VIRAL CARCINOGENESIS: FUNCTIONAL ASPECTS NLM AIDSLINE Important note: Information in this article was accurate in 1988. The state of the art may have changed since the publication date.

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VIRAL CARCINOGENESIS: FUNCTIONAL ASPECTS

Alfred Benzon Symp; 24:1-467 1987. Unique Identifier : AIDSLINE ICDB/88647938
Anonymous; No affiliation given

Abstract: Proceedings of the Alfred Benzon Symposium 24 on functional aspects of viral carcinogenesis, held June 15-19, 1986 in Copenhagen, Denmark, are presented in eight sections. The first, enhancers and transcriptional factors, discusses the following topics: transcriptional control and oncogenicity of murine leukemia viruses, determinants of cell type specificity within the immunoglobulin heavy chain gene enhancer, transcription from unconventional promoters: dihydrofolate reductase and SV40 late; and identification of cellular proteins that interact with the polyoma virus enhancer. The section on transcriptional and translation control addresses the following topics: structure and function of the HTLV-III genome, replication and pathogenesis of human retroviruses, and activation and inhibition of mos transformation by proviral long terminal repeats and c-mos-associated cellular sequences. A section on transcriptional control and modifications discusses these topics: some remarkable properties of cell lines and transgenic mice which received the gene encoding the large T protein of polyoma virus, activation of cellular transcription by simian virus 40 large T antigen, role of papillomaviruses in human cancer, cis-acting elements and trans-acting factors involved in the expression and regulation of the a genes of herpes simplex virus type 1, influence of adenovirus transformation on cellular gene expression, and an adenovirus oncogene post-transcriptionally modulates mRNA accumulation. Pim-1 activation in T-cell lymphomas and activation of the cellular oncogenes int-1 and int-2 are discussed in the section on gene activation by integration. Chromosome aberration and oncogene activation in two histologically related human and rat B-cell tumors and constitutive c-myc expression and lymphoid neoplasia are discussed in the section on gene activation by translocation. Multiple skin pathologies in transgenic mice harboring the bovine papilloma virus (BPV) and multiple BPV genes influence transformation of mouse cells are discussed in the section on transformation by BPV. In the section on cytoskeleton and activation of c-onc, the following topics are discussed: interaction between herpes simplex virus and the cellular cytoskeleton structures; changes in the levels of expression of human tropomyosins IEF 52, 55, and 56 in normal and SV40-transformed MRC-5 fibroblasts; induction of c-fos and c-myc by growth factors: role in growth control; and v-myc regulation of c-myc expression. The final section, on signal pathways, presents the following papers: functional expression of human EGF-receptor and its mutants in mouse 3T3 cells, conversion of a putative growth factor receptor into an oncogene protein, a mutational analysis of ras function, regulation of the expression of the cellular src proto-oncogene product, structure and function of normal cellular and mutant viral erbA oncogenes, mechanism of transformation by the fms oncogene and the relationship of its product to the CSF-1 receptor, and acute transformation by simian sarcoma virus is mediated by an externalized PDGF-like growth factor. Discussions at the end of each presented paper are included.
Keywords: Animal *Cell Transformation, Neoplastic Cell Transformation, Viral Congresses Gene Expression Regulation Genes, Viral Human Neoplasms/GENETICS/*MICROBIOLOGY Oncogenes *Oncogenic Viruses/GENETICS/IMMUNOLOGY Proto-Oncogene Proteins/GENETICS CONGRESS MONOGRAPH

KWDanimalKWDcelltransformation,neoplasticcelltransformation,viralcongressesgeneexpressionregulationgenes,viralhumanneoplasms/genetics/KWDmicrobiologyoncogenesKWDoncogenicviruses/genetics/immunologyproto-oncogeneproteins/geneticscongressmonograph
881230
M88C0649

Copyright © 1988 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

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