Five groups of double-stranded DNA viruses and diploid RNA viruses of the retroviral group are associated epidemiologically, experimentally, or both with animal and human neoplasia. DNA tumor viruses associated with cancer on epidemiological grounds include papilloma viruses and urogenital cancer, herpes viruses and Burkitt' s lymphoma and nasopharyngeal-carcinoma, and hepatitis viruses and liver cancer. No biochemically defined oncogenes have yet been described for any of these viruses; however, preliminary evidence suggests the existence of transforming sequences in both papilloma and herpes viruses.
Although studied in great molecular detail with elucidation of clearly defined oncogenes, polyoma viruses and adenoviruses have not been associated with naturally occurring tumors in vivo. Their oncogenes are structurally dissimilar to retroviral oncogenes, yet these two gene classes appear to subserve similar functions.
The RNA tumor viruses were the first infectious agents unequivocally associated with neoplasia. A large number of such viruses have been isolated from chickens, rodents, cats, and monkeys. Many transduce one or two oncogene sequences necessary and sufficient for efficient cellular transformation. These oncogenes were derived originally from host sequences. Virally transduced oncogenes comprise some 20 independent species falling into a smaller number (some five to seven) of functional categories. The retroviral life cycle, employing a double - stranded DNA intermediate (the provirus) that integrates into host DNA, suggests a mechanism where by the virus could acquire cellular sequences.
Both RNA and DNA viruses are associated with cancer. There are five major categories of DNA rumor viruses, each of which has a double - stranded DNA genome. No known single -stranded DNA virus is associated with oncogenesis. Of the RNA viruses, only one group is associated with cancer: the single-stranded but diploid oncorna viruses.
Oncogenes and Human Cancels
Overview
Nearly all of the known retroviral oncogenes have proto-oncogene counterparts detectable in human DNA. Many of these proto-oncogenes activated through a variety of mechanisms have been associated with human cancers. Perturbations in the structure or expression of certain proto -oncogenes appear to be the general means by which this activation occurs.
Examples of structural changes are seen in single amino acid substitutions in the ras family of genes isolated iron human leukemias, colon carcinomas, and bladder carcinomas. In chronic myelogenous leukemia, the translocation between chromosomes 9q and 22q results in the formation of a novel fusion gene termed bcr-abl whose gene product differs from that of the normal c-abl protein in size and in the ability to autophosphorylate.
Perturbations in the expression of a proto-oncogene can be due to the presence of abnormal regulatory elements as in the case of translocations involving c-myc seen in Burkitt' s lymphomas, or due to amplification which augments expression by increasing the gene copy number. Amplifications of N-myc in neuroblastoma, and erB-/neu in human breast cancer have been correlated with a more advanced stage and a poorer prognosis.
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