Reticuloendotheliosis virus (REV-T) induces immature lymphoid tumors in the chicken. The ability of REV-T to induce tumors in different types of lymphoid tissues will be examined. The phenotype of the REV-T induced tumor is consistent with the hypothesis that tumor development is accompanied by inhibition of lymphoid differentiation. Experiments will evaluate this hypothesis and also determine whether inactivation of the protein responsible for tumor development, v-rel, is accompanied by the reinitiation of lymphoid differentiation. These experiments will require the use of a helper-free REV-T. Purification of specific populations of lymphoid cells will be infected in vitro with this virus and injected into recipient animals for in vivo tumor development. The phenotypes of the target cell and the tumor cell will be compared to determine their relationship. A mutant of REV-T that is temperature sensitive for functional v-rel will be prepared in order to study the effect of v-rel inactivation on lymphoid differentiation.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
1R01CA041450-01
Application #
3181923
Study Section
Virology Study Section (VR)
Project Start
1986-03-01
Project End
1989-02-28
Budget Start
1986-03-01
Budget End
1987-02-28
Support Year
1
Fiscal Year
1986
Total Cost
Indirect Cost
Name
University of Texas Sw Medical Center Dallas
Department
Type
Overall Medical
DUNS #
City
Dallas
State
TX
Country
United States
Zip Code
75390
Zhang, G; Humphries, E H (1996) v-rel and c-rel induce a membrane protein, p75, on avian hematopoietic cells. Oncogene 12:1153-7
Zhang, G; Slaughter, C; Humphries, E H (1995) v-rel Induces ectopic expression of an adhesion molecule, DM-GRASP, during B-lymphoma development. Mol Cell Biol 15:1806-16
Hrdlickova, R; Nehyba, J; Roy, A et al. (1995) The relocalization of v-Rel from the nucleus to the cytoplasm coincides with induction of expression of Ikba and nfkb1 and stabilization of I kappa B-alpha. J Virol 69:403-13
Filardo, E J; Lee, M F; Humphries, E H (1994) Structural genes, not the LTRs, are the primary determinants of reticuloendotheliosis virus A-induced runting and bursal atrophy. Virology 202:116-28
Hrdlickova, R; Nehyba, J; Humphries, E H (1994) In vivo evolution of c-rel oncogenic potential. J Virol 68:2371-82
Nehyba, J; Hrdlickova, R; Humphries, E H (1994) Evolution of the oncogenic potential of v-rel: rel-induced expression of immunoregulatory receptors correlates with tumor development and in vitro transformation. J Virol 68:2039-50
Hrdlickova, R; Nehyba, J; Humphries, E H (1994) v-rel induces expression of three avian immunoregulatory surface receptors more efficiently than c-rel. J Virol 68:308-19
Humphries, E H; Zhang, G (1992) V-rel and C-rel modulate the expression of both bursal and non-bursal antigens on avian B-cell lymphomas. Curr Top Microbiol Immunol 182:475-83
Barth, C F; Ewert, D L; Olson, W C et al. (1990) Reticuloendotheliosis virus REV-T(REV-A)-induced neoplasia: development of tumors within the T-lymphoid and myeloid lineages. J Virol 64:6054-62
Huffnagle, G B; Ratcliffe, M J; Humphries, E H (1989) Bu-2, a novel avian cell surface antigen on B cells and a population of non-lymphoid cells, is expressed homogeneously in germinal centers. Hybridoma 8:589-604

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