By GEORGE F. & GEORGE KLIEN (eds.) VANDE WOUDE
Meant for uncomplicated and scientific researchers, immunologists, virologists and molecular biologists, this publication is a part of a chain which offers severe overviews on chosen points of either melanoma examine and the fundamental underlying sciences.
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Extra resources for Advances in Cancer Research, Vol. 56
Abnormal Gene Regulation in Burkitt's Lymphoma The levels of c-myc mRNA and proteins in BL, although often elevated over normal o r quiescent cells, are not necessarily higher than those in 32 CHARLOTTE A. , 1990). This suggests that the absolute level of the c-myc product may not be as important to the establishment of the transformed phenotype as either qualitative differences between the c-myc products of normal and BL cells, or the fact that the translocated c-myc allele has escaped the regulatory pathways that would repress c-myc expression and permit developmental progression or quiescence in normal B cells.
On the reciprocal chromosome, the IgH locus VDJ regions, often with the IgH enhancer, become juxtaposed to the 5‘ region of c-myc (Cory, 1986). , 1984). , 1989). The breakpoint for the i m n p noglobulin light chains is usually 5’ to the variable region and the two loci are joined in the same transcriptional orientation (Varmus, 1984; Cory, 1986). As the most common sites of translocation breakpoints are in the IgH switch or VDJ join regions, it has been hypothesized that translocations arise as a result of aberrant immunoglobulin recombination events (Cory, 1986).
When stimulated by concanavalin A, these cells exhibit a 5-fold increase in transcription elongation through block signals in exon 1, concurrent with a 10-fold increase in steady-state c-myc RNA. , 1987). Several approaches have been taken to define the DNA or RNA sequences within the c-myc gene which program this attenuation-like mechanism. This region contains a potential stem-loop structure followed by a T5tract, a configuration resembling p-independent transcription terminators in prokaryotes (Platt, 1986), and resembling sequences that may be involved in human c-myc block to transcription elongation (see below).
Advances in Cancer Research, Vol. 56 by GEORGE F. & GEORGE KLIEN (eds.) VANDE WOUDE