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R. Kingston, A. Baldwin, P. Sharp (1984)Regulation of heat shock protein 70 gene expression by c-myc
H. Armelin, M. Armelin, K. Kelly, T. Stewart, P. Leder, B. Cochran, C. Stiles (1984)Functional role for c-myc in mitogenic response to platelet-derived growth factor
K. Alitalo, M. Schwab, Charlene Lin, H. Varmus, J. Bishop (1983)Homogeneously staining chromosomal regions contain amplified copies of an abundantly expressed cellular oncogene (c-myc) in malignant neuroendocrine cells from a human colon carcinoma.
Proceedings of the National Academy of Sciences of the United States of America, 80 6
J. Bishop (1983)Cellular oncogenes and retroviruses.
Annual review of biochemistry, 52
M. Greenberg, E. Ziff (1984)Stimulation of 3T3 cells induces transcription of the c-fos proto-oncogene
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The EMBO Journal, 2
E. Gelmann, M. Psallidopoulos, T. Papas, R. Favera (1983)Identification of reciprocal translocation sites within the c-myc oncogene and immunoglobulin μ locus in a Burkitt lymphoma
Jerry Adams, S. Gerondakis, E. Webb, L. Corcoran, S. Cory, Walter (1983)Cellular myc oncogene is altered by chromosome translocation to an immunoglobulin locus in murine plasmacytomas and is rearranged similarly in human Burkitt lymphomas.
Proceedings of the National Academy of Sciences of the United States of America, 80 7
S. Hann, R. Eisenman (1984)Proteins encoded by the human c-myc oncogene: differential expression in neoplastic cells
Molecular and Cellular Biology, 4
R. Favera, F. Wong-Staal, R. Gallo (1982)onc gene amplification in promyelocytic leukaemia cell line HL-60 and primary leukaemic cells of the same patient
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Science, 222 4625
M. Einat, D. Resnitzky, A. Kimchi (1985)Close link between reduction of c-myc expression by interferon and G0/G1 arrest
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S. Hann, H. Abrams, L. Rohrschneider, R. Eisenman (1983)Proteins encoded by v-myc and c-myc oncogenes: Identification and localization in acute leukemia virus transformants and bursal lymphoma cell lines
R. Taub, K. Kelly, J. Battey, S. Latt, G. Lenoir, U. Tantravahi, Zhiming Tu, P. Leder (1984)A novel alteration in the structure of an activated c-myc gene in a variant t(2;8) burkitt lymphoma
G. Klein (1983)Specific chromosomal translocations and the genesis of B-cell-derived tumors in mice and men
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Proceedings of the National Academy of Sciences of the United States of America, 80 21
H. Land, L. Parada, R. Weinberg (1983)Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes
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Michael Green, R. Treisman, T. Maniatis (1983)Transcriptional activation of cloned human β-globin genes by viral immediate-early gene products
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Proceedings of the National Academy of Sciences of the United States of America, 82 2
R. Ralston, J. Bishop (1983)The protein products of the myc and myb oncogenes and adenovirus E1a are structurally related
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P. Tsichlis, P. Strauss, Li-Fu Hu (1983)A common region for proviral DNA integration in MoMuLV-induced rat thymic lymphomas
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Proceedings of the National Academy of Sciences of the United States of America, 81 13
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Proceedings of the National Academy of Sciences of the United States of America, 81 10
Kari Alitalo, Kari Alitalo, G. Ramsay, J. Bishop, Pfeifer So, W. Colby, A. Levinson (1983)Identification of nuclear proteins encoded by viral and cellular myc oncogenes
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Proceedings of the National Academy of Sciences of the United States of America, 78 3
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Proceedings of the National Academy of Sciences of the United States of America, 81 21
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C. Shih, M. Linial, M. Goodenow, W. Hayward (1984)Nucleotide sequence 5' of the chicken c-myc coding region: localization of a noncoding exon that is absent from myc transcripts in most avian leukosis virus-induced lymphomas.
Proceedings of the National Academy of Sciences of the United States of America, 81 15
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Proceedings of the National Academy of Sciences of the United States of America, 80 2
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E. Webb, Jerry Adams, S. Cory (1984)Variant (6 ; 15) translocation in a murine plasmacytoma occurs near an immunoglobulin κ gene but far from the myc oncogene
S. Palmieri, P. Kahn, T. Graf (1983)Quail embryo fibroblasts transformed by four v‐myc‐containing virus isolates show enhanced proliferation but are non tumorigenic.
The EMBO Journal, 2
Gerard Selten, H. Cuypers, Maarten Zijlstral, Cees, Meliefl, A. Berns (1984)Involvement of c‐myc in MuLV‐induced T cell lymphomas in mice: frequency and mechanisms of activation.
The EMBO Journal, 3
A. Geser, G. Lenoir, M. Anvret, G. Bornkamm, G. Klein, E. Williams, D. Wright, G. de‐Thé (1983)Epstein-Barr virus markers in a series of Burkitt's lymphomas from the West Nile District, Uganda.
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Terence Rabbitts, A. Forster, P. Hamlyn, R. Baer, R. Baer (1984)Effect of somatic mutation within translocated c-myc genes in Burkitt's lymphoma
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Proceedings of the National Academy of Sciences of the United States of America, 81 1
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Proceedings of the National Academy of Sciences of the United States of America, 79 8
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Proceedings of the National Academy of Sciences of the United States of America, 75 6
Lymphocytes exist in a dynamic state that alternates between small quiescent cells and large, antigen-activated, proliferating cells. Their failure to activate properly or to turn off a proliferative program is a likely step in the development of lymphoid malignancies. Understanding the genetic mechanisms that regulate the expression of the alternately quiescent and activated phenotypes is a fundamental question for immunology and oncology. Significant progress in the identification of DNA elements that appear to play a role in the regulation of proliferation and differentiation has come about as a consequence of the isolation of oncogenes, pieces of genetic information that are involved in the malignant transformation of cells. Oncogenes were first isolated as part of the small genomes of rare RNA tumor viruses, called acute transforming retroviruses. These viruses effiÂ ciently transform cells in culture and in animals. Acute retroviruses are The US Government has the right to retain a nonexclusive, royalty-free license in and to any copyright covering this paper. KELLY & SIEBENLIST distinct from slow transforming retroviruses that, by contrast, do not possess oncogenes. Accordingly, slow viruses are common in nature, do not transform cells in culture, and only rarely cause tumors in vivo. Normal vertebrate cells
Annual Review of Immunology – Annual Reviews
Published: Apr 1, 1986
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