By GEORGE F. & GEORGE KLIEN (eds.) VANDE WOUDE
Meant for simple and scientific researchers, immunologists, virologists and molecular biologists, this publication is a part of a sequence which offers serious overviews on chosen points of either melanoma learn and the fundamental underlying sciences.
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Additional resources for Advances in Cancer Research, Vol. 56
When BL cells with intact but translocated c-myc alleles o r those with rearranged translocated alleles were fused to an EBV-transformed lymphoblastoid line, immunoglobulins from the BL chromosomes were expressed, but c-myc expression from the translocated chromosome was repressed. , 1984). T h e apparent contradiction between these results and those of the BL X PC cell fusions can be resolved if one considers that this particular lymphoblastoid line, which was passaged to a highly malignant state and which expressed high levels of endogenous c-myc, is competent for transcription of sequences associated with either normal c-myc or the immunoglobulin enhancer.
86, 9682-9686. , Levine, R. , Kindy, M. , Sonenshein, G. , and Campisi, J. (1986). J . Bzol. Chem. 261,9161-9166.
28 CHARLOTTE A. SPENCER AND MARK GROUDlNE TABLE I1 CHARACTERISTIC FEATURES OF BURKITT’S LYMPHOMA c-myc ALLELES 1. Reciprocal chromosomal translocations of the c-myc gene on chromosome 8 and one of the immunoglobulin loci on chromosomes 2, 14, or 22. Breakpoints are variable. See Fig. 3 2. Elevated levels and/or constitutive synthesis of c - m y RNA from the translocated allele. Very low levels of c-myc transcripts originate from the nontranslocated allele 3. Mutations or truncation of exon 1 in the translocated allele 4.
Advances in Cancer Research, Vol. 56 by GEORGE F. & GEORGE KLIEN (eds.) VANDE WOUDE