[PDF][PDF] A single oncogenic enhancer rearrangement causes concomitant EVI1 and GATA2 deregulation in leukemia

S Gröschel, MA Sanders, R Hoogenboezem, E de Wit… - Cell, 2014 - cell.com
Chromosomal rearrangements without gene fusions have been implicated in
leukemogenesis by causing deregulation of proto-oncogenes via relocation of cryptic …

[PDF][PDF] A remote GATA2 hematopoietic enhancer drives leukemogenesis in inv (3)(q21; q26) by activating EVI1 expression

H Yamazaki, M Suzuki, A Otsuki, R Shimizu… - Cancer cell, 2014 - cell.com
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 leukemic oncogene EVI1 hijacks a MYC super-enhancer by CTCF-facilitated loops

S Ottema, R Mulet-Lazaro… - Nature …, 2021 - nature.com
Chromosomal rearrangements are a frequent cause of oncogene deregulation in human
malignancies. Overexpression of EVI1 is found in a subgroup of acute myeloid leukemia …

The leukemia-associated gene MDS1/EVI1 is a new type of GATA-binding transactivator

J Soderholm, H Kobayashi, C Mathieu, JD Rowley… - Leukemia, 1997 - nature.com
EVI1, located at chromosome band 3q26, encodes a 1051 amino acid zinc finger protein
inappropriately expressed in the leukemic cells of 2–5% of acute myeloid leukemia (AML) …

Cooperation of BCR-ABL and AML1/MDS1/EVI1 in blocking myeloid differentiation and rapid induction of an acute myelogenous leukemia

GM Cuenco, R Ren - Oncogene, 2001 - nature.com
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 …

EVI1 is critical for the pathogenesis of a subset of MLL-AF9–rearranged AMLs

EMJ Bindels, M Havermans, S Lugthart… - Blood, The Journal …, 2012 - ashpublications.org
The proto-oncogene EVI1 (ecotropic viral integration site-1), located on chromosome band
3q26, is aberrantly expressed in human acute myeloid leukemia (AML) with 3q26 …

Molecular mechanisms of leukemogenesis by AML1/EVI-1

K Mitani - Oncogene, 2004 - nature.com
Abstract The AML1/EVI-1 chimeric gene is generated by the t (3; 21)(q26; q22) translocation
and plays a pivotal role in progression of hematopoietic stem cell malignancies such as …

The t (3; 21) fusion product, AML1/Evi-1, interacts with Smad3 and blocks transforming growth factor-β–mediated growth inhibition of myeloid cells

M Kurokawa, K Mitani, Y Imai, S Ogawa… - Blood, The Journal …, 1998 - ashpublications.org
Abstract The t (3; 21)(q26; q22) chromosomal translocation associated with blastic crisis of
chronic myelogenous leukemia results in the formation of the AML1/Evi-1 chimeric protein …

Atypical 3q26/MECOM rearrangements genocopy inv(3)/t(3;3) in acute myeloid leukemia

S Ottema, R Mulet-Lazaro, HB Beverloo… - Blood, The Journal …, 2020 - ashpublications.org
Acute myeloid leukemia (AML) with inv (3)/t (3; 3)(q21q26) is a distinct World Health
Organization recognized entity, characterized by its aggressive course and poor prognosis …

Modeling the evolution of ETV6-RUNX1–induced B-cell precursor acute lymphoblastic leukemia in mice

L van der Weyden, G Giotopoulos… - Blood, The Journal …, 2011 - ashpublications.org
Abstract The t (12; 21) translocation that generates the ETV6-RUNX1 (TEL-AML1) fusion
gene, is the most common chromosomal rearrangement in childhood cancer and is …