J
J. Michael Bishop
Researcher at University of California, San Francisco
Publications - 170
Citations - 27667
J. Michael Bishop is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: RNA & Avian sarcoma virus. The author has an hindex of 88, co-authored 170 publications receiving 26969 citations. Previous affiliations of J. Michael Bishop include Foundation University, Islamabad.
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Journal ArticleDOI
Molecular themes in oncogenesis
TL;DR: It seems likely that most malignancies arise from the collaborative effects of dominant and recessive lesions, andumeration of the number of tumor suppressor genes afflicted in any given tumor may be greater.
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Amplified DNA with limited homology to myc cellular oncogene is shared by human neuroblastoma cell lines and a neuroblastoma tumour.
Manfred Schwab,Kari Alitalo,Karl-Heinz Klempnauer,Harold E. Varmus,J. Michael Bishop,Fred Gilbert,Garrett M. Brodeur,Milton I. Goldstein,Jeffrey M. Trent +8 more
TL;DR: It is shown here that a DNA domain detectable by partial homology to the myc oncogene is amplified up to 140-fold in cell lines derived from different human neuroblastomas and in a neuroblastoma tumour, but not in other tumour cells showing cytological evidence for gene amplification.
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Reversible Tumorigenesis by MYC in Hematopoietic Lineages
TL;DR: It is concluded that even though tumorigenesis is a multistep process, remediation of a single genetic lesion may be sufficient to reverse malignancy.
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Senescence of human fibroblasts induced by oncogenic Raf
TL;DR: It is concluded that the kinase cascade initiated by Raf can regulate the expression of p16(Ink4a) and the proliferative arrest and senescence that follows and may provide a defense against neoplastic transformation when the MAP kinase signaling cascade is inappropriately active.
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MYC inactivation uncovers pluripotent differentiation and tumour dormancy in hepatocellular cancer
Catherine M. Shachaf,Andrew M. Kopelman,Constadina Arvanitis,Asa Karlsson,Shelly Beer,Stefanie Mandl,Michael Bachmann,Alexander D. Borowsky,Boris H. Ruebner,Robert D. Cardiff,Qiwei Yang,J. Michael Bishop,Christopher H. Contag,Dean W. Felsher +13 more
TL;DR: It is reported that inactivation of the MYC oncogene is sufficient to induce sustained regression of invasive liver cancers and how oncogenic inactivation may reverse tumorigenesis in the most clinically difficult cancers is shown.