Establishment of an Undifferentiated Leukemia Cell Line (Kasumi‐3) with t(3;7)(q27;q22) and Activation of the EVI1 Gene

Asou, Hiroya; Suzukawa, Kazumi; Kita, K; Nakase, Kazunori; Ueda, Haruo; Morishita, Kazuhiro; Kamada, Nanao

doi:10.1111/j.1349-7006.1996.tb00216.x

Cited by 35 publications

(25 citation statements)

References 14 publications

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“…Several myeloid leukemia cell lines (K562 and U937) and EVI1 rearranged cell lines (Kasumi-3 and UCSD-AML1) were included as positive controls for EVI1 overexpression. [12][13][14][15] The study was approved by the ethics committee of the Ghent University Hospital (2003/273). Patients' characteristics and karyotypes are described in Table 1.…”

Section: Patients and Cell Linesmentioning

confidence: 99%

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EVI1 overexpression in t(3;17) positive myeloid malignancies results from juxtaposition of EVI1 to the MSI2 locus at 17q22

Weer

Speleman²,

Cauwelier³

et al. 2008

Haematologica

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Chromosomal translocations involving the EVI1 locus are a recurrent finding in myeloid leukemia and are associated with poor prognosis. In this study, we performed a detailed molecular characterization of the recurrent translocation t(3;17)(q26;q22) in 13 hematologic malignancies. The EVI1 gene locus was rearranged in all 13 patients and was associated with EVI1 overexpression. In 9 out of 13 patients, the 17q breakpoints clustered in a 250 kb region on band 17q22 encompassing the MSI2 (musashi homologue 2) gene.Expression analyses failed to demonstrate ectopic MSI2 expression or the presence of an MSI2/EVI1 fusion gene. In conclusion, we show for the first time that the t(3;17) is indeed a recurrent chromosomal aberration in myeloid malignancies. In keeping with findings in other recurrent 3q26 rearrangements, overexpression of the EVI1 gene appears to be the major contributor to leukemogenesis in patients with a t(3;17).

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Section: Patients and Cell Linesmentioning

confidence: 99%

“…8,17 For normalization three housekeeping genes (RPL13A, YWHAZ and HPRT1) were selected in view of their stability in bone marrow samples as analyzed using the Genorm software. 17 The EVI1 overexpressing cell line Kasumi-3 carrying a t(3;7)(q26;q22) translocation 12 was used as a positive control.…”

Section: Real-time Quantitative Rt-pcrmentioning

confidence: 99%

EVI1 overexpression in t(3;17) positive myeloid malignancies results from juxtaposition of EVI1 to the MSI2 locus at 17q22

Weer

Speleman²,

Cauwelier³

et al. 2008

Haematologica

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“…69,70 In addition to the t(3;12) and t(3;21), EVI1 is involved in several other chromosomal translocations such as the t(2;3)(p13;q26), t(2;3)(q23;q26), t(3;7)(q26;q22), t(3;13) (q27;q13-14), and t(3;17)(q26;q22). [71][72][73][74][75][76][77] Although these rearrangements result in EVI1 overexpression, as determined by RT-PCR of the 3Ј region of the gene, it is not known yet whether the inappropriate expression relates to EVI1 only or to a fusion protein which includes EVI1. Table 2 summarizes the location of breakpoints in the rearrangements involving EVI1 which have been reported.…”

Section: Involvement Of Evi1 In Myeloid Leukemiasmentioning

confidence: 99%

The EVI1 gene in myeloid leukemia

Nucifora

1997

Leukemia

119

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Leukemia is an acquired genetic disease caused by the accumulation of chromosomal abnormalities which modify either the biochemical property or the level of expression of proteins. Frequent genetic abnormalities identified in human leukemia are chromosomal rearrangements such as chromosomal translocations and inversions. Chromosome band 3q26 is the site of the breakpoint of recurring translocations and inversions observed in patients with myeloid leukemias. Two genes located at 3q26 have been implicated in development or progression of myeloid leukemia. They are MDS1 and EVI1. MDS1, first identified as part of a fusion transcript resulting from the t(3;21)(q26;q22), encodes a small protein of unknown function. EVI1 encodes a zinc finger protein inappropriately overexpressed by chromosomal rearrangements (in man) or by retroviral insertion (in the mouse). Both genes are rearranged by the t(3;21)(q26;q22) and by the t(3;12)(p13;q22). As a result of the translocation, they are expressed as fusion genes either with AML1 or with TEL. EVI1 and MDS1 are unusual in that they can either encode separate proteins, or they can be expressed as one protein which we named MDS1/EVI1. EVI1 and MDS1/EVI1 have opposite functions as transcription factors. In this report, we review the current information on the two genes, and on their involvement in myeloid leukemia.

