H. Eagle M.D.¹, G. E. Foley Sc.D.¹, H. Koprowski M.D.¹, H. Lazarus ¹, E. M. Levine Ph.D.¹, and R. A. Adams Ph.D.¹

¹ From the Institute of Cell Biology, Division of Biological Sciences, Albert Einstein College of Medicine, Bronx, New York 10461, the Children's Cancer Research Foundation