Transformation of Brown Leghorn chicken embryo fibroblasts by avian myeloblastosis virus proviral DNA

Soret, Johann; Krycève-Martinerie, Cécile; Crochet, J; Perbal, Bernard

doi:10.1128/jvi.55.1.193-205.1985

Cited by 15 publications

(5 citation statements)

References 55 publications

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“…As expected from the M7B cDNA structure (see above), the B3HI92 probe detected the 4.0-kb chimeric c-myb mRNA expressed in T9 cells (Fig. 6) and endogenous viral sequences previously described for CEF (70). The B3HI92 probe detected RNA species whose sizes were in agreement with those of genomic (also revealed by pol and env probes) and env subgenomic viral species (Fig.…”

Section: Downloaded Fromsupporting

confidence: 79%

“…BM2 cells were grown in Dulbecco's modified Eagle medium supplemented with 10% fetal calf serum, 10% tryptose phosphate broth, and 2% heat-inactivated chicken serum. CEF were prepared from 13-dayold C/E Brown Leghorn embryos (gsϩ, chfϩ, VϪ) of the Edinburgh strain and cultured as described elsewhere (70). All cultures were performed at 37ЊC in a 5% CO 2 atmosphere.…”

Section: Cells Media and Viruses The T9 T-cell Lymphoma Cell Line mentioning

confidence: 99%

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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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confidence: 79%

Section: Cells Media and Viruses The T9 T-cell Lymphoma Cell Line mentioning

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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“…The ratio of MAV-specific DNA fragments to endogenous DNA fragments in the control tissues was found to be lower than in fibroblasts infected in culture (20) and was considerably increased in tumor DNA, as shown by the heavy bands obtained with gag and with env probes (Fig. 3A and B).…”

Section: The Identification Of Ecori 5'-proximal Junction Fragmentsmentioning

confidence: 83%

“…2). Because the pattern of endogenous sequences varies slightly from one animal to another (20), and since all tissues of tumor-bearing animals contain viral particles (24), we used fibroblast DNA from each infected chicken as controls.…”

Section: The Identification Of Ecori 5'-proximal Junction Fragmentsmentioning

confidence: 99%

Induction of nephroblastoma by myeloblastosis-associated virus type 1: state of proviral DNAs in tumor cells

Soret

Dambrine

Perbal

1989

J Virol

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“…CEFs were prepared from 13 day old C/E brown leghorn embryos (gs+, chf+, V−) of the Edinburgh strain, and cultured as described elsewhere. 39 All cultures were performed at 37°C in a 5% CO 2 atmosphere.…”

Section: Cellsmentioning

confidence: 99%

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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Transformation of Brown Leghorn chicken embryo fibroblasts by avian myeloblastosis virus proviral DNA

Cited by 15 publications

References 55 publications

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

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

Induction of nephroblastoma by myeloblastosis-associated virus type 1: state of proviral DNAs in tumor cells

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

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