Abbas Ar-Rushdi

Transcriptional control of the expression of mouse globin genes in myeloma x erythroleukemia cell hybrids.

Fusions were made between thymidine kinase deficient (TK−) Friend cells inducible for hemoglobin production, and immunoglobulin-producing, hypoxanthine-guanine phosphoribosyltransferase-deficient (HGPRT−) myeloma cells. Hybrids were selected in hypoxanthine-aminopterin-thymidine (HAT) and identified by isozyme analysis and chromosome counts. All hybrids resembled the myeloma cell line in mode of growth and were immunoglobulin secretors. All hybrids did not express hemoglobin and were uninducible for hemoglobin production with dimethyl sulfoxide (DMSO). Hybridization of genomic globin DNA probes with hybrid-derived nuclear and cytoplasmic mRNAs blotted to nitrocellulose filter indicated that lack of expression of the globin genes in the hybrids was due to lack of transcription.

The Translocated c-myc Oncogene of Burkitt Lymphoma is Differentially Regulated in Lymphoblastoid vs Plasma Cells

We have shown that the c-myc oncogene translocates from its normal position on band q24 of chromosome 8 to the heavy chain locus on chromosome 14 in Burkitt lymphomas with the t(8;14) chromosome translocation, while the c-myc oncogene remains on chromosome 8 and either the lambda or the kappa chain locus translocates to a region distal to the c-myc oncogene in Burkitt lymphoma with the t(8;22) and t(2;8) translocations, respectively (Dalla Favera 1982, 1983; Erikson 1983, 1983a; Croce 1983). Independently of whether it is structurally rearranged, the c-myc oncogene involved in the translocation is transcriptionally active, while the c-myc oncogene on the normal chromosome 8 is transcriptionally silent (Erikson 1983, 1983a; Croce 1983; Nishikura 1983; ar-Rushdi 1983). We have also shown that while the c-myc oncogene involved in the translocation escapes normal transcriptional control, the untranslocated c-myc oncogene on normal chromosome 8 is repressed in plasma cells (Erikson 1983; 1983a; Croce 1983; Nishikura 1983; ar-Rushdi 1983). To determine whether the activation of the translocated c-myc oncogene depends on the differentiated state of the B cells harboring the c-myc oncogene involved in the translocation, we have hybridized different human Burkitt lymphoma cells with human lymphoblastoid cells and with mouse plasmacytoma cells and examined the hybrids for the expression of the normal and of the involved c-myc oncogene.