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Cell Growth & Differentiation, Vol 8, Issue 1 35-45, Copyright © 1997 by American Association of Cancer Research
ARTICLES |
SL Fu and JS Lipsick
Department of Pathology, Stanford University, California 94305-5324, USA.
Both viral Myb (v-Myb) and cellular Myb (c-Myb) are nuclear sequence-specific DNA-binding proteins that can function as transcriptional activators. v-Myb, encoded by avian myeloblastosis virus, induces acute monoblastic leukemia in chickens and transforms avian myelomonocytic cells in culture. The normal c-Myb protein is essential for hematopoietic development. Previous reports suggested that truncation of c-Myb is required for oncogenic transformation of avian myelomonocytic cells in culture. In this study, we demonstrate that constitutive expression of full-length c-Myb can transform avian myelomonocytic cells isolated from embryonic yolk sacs by using a strategy to enhance the efficiency of infection and/or expression of c-myb-containing viruses. c-Myb-transformed myelomonocytic cells display a different phenotype than cells transformed by v-MybAMV or other Myb mutants. c-Myb-transformed yolk sac cells are heterogeneous populations with characteristics of both the macrophage and granulocyte lineages. Our results demonstrate that constitutive expression of full-length c-Myb is sufficient to activate its oncogenic potential, but that the target cells for c-Myb are relatively rare and presumably quite immature.
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| Cancer Research | Clinical Cancer Research |
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| Molecular Cancer Research | Cell Growth & Differentiation |