Murine leukemia virus-induced T-cell lymphomagenesis: Integration of proviruses in a distinct chromosomal region

Cuypers, H. T. M.; Selten, Gerard C.M.; Quint, Wim; Zijlstra, Maarten; Maandag, E R; Boelens, Wilbert C.; Wezenbeek, P. van; Melief, C. J. M.; Berns, Anton

doi:10.1016/0092-8674(84)90309-x

Cited by 609 publications

(472 citation statements)

References 46 publications

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“…The Bcl-X, neo, LacZ and U3MPSV probes were used as described in Materials and methods. U3 hybridizing bands which colocalize with the bcl-X rearranged bands are indicated by arrows integration of solo LTR can also lead to the disregulation of gene expression we have used a probe speci®c for the U3 sequence of the MPSV LTR to identify that type of integration (Cuypers et al, 1984;Robinson and Gagnon, 1986). Figure 4b shows that as expected the U3 probe hybridizes with the same band as the Neo probe for Baf-Bcl-X-1, Baf-Bcl-X-2 and Baf-Bcl-X-3 mutants.…”

Section: Selection Of Pleiotropic Apoptosis Resistant Mutants Followimentioning

confidence: 99%

Bcl-X is the major pleiotropic anti-apoptotic gene activated by retroviral insertion mutagenesis in an IL-3 dependent bone marrow derived cell line

1998

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In order to identify genes capable of inhibiting apoptosis induced by di erent pathways, without inducing proliferation we have performed retroviral insertion mutagenesis in the IL-3 dependent bone marrow derived Baf-3 cell line. Out of 200 mutants obtained in three separate mutagenesis experiments, four mutants were resistant to multiple apoptosis inducing pathways (including growth factor starvation, staurosporine, etoposide and cyclosporin A) and did not proliferate in the absence of IL-3. These four mutants overexpress the bcl-X gene following a retroviral insertion 5' of the translation initiation site. These results indicate that the bcl-X gene is a major pleiotropic anti-apoptotic gene in Baf-3 cells. They also suggest that the Bcl-2 family of genes might be the only one capable of inhibiting apoptosis induced by multiple pathways without inducing cell proliferation.

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Section: Selection Of Pleiotropic Apoptosis Resistant Mutants Followimentioning

confidence: 99%

Bcl-X is the major pleiotropic anti-apoptotic gene activated by retroviral insertion mutagenesis in an IL-3 dependent bone marrow derived cell line

1998

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“…The Pim family of serine (Ser)/threonine (Thr) protein kinases were initially identified as a target for proviral activation by Moloney murine leukemia virus (Cuypers et al, 1984;Selten et al, 1985). The Pim proteins have been implicated in the control of tumorigenesis, cell cycle progression and apoptosis (Wang et al, 2001;Mikkers et al, 2004;Amaravadi and Thompson, 2005;Bachmann and Moroy, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…The Pim proteins have been implicated in the control of tumorigenesis, cell cycle progression and apoptosis (Wang et al, 2001;Mikkers et al, 2004;Amaravadi and Thompson, 2005;Bachmann and Moroy, 2005). In animal models, Pim protein kinases have been shown to enhance development of lymphoma induced by c-Myc, and to be overexpressed in hepatocellular cancer (Cuypers et al, 1984;Selten et al, 1985;van Lohuizen et al, 1989). In humans, the protein levels of Pim have been shown to be elevated in lymphomas (Ionov et al, 2003), leukemias (Adam et al, 2006) and prostate cancer (Cibull et al, 2006;Xu et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Negative regulation of Pim-1 protein kinase levels by the B56β subunit of PP2A

Arnold

Lilly

et al. 2007

Oncogene

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The Pim protein kinases are serine threonine protein kinases that regulate important cellular signaling pathway molecules, and enhance the ability of c-Myc to induce lymphomas. We demonstrate that a cascade of events controls the cellular levels of Pim. We find that overexpression of the protein phosphatase (PP) 2A catalytic subunit decreases the activity and protein levels of Pim-1. This effect is reversed by the application of okadaic acid, an inhibitor of PP2A, and is blocked by SV40 small T antigen that is known to disrupt B subunit binding to PP2A A and C subunits. Pim-1 can coimmunoprecipitate with the PP2A regulatory B subunit, B56b, but not B56a, c, d, e or B55a. Using short hairpin RNA targeted at B56b, we demonstrate that decreasing the level of B56b increases the half-life of Pim-1 from 0.7 to 2.8 h, and decreases the ubiquitinylation level of Pim-1. We also find that Pin1, a prolyl-isomerase, is capable of binding Pim-1 and leads to a decrease in the protein level of Pim-1. On the basis of these observations, we hypothesize that phosphorylated Pim-1 binds Pin1 allowing the interaction of PP2A through B56b. Dephosphorylation of Pim-1 then allows for ubiquitinylation and protein degradation of Pim-1.

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“…14,15 Thus, we reasoned that if thymomagenesis by bcrMoloney thymomagenesis is frequently associated with recurring proviral integration near c-myc, 30,36 N-myc, 29 Pim-1, 37 abl/M virus is also not affected by insertional activation of …”

Section: Thymomas Induced With the Different Viruses Contain Multiplementioning

confidence: 99%

Recurring proviral integration suggests a role for proto-oncogene activation in thymomas induced with Mo-MuLV-rescued BCR/ABL virus

Clark¹

1997

Leukemia

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Murine leukemia virus-induced T-cell lymphomagenesis: Integration of proviruses in a distinct chromosomal region

Cited by 609 publications

References 46 publications

Bcl-X is the major pleiotropic anti-apoptotic gene activated by retroviral insertion mutagenesis in an IL-3 dependent bone marrow derived cell line

Bcl-X is the major pleiotropic anti-apoptotic gene activated by retroviral insertion mutagenesis in an IL-3 dependent bone marrow derived cell line

Negative regulation of Pim-1 protein kinase levels by the B56β subunit of PP2A

Recurring proviral integration suggests a role for proto-oncogene activation in thymomas induced with Mo-MuLV-rescued BCR/ABL virus

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