Comparative Expression Analysis of the Antagonistic Transcription Factors EVI1 and MDS1-EVI1 in Murine Tissues and duringin VitroHematopoietic Differentiation

Wimmer, Katharina; Vinatzer, Ursula; Zwirn, P; Fonatsch, Christa; Wieser, Rotraud

doi:10.1006/bbrc.1998.9588

Cited by 19 publications

(23 citation statements)

References 19 publications

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“…Figure 1a (bottom) shows the amplification of the Hprt gene, used for normalization of the intensity (shown in Figure 1b). Our results partially contrast with previously reported results 29 in that our data show that Mds1/Evi1 is expressed clearly in undifferentiated ES cells and that the two genes are regulated differentially. To determine whether the two genes are expressed specifically in the hematopoietic compartment of the developing EBs, we used RNA extracted from hematopoietic colonies after we plated cells from disrupted EBs in methylcellulosebased medium as described in Materials and methods.…”

Section: Mds1/evi1 and Evi1 Are Expressed Differentially In Es Cellscontrasting

confidence: 99%

“…The primers for amplification of the murine genes Evi1 and Mds1/Evi1 and the murine housekeeping gene Hprt have been described. 28,29 The PCR reactions were carried out as previously described. 29 Equal volumes of the cDNA reaction mix were used to amplify Evi1 and Mds1/Evi1.…”

Section: Rna Isolation and Rt-pcrmentioning

confidence: 99%

“…28,29 The PCR reactions were carried out as previously described. 29 Equal volumes of the cDNA reaction mix were used to amplify Evi1 and Mds1/Evi1. The PCR products were separated by electrophoresis on 2% agarose gel, and the fragments were identified by ethidium bromide staining and ultraviolet illumination.…”

Section: Rna Isolation and Rt-pcrmentioning

confidence: 99%

“…29 The EBs are similar to developing embryos and contain cells of many different lineages in addition to hematopoietic cells. Therefore, to determine whether the two genes are expressed specifically in hematopoietic colonies, we induced ES cells to differentiate in EBs and in secondary colonies, and we extracted total RNA for RT-PCR analysis as described in Materials and methods.…”

Section: Mds1/evi1 and Evi1 Are Expressed Differentially In Es Cellsmentioning

confidence: 99%

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Forced expression of the leukemia-associated gene EVI1 in ES cells: a model for myeloid leukemia with 3q26 rearrangements

et al. 1999

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Chromosome band 3q26 is the locus of two genes, MDS1/EVI1 and EVI1. The proteins encoded by these genes are nuclear factors each containing two separate DNA-binding zinc finger domains. The proteins are identical, aside from the N-terminal extension of MDS1/EVI1, which is missing in EVI1. However, they have opposite functions as transcription factors. In contrast to MDS1/EVI1, EVI1 is often activated inappropriately by chromosomal rearrangements at 3q26 leading to inappropriate expression of the protein in hematopoietic cells and to myeloid leukemias, which are often characterized by abnormal megakaryopoiesis. We previously showed that the two proteins affect replication and differentiation of progenitor hematopoietic cell lines in opposite ways: whereas EVI1 inhibits the response of 32Dc13 cells to G-CSF and TGF␤1, MDS1/EVI1 has no effect on the G-CSF-induced differentiation of the 32Dc13 cells, and it enhances the growth-inhibitory effect of TGF␤1. In the present study, we analyzed the endogenous expression of the two genes during in vitro hematopoietic differentiation of murine embryonic stem (ES) cells and evaluated the effects of their forced expression on the ability of ES cells to produce differentiated hematopoietic colonies. We found that the expression of the two genes is independently and tightly controlled during differentiation. In addition, the forced expression of EVI1 led to a much higher rate of cell growth before and during differentiation, whereas the expression of MDS1/EVI1 repressed cell growth and strongly reduced the number of differentiated hematopoietic colonies. Finally, our study also found that the forced expression of EVI1 resulted in the differentiation of abnormally high numbers of megakaryocytic colonies, thus providing one of the first experimental models showing a clear correlation between inappropriate expression of EVI1 and abnormalities in megakaryopoiesis.

