MDS1 and EVI1 complex locus (MECOM) on
chromosome 3q26 define an aggressive subtype of acute myeloid leukemia (AML) that is …

Chromosomal rearrangements without gene fusions have been implicated in
leukemogenesis by causing deregulation of proto-oncogenes via relocation of cryptic …

Deregulation of the EVI1 proto-oncogene by the GATA2 distal hematopoietic enhancer
(G2DHE) is a key event in high-risk acute myeloid leukemia carrying 3q21q26 aberrations …

Chromosomal inversion between 3q21 and 3q26 results in high-risk acute myeloid leukemia
(AML). In this study, we identified a mechanism whereby a GATA2 distal hematopoietic …

The development of acute myelogenous leukemia (AML), which is characterized by a block
of myeloid differentiation, is a multi-step process that involves several genetic abnormalities …

Acute myeloid leukemia (AML) driven by the activation of EVI1 due to chromosome
3q26/MECOM rearrangements is incurable. Because transcription factors such as EVI1 are …

Disruption of epigenetic regulation is a hallmark of acute myeloid leukemia (AML), but
epigenetic therapy is complicated by the complexity of the epigenome. Herein, we …

Ecotropic viral integration site 1 (EVI1) is an important transcription factor for
leukemogenesis. EVI1 is a member of a group of transcription factors with C-terminal …