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A class of mouse neoplasms termed Abelson virus-induced plasmacytoid lymphosarcomas has previously been found to express abnormal myb transcripts due to a helper virus insertion into the 5' end of the c-myb locus. We have established clonal cell lines from these tumors and have shown that they all express markers characteristic of myelomonocytic, rather than lymphoid, cells. Treatment of the plasmacytoid lymphosarcoma lines with phorbol 12-myristate 13-acetate led to various degrees of growth arrest, presumably due to myelomonocytic differentiation. To date, characterization of myeloid cell lines with varying responses to phorbol 12-myristate 13-acetate has not been reported. The different clonal plasmacytoid lymphosarcoma lines should, therefore, provide a good model to help elucidate the role of altered myb locus and other protooncogenes in myelomonocytic leukemia. Contrary to studies on induced differentiation of myelomonocytic cells with normal myb locus, our results on plasmacytoid lymphosarcoma cells indicate that reduced myb and myc expression may not be obligatory for growth arrest to occur. The present study, however, supports the previous notion that the myb transforming ability may be restricted to cells of the myelomonocytic lineage. In addition, we found that only the more mature cells can undergo prolonged phorbol 12-myristate 13-acetate-induced growth arrest, suggesting that the maintenance of these leukemic cells in their proliferative state, presumably by the myb gene product, can be overcome with appropriate differentiation signal(s).

proceedings of the national academy of sciences of the united states of america

Phorbol ester-induced growth arrest of murine myelomonocytic leukemic cells with virus-disrupted myb locus is not accompanied by decreased myc and myb expression.