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February 15, 1995

The Genetic Origins of Neoplasia

Author Affiliations

From the Department of Molecular Biology and the Lewis Thomas Laboratory, Princeton University, Princeton, NJ. Research in the laboratory of Dr Levine has been sponsored by the National Cancer Institute, Onyx Pharmaceuticals, and Imclone Systems. He has stock options in Onyx Pharmaceuticals and Imclone Systems.

JAMA. 1995;273(7):592. doi:10.1001/jama.1995.03520310090035

The last 15 years have witnessed a conceptual breakthrough in our understanding of the molecular and genetic basis of the origins of neoplasia in humans. This happened methodically, experiment by experiment, with no one observation yielding the entire picture. Over time, a large number of observations slowly came together, and, for that reason, we often do not give enough credit to the science, or the scientists, for this remarkable achievement.

Mutations in three broad categories of genes have been shown to contribute to the origins and progression of neoplasia in humans: the oncogenes, the tumor suppressor genes, and the mutator genes. Almost 100 different oncogenes have been identified in animals and humans and shown to contain mutations in a wide variety of tumors. Most of these oncogenes were discovered with the use of retro viruses that insert adjacent to an oncogene and activate it or capture the oncogene in a

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