Transformation of chicken myelomonocytic cells by a retrovirus expressing the v-myb oncogene from the long terminal repeats of avian myeloblastosis virus but not Rous sarcoma virus

Press, Richard D.; Kim, A; Ewert, Donald L.; Reddy, E. S. P.

doi:10.1128/jvi.66.9.5373-5383.1992

Cited by 9 publications

(5 citation statements)

References 33 publications

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“…The low incidence of myeloid tumors induced with these constructs may be due either to the nature of the mutation or to the vector. Retroviruses containing either the RSV LTR or the subgroup A env gene, which are present in the RCASBP vector (and in EU-8 ALV), have been reported to infect myeloid cells poorly (34,41). In contrast to our results, Press et al (43) observed a low incidence of lymphoma, coupled with activation of endogenous c-myb by insertional mutagenesis, with a retroviral vector expressing a minimally truncated Myb.…”

Section: Aberrant Splicing From Eu-8 Alv Generates a Truncated Myb Prcontrasting

confidence: 99%

“…Their constructs were similar to ours except that their LTR was derived from avian myeloblastosis virus, whereas our vectors used an RSV LTR. These two LTRs show tissue-specific differences in expression in cultured cells (41). Press et al (42) also observed fibrosarcoma induction by vectors expressing C-terminally truncated myb.…”

Section: Aberrant Splicing From Eu-8 Alv Generates a Truncated Myb Prmentioning

confidence: 98%

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Minimal truncation of the c-myb gene product in rapid-onset B-cell lymphoma

Jiang

Kanter

Dunkel

et al. 1997

J Virol

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Oncogenic activation of c-myb by insertional mutagenesis has been implicated in rapid-onset B-cell lymphomas induced by the nonacute avian leukosis virus EU-8. In these tumors, proviruses are integrated either upstream of the c-myb coding region or within the first intron of c-myb. Tumors with either type of integration contained identical chimeric mRNAs in which the viral 5 splice site was juxtaposed to the 3 splice site of c-myb exon 2 and myb exon 1 was eliminated. Both classes of integrations generated truncated Myb proteins that were indistinguishable by Western analysis. In contrast to most other examples of c-myb activation, the truncation consisted of only 20 N-terminal amino acids and did not disrupt either the DNA binding domain near the N terminus or the negative regulatory domain near the C terminus of Myb. The significance of the 20-amino-acid Myb truncation to tumorigenesis was tested by infection of chicken embryos with retroviral vectors expressing different myb gene products. While virus expressing either wild-type c-myb or c-myb mutated at the N-terminal casein kinase II sites was only weakly oncogenic at 10 weeks, the minimally truncated myb virus induced a high incidence of rapid-onset tumors, including B-cell lymphomas, sarcomas, and adenocarcinomas.

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Section: Aberrant Splicing From Eu-8 Alv Generates a Truncated Myb Prcontrasting

confidence: 99%

Section: Aberrant Splicing From Eu-8 Alv Generates a Truncated Myb Prmentioning

confidence: 98%

Minimal truncation of the c-myb gene product in rapid-onset B-cell lymphoma

Jiang

Kanter

Dunkel

et al. 1997

J Virol

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“…32 A similar truncation conferred a transforming potential on myb, when assessed in primary chicken fibroblasts, 67 and related chimaeric mRNA was isolated from B lymphomas and fibrosarcomas induced by avian leukosis virus. 68 To our knowledge, this is the only report of a RAV insertional activation of c-myb in a T lymphoma. Liu et al reported that MEQ can transform established Rat-2 fibroblasts but MEQ alone is not capable of transforming primary cells.…”

Section: Discussionmentioning

confidence: 78%

Alterations of the MDV oncogenic regions in an MDV transformed lymphoblastoid cell line

