Important note: Information in this article was accurate in 1988. The state of the art may have changed since the publication date.
VIRUSES AND CANCER
The Basic Science of Oncology. Tannock IF, Hill RP, eds. New York, Pergamon Press, p. 52-71, 1987.. Unique Identifier : AIDSLINE ICDB/88639527 Sheinin R; Mak TW; Clark SP; Dept. of Microbiology, Univ. of Toronto, Toronto, Ontario, Canada
Abstract:
Experimental methods of cancer virology and characteristics of DNA and RNA tumor viruses are reviewed. Topics include in vivo assay for tumor viruses, viral infection, in vitro assays, families of tumor viruses, integration of viral DNA, expression of viral genes, human tumors and viruses, specific DNA viruses, characteristics of retroviruses and the retrovirus genome, mechanisms of transformation by retroviruses, retroviruses and mammary cancer, and human T-cell lymphotropic viruses. Tumors that occur spontaneously in a variety of animals are caused by DNA- or RNA-containing viruses. In vitro, these viruses cause genetic and morphological transformation of infected cells. An essential step in malignant transformation of normal cells by most tumor viruses is integration of all or part of the viral DNA (or DNA copy of retroviral RNA) into the host-cell genome. Such viral DNA then acquires immortality as a chromosomal parasite. Expression of specific viral genes leads to the synthesis of new polypeptide(s) which may cause malignant transformation directly, if that protein is the product of a viral oncogene. The viral genes or their protein products may also act indirectly by activating a cellular oncogene. Six of the seven known families of DNA-containing viruses have members that can induce tumors in animals and/or cause genetic transformation and immortalization of cells in vitro. There is evidence that (1) the human hepatitis B virus is a major cause of primary hepatocellular carcinoma, (2) the human papillomaviruses cause benign warts and papillomas and are implicated in the etiology of cervical cancer, and (3) Epstein-Barr herpes virus is the etiological agent of Burkitt's lymphoma and, possibly, nasopharyngeal carcinoma. Retroviral oncogenes may undergo mutation events that enhance their expression and, therefore, the oncogenicity of the virus housing them. Oncogenic viruses that induce rapid formation of tumors in animals have acquired oncogenes which are regulated by the viral promoter and enhancer sequences. Other viruses induce tumors after a longer latency period and are active because they promote expression of cellular oncogenes adjacent to, or even remote from, their site of insertion in the cellular genome. There is evidence that retroviruses cause adult T-lymphocytic leukemia and acquired immunodeficiency syndrome in humans. (46 Refs)
Keywords: Animal Carcinoma, Hepatocellular/GENETICS Cell Transformation, Neoplastic Cell Transformation, Viral Cervix Neoplasms/GENETICS DNA, Viral/GENETICS Gene Expression Regulation Hepatitis B Virus/GENETICS Human HTLV-BLV Viruses/GENETICS Liver Neoplasms/GENETICS Mammary Neoplasms, Experimental/GENETICS Mammary Tumor Viruses, Mouse/GENETICS Oncogenic Viruses/GENETICS Papillomavirus/GENETICS Retroviridae/GENETICS Tumor Virus Infections/*GENETICS Virus Replication MONOGRAPH
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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.