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Section: Mds1/evi1 and Evi1 Are Expressed Differentially In Es Cellscontrasting

confidence: 99%

Section: Rna Isolation and Rt-pcrmentioning

confidence: 99%

Section: Rna Isolation and Rt-pcrmentioning

confidence: 99%

Section: Mds1/evi1 and Evi1 Are Expressed Differentially In Es Cellsmentioning

confidence: 99%

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Forced expression of the leukemia-associated gene EVI1 in ES cells: a model for myeloid leukemia with 3q26 rearrangements

et al. 1999

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“…44 MDS1 can be expressed in normal human tissue as a unique transcript and as a normal fusion transcript with EVI1.…”

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confidence: 99%

The New Clinicopathologic and Molecular Findings in Myeloid Neoplasms With inv(3)(q21q26)/t(3;3)(q21;q26.2)

Wang

Rashidi

2016

Archives of Pathology &Amp; Laboratory Medicine

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Context.-Inv(3)(q21q26)/t(3;3)(q21;q26.2) is the most common form of genetic abnormality of the so-called 3q21q26 syndrome. Myeloid neoplasms with 3q21q26 aberrancies include acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and blast crisis of myeloproliferative neoplasms. Recent advances on myeloid neoplasms with inv(3)/t(3;3) with regard to clinicopathologic features and novel molecular or genomic findings warrant a comprehensive review on this topic.Objective.-To review the clinicopathologic features and molecular as well as genomic alterations in myeloid neoplasms with inv(3)/t(3;3).Data Sources.-The data came from published articles in English-language literature.Conclusions.-At the clinicopathologic front, recent studies on MDS with inv(3)/t(3;3) have highlighted their overlapping clinicopathologic features with and similar overall survival to that of inv(3)/t(3;3)-harboring AML regardless of the percentage of myeloid blasts. On the molecular front, AML and MDS with inv(3)/t(3;3) exhibit gene mutations, which affect the RAS/receptor tyrosine kinase pathway. Furthermore, functional genomic studies using genomic editing and genome engineering have shown that the reallocation of the GATA2 distal hematopoietic enhancer to the proximity of the promoter of ectopic virus integration site 1 (EVI1) without the formation of a new oncogenic fusion transcript is the molecular mechanism underlying these inv(3)/t(3;3) myeloid neoplasms. Although the AML and MDS with inv(3)/t(3;3) are listed as a separate category of myeloid malignancies in the 2008 World Health Organization classification, the overlapping clinicopathologic features, similar overall survival, and identical patterns at the molecular and genomic levels between AML and MDS patients with inv(3)/t(3;3) may collectively favor a unification of AML and MDS with inv(3)/t(3;3) as AML or myeloid neoplasms with inv(3)/t(3;3) regardless of the blast count.(Arch Pathol Lab Med. 2016;140:1404-1410; doi: 10.5858/arpa.2016-0059-RA) B efore we review the recent advances of myeloid neoplasms with inv(3)(q21q26)/t(3;3)(q21;q26.2) [referred to as inv(3)/t(3;3) hereafter], the clinicopathologic features of inv(3)/t(3;3) are worth being mentioned here. The structural changes involving the long arm of chromosome 3 at bands 3q21 and 3q26.2 in the forms of inversion and translocation-namely, paracentric inversion [inv(3)(q21q26.2), referred to as inv (3) hereafter] and homologous translocations [t(3;3)(q21;q26.2), referred to as t(3;3) hereafter]-in myeloid neoplasms have long been recognized. [1][2][3][4][5] Together inv(3), t(3;3), and sometimes insertions (ins) [ins(3;3)(q26;q21q26)] or duplications (dup) [dup(3)(q21-q26)] of these chromosomal regions are collectively termed as a 3q21q26 syndrome.5 Myeloid neoplasms with 3q21q26 anomalies are not only seen in acute myeloid leukemias (AMLs), 6,7 but also in myelodysplastic syndromes (MDS) 5; blast crisis of myeloproliferative neoplasm (MPN), such as chronic myelogenous leukemia 8 or leukemic transformation of essen...

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Conservation and expression of a novel alternatively spliced Evi1 exon

Alzuherri

McGilvray

Kilbey

et al. 2006

Gene

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Comparative Expression Analysis of the Antagonistic Transcription Factors EVI1 and MDS1-EVI1 in Murine Tissues and duringin VitroHematopoietic Differentiation

Cited by 19 publications

References 19 publications

Forced expression of the leukemia-associated gene EVI1 in ES cells: a model for myeloid leukemia with 3q26 rearrangements

Forced expression of the leukemia-associated gene EVI1 in ES cells: a model for myeloid leukemia with 3q26 rearrangements

The New Clinicopathologic and Molecular Findings in Myeloid Neoplasms With inv(3)(q21q26)/t(3;3)(q21;q26.2)

Conservation and expression of a novel alternatively spliced Evi1 exon

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