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The Harold Varmus Papers

Oncogenesis without Viral Oncogenes by Avian Leukosis and Mouse Mammary Tumor Viruses pdf (77,871 Bytes) transcript of pdf
Oncogenesis without Viral Oncogenes by Avian Leukosis and Mouse Mammary Tumor Viruses
Varmus and Nusse here gave a summary of their research on cancer-causing retroviruses that do not carry their own oncogene, but instead induce cancer by triggering so-called insertion mutations in genes near the site where the viral genes are inserted into the genome of the host cell.
Number of Image Pages:
1 (77,871 Bytes)
Date Supplied:
ca. March 1983
Varmus, Harold
Nusse, Roel
Fung, Yuen-Kai
Payne, Gregory
Westaway, David
Luciw, Paul
Original Repository: University of California, San Francisco. Archives and Special Collections. Harold E. Varmus Papers
Reproduced with permission of the Regents of the University of California.
Medical Subject Headings (MeSH):
Mammary Tumor Virus, Mouse
Avian Leukosis
Exhibit Category:
Retroviruses and the Genetic Origins of Cancer, 1970-1993
Box Number: 2
Folder Number: 7
Unique Identifier:
Document Type:
Abstracts (summaries)
Physical Condition:
Series: UCSF Collections
SubSeries: Collection Number MSS 84-25
SubSubSeries: Correspondence, 1971-1984
Folder: Correspondence, 1983
Oncogenesis Without Viral Oncogenes By Avian Leukosis And Mouse Mammary Tumor Viruses
Harold E. Varmus*, Roel Nusse, Yuen-Kai Fung, Gregory Payne, David Westaway, and Paul Luciw
Department of Microbiology and Immunology, University of California, San Francisco, CA. 94143 U.S.A.
We have been exploring the behavior of certain oncogenic retroviruses that lack their own oncogenes but can activate cellular genes by insertional mutation. In B cell lymphomas induced in chickens by avian leukosis virus (ALV), an elevated level of expression of a cellular oncogene (c-myc), is observed with three different arrangements of integrated ALV DNA within the c-myc locus (1). The results imply that proviral DNA can activate expression of host genes either directly, by providing a viral promoter, or indirectly, by affecting the efficiency of a host promoter. Analysis of DNA cloned from interrupted c-myc loci in B cell lymphomas and studies of the expression of the herpes simplex virus thymidine kinase gene joined in vitro to retroviral DNA (2) indicate that retroviral sequences sufficient for both the direct and indirect mechanisms lie within or immediately adjacent to an LTR. Related mechanisms appear to operate during oncogenesis by the mouse mammary tumor virus (MMTV). Most of the MMTV-induced mammary tumors in C3H mice harbor proviral DNA within a 20 kb domain of the mouse genome that we have called int-1 (3). The insertions occur in several clusters throughout this region, on both sides of a transcriptional unit that is silent in normal mammary glands but expressed at a low level in tumors with an interrupted int-1 locus. We interpret these findings to mean that rare insertions of MMTV DNA into s-1 can initiate tumorigenesis by activating a heretofore unrecognized cellular oncogene.
1. G.S. Payne, J.M. Bishop and H.E. Varmus. Nature 295:209-217, 1982.
2. P. Luciw, J.M. Bishop, H.E. Varmus and M. Capecchi. Cell, in press.
3. R. Nusse and H.E. Varmus. Cell 31:99-109, 1982.
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