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“…ϩ HPCs isolated from either bone marrow or cord blood (50). We have previously shown that the Kasumi-3 cell line supports all of the hallmarks of HCMV latency, including reactivation resulting in the production of infectious virus (23).…”

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confidence: 99%

Human Cytomegalovirus US28 Is Important for Latent Infection of Hematopoietic Progenitor Cells

Humby

O’Connor

2016

J Virol

102

163

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Human cytomegalovirus (HCMV) resides latently in hematopoietic progenitor cells (HPCs). During latency, only a subset of HCMV genes is transcribed, including one of the four virus-encoded G protein-coupled receptors (GPCRs), US28. Although US28 is a multifunctional lytic protein, its function during latency has remained undefined. We generated a panel of US28 recombinant viruses in the bacterial artificial chromosome (BAC)-derived clinical HCMV strain TB40/E-mCherry. We deleted the entire US28 open reading frame (ORF), deleted all four of the viral GPCR ORFs, or deleted three of the HCMV GPCRs but not the US28 wild-type protein. Using these recombinant viruses, we assessed the requirement for US28 during latency in the Kasumi-3 in vitro latency model system and in primary ex vivo-cultured CD34 ؉ HPCs. Our data suggest that US28 is required for latency as infection with viruses lacking the US28 ORF alone or in combination with the remaining HCMV-encoded GPCR results in transcription from the major immediate early promoter, the production of extracellular virions, and the production of infectious virus capable of infecting naive fibroblasts. The other HCMV GPCRs are not required for this phenotype as a virus expressing only US28 but not the remaining virus-encoded GPCRs is phenotypically similar to that of wild-type latent infection. Finally, we found that US28 copurifies with mature virions and is expressed in HPCs upon virus entry although its expression at the time of infection does not complement the US28 deletion latency phenotype. This work suggests that US28 protein functions to promote a latent state within hematopoietic progenitor cells. IMPORTANCEHuman cytomegalovirus (HCMV) is a widespread pathogen that, once acquired, remains with its host for life. HCMV remains latent, or quiescent, in cells of the hematopoietic compartment and upon immune challenge can reactivate to cause disease. HCMV-encoded US28 is one of several genes expressed during latency although its biological function during this phase of infection has remained undefined. Here, we show that US28 aids in promoting experimental latency in tissue culture. The betaherpesvirus human cytomegalovirus (HCMV) is a ubiquitous pathogen that, once acquired, remains with its host for life. HCMV establishes a latent infection in CD34 ϩ hematopoietic progenitor cells (HPCs), and individuals with a competent immune system are, for the most part, asymptomatic for disease. Under weakened immune conditions, however, the virus can reactivate, causing severe morbidity and often mortality. In developed countries, such as the United States, approximately 80% of the population is HCMV positive by 40 years of age (reviewed in reference 1). In adults, HCMV-associated disease is due mostly to reactivation of latent infection, whereas primary infections rarely cause significant health burdens in this population (reviewed in reference 1). Current treatments administered in clinical settings to sequester HCMV infection include those that predominantly target la...

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Establishment of an Undifferentiated Leukemia Cell Line (Kasumi‐3) with t(3;7)(q27;q22) and Activation of the EVI1 Gene

Cited by 35 publications

References 14 publications

EVI1 overexpression in t(3;17) positive myeloid malignancies results from juxtaposition of EVI1 to the MSI2 locus at 17q22

EVI1 overexpression in t(3;17) positive myeloid malignancies results from juxtaposition of EVI1 to the MSI2 locus at 17q22

The EVI1 gene in myeloid leukemia

Human Cytomegalovirus US28 Is Important for Latent Infection of Hematopoietic Progenitor Cells

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