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Article
November 24, 1989

Short-circuiting Oncogenes May Become Basis of New Cancer Therapies

JAMA. 1989;262(20):2785. doi:10.1001/jama.1989.03430200013002

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Abstract

NEW APPROACHES to cancer therapy that target environments conducive to oncogene expression rather than the genes themselves may be on the horizon.

That was the impression conveyed by two speakers at the 12th Annual Bristol-Myers Symposium on Cancer Research, held recently in Toronto, Canada. Implicit in their message was that the proteins for which oncogenes code have a variety of functions that, if properly understood, can be intercepted to reverse, and even avert, malignancy.

That line of reasoning makes sense, given that each of the 60 or so known oncogenes codes for a protein that has a normal cellular function. The knowledge that oncogenes are normal cellular genes rather than viral genes inserted via retroviral infection stems from work done during the late 1970s by J. Michael Bishop, MD; Howard Varmus, MD; and Dominique Stehlin, PhD.

Their experiments at the University of California, San Francisco, established the paradigm that oncogenes

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