Important note: Information in this article was accurate in 1988. The state of the art may have changed since the publication date.
MECHANISMS OF LYMPHOMA INDUCTION BY RETROVIRUSES
Progress in Immunology VI. Sixth International Congress of Immunology. Cinader B, Miller RG, eds. New York, Academic Press, p. 664-74, 1986.. Unique Identifier : AIDSLINE ICDB/88640042 Melief CJ; Zijlstra M; Vasmel WL; Matthews E; Slater RM; Berns AM; The Netherlands Cancer Inst., Antoni van Leeuwenhoek Huis, 1006; CX Amsterdam, The Netherlands
Abstract:
Molecular genetic mechanisms of lymphoma induction by retroviruses (RVs) are discussed under the following headings: structure of lymphomagenic RVs, modes of transmission of lymphomagenic RVs, RV insertions in the vicinity of cellular oncogenes (RV insertional mutagenesis of the c-myc gene by avian leukosis virus and RV insertional mutagenesis of the c-myc and pim-1 genes by murine leukemia viruses), mode of action of viral and cellular oncogenes, chromosome aberrations in virus- and nonvirus-induced lymphomas, modulation of lymphoma development by the major histocompatibility complex (MHC) of the mouse, and mechanism of lymphoma induction by human T cell leukemia virus type I (HTLV-I). Acutely-transforming RVs with built-in viral oncogenes (v-onc) rarely cause lymphomas, whereas slowly-transforming RVs lacking v-onc very often cause lymphomas in a variety of mammalian species, including man. Many such viruses induce lymphomas by insertional mutagenesis of cellular oncogenes (c-onc). Examples described here are c-myc deregulation by avian leukosis virus and c-myc and/or pim-1 deregulation by murine leukemia virus. The chromosomal translocations activating c-myc provide an interesting parallel with c-myc activation by RV insertion. As in the case of RV-activated c-myc, the coding second and third exons of c-myc are always intact, despite considerable variability of the translocation breakpoints in or around the c-myc and Ig genes. The c-myc activation probably proceeds by several mechanisms, although an IgH enhancer may be the activation element in translocations involving IgH. Lymphoma incidence and type are modulated by the MHC in the mouse. The pathogenesis of the early T-cell lymphomas in mice of susceptible MHC types appears to differ from that of late B-cell lymphomas in mice of resistant MHC types, despite the fact that both the early T- and the late B-cell lymphomas show frequent DNA reintegrations of ecotropic and MCF viruses. Lymphoma induction by HTLV-I involves a unique transactivating protein (tat product), which probably induces lymphomas by activating the expression of growth-promoting genes specific for lymphoid cells. (47 Refs)
Keywords: Animal Chromosome Aberrations DNA, Neoplasm/GENETICS *Gene Expression Regulation Genes, MHC Class II Human HTLV-BLV Infections/*GENETICS HTLV-BLV Viruses/*GENETICS Major Histocompatibility Complex Mice *Oncogenes RNA, Neoplasm/GENETICS Transcription, Genetic *Translocation (Genetics) MEETING PAPER
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Important note: Information in this article was accurate in 1988. The state of the art may have changed since the publication date.