Rouzic

Thoraval²,

Afanassieff³

et al. 2002

Molecular Pathology

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Aims: Lymphoblastoid cell lines derived from Marek's disease virus (MDV) induced tumours have served as models of MDV latency and transformation. They are stable and can be cultured with no detectable MDV genomic alterations upon repeated passaging. An MDV transformed lymphoblastoid T cell line (T9 cell line) has been reported to contain a disrupted MDV BamHI-H fragment and a Rous associated virus insertional activation of the c-myb protooncogene. In an attempt to define the respective participation of c-myb and MDV in the transformed phenotype of T9 cells, an analysis of MDV oncogenic sequences (BamHI-H, BamHI-A, and EcoQ fragments) was performed in these cells. Methods: Using two different passages of the T9 cell line (late and early passages), the organisation of the MDV oncogenic regions and their expression in these cells were analysed. In vivo assessment of the oncogenicity of the virus contained within these cells was assessed by injecting them into 1 day old chickens. Results: In T9 cells maintained in culture for up to six months (late T9), the MDV ICP4 gene was disrupted, whereas the meq gene was actively transcribed. The alterations of the MDV genome in these cells correlated with the inability of the virus to induce the classic signs of Marek's disease in 1 day old chickens. However, early T9 cells submitted to a limited number of passages induced classic MDV pathogenicity, as efficiently as the MDV control cell line (T5), and did not show gross structural changes in the oncogenic MDV sequences. Conclusions: Although the expression pattern of the MDV oncogenes in early T9 cells was identical to the one reported for other MDV transformed cells, longterm culture of an MDV transformed cell line containing a RAV insertional activation of the c-myb protooncogene led to the disruption of the MDV BamHI-H and BamHI-A oncogenic regions. In the late T9 cells MEQ was the only detected MDV oncoprotein. These results suggest that in the late T9 cells the truncated MYB protein compensates for the loss of MDV oncoproteins and reinforce the possibility that MEQ and MYB cooperate in the maintenance of the transformed state and the tumorigenic potential of these cells.

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“…Aminoproximal truncation of the c-myb gene has also been shown to occur as the result of v-myb sequence transduction by AMV and E26 avian retroviruses (35,66) and upon retroviral integration in murine myeloid leukemias (5,46,48,49,69) and in avian B lymphomas (33,60). In most of these cases, the oncogenic activation of c-myb results in the expression of truncated MYB proteins deprived of the casein kinase II phosphorylation site and of the 5Ј-proximal (R1) DNA-binding repeat which has been proposed to play a role in the restricted transforming potential of c-myb (38,43,62). According to the previously established nomenclature (72), the RAV-1 insertion occurred upstream from c-myb exons 3 (33) and 2 (60) in B-cell lymphomas.…”

Section: Discussionmentioning

confidence: 99%

Retroviral insertional activation of the c-myb proto-oncogene in a Marek's disease T-lymphoma cell line

Rouzic

Perbal

1996

J Virol

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Marek's disease virus (MDV) is an avian herpesvirus that causes, in chickens, a lymphoproliferative disease characterized by malignant transformation of T lymphocytes. The rapid onset of polyclonal tumors indicates the existence of MDV-encoded oncogenic products. However, the molecular basis of MDV-induced lymphoproliferative disease and latency remains largely unclear. Several lines of evidence suggest that MDV and Rous-associated virus (RAV) might cooperate in the development of B-cell lymphomas induced by RAV. Our present results indicate for the first time that MDV and RAV might also act synergistically in the development of T-cell lymphomas. We report an example of an MDV-transformed T-lymphoblastoid cell line (T9) expressing high levels of a truncated C-MYB protein as a result of RAV integration within one c-myb allele. The chimeric RAV-c-myb mRNA species initiated in the 5 long terminal repeat of RAV are deprived of sequences corresponding to c-myb exons 1 to 3. The attenuation of MDV oncogenicity has been strongly related to structural changes in the MDV BamHI-D and BamHI-H DNA fragments. We have established that both DNA restriction fragments are rearranged in the T9 MDV-transformed cells. Our results suggest that retroviral insertional activation of the c-myb proto-oncogene is a critical factor involved in the maintenance of the transformed phenotype and the tumorigenic potential of this T-lymphoma cell line.

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Transformation of chicken myelomonocytic cells by a retrovirus expressing the v-myb oncogene from the long terminal repeats of avian myeloblastosis virus but not Rous sarcoma virus

Cited by 9 publications

References 33 publications

Minimal truncation of the c-myb gene product in rapid-onset B-cell lymphoma

Minimal truncation of the c-myb gene product in rapid-onset B-cell lymphoma

Alterations of the MDV oncogenic regions in an MDV transformed lymphoblastoid cell line

Retroviral insertional activation of the c-myb proto-oncogene in a Marek's disease T-lymphoma cell line

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