Advances in Cancer Research, Vol. 56 by GEORGE F. & GEORGE KLIEN (eds.) VANDE WOUDE

By GEORGE F. & GEORGE KLIEN (eds.) VANDE WOUDE

Meant for easy and medical researchers, immunologists, virologists and molecular biologists, this publication is a part of a chain which offers severe overviews on chosen facets of either melanoma examine and the fundamental underlying sciences.

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T h e c-myc promoter usage shifts to P I and the block to transcription elongation is lost in the translocated allele (shown by heavy black arrows over all three exons). The absolute levels of transcription of c-myc vary between BL cell lines. At this postulated transition step in the development of BL, the normal c-myc allele is still under normal regulation. (D) After maturation to the BL cell phenotype, the normal c-myc allele is permanently repressed transcriptionally and at the level of chromatin structure.

T h e 1O-fold increase in the block to transcription elongation in HL60 cells treated with DMSO was observed within 30 min of treatment (Eick and Bornkamm, 1986). Between 24 and 48 hr after treatment, the level of transcription initiation in exon 1 also declines, concurrent with loss of DNase I hypersensitive sites 112, 1111, and 1112. , 1988). From these experiments, it appears that the block to transcription elongation can control c-myc RNA levels during differentiation. , 1987; M. Groudine, unpublished observations).

Truncations of exon 1 could contribute to c-my deregulation because expression from cryptic intron 1 promoters would not be subject to normal c-myc regulatory influences such as transcription initiation signals and the block to transcription elongation in exon 1. , 1984) indicate that truncation alone is not sufficient to deregulate o r activate c-my expression. , 1985a). A longer half-life for transcripts from these BLs could contribute to high levels of c-myc RNA. However, many BL lines retain exon 1 and initiate transcription from P I and P2 start sites.

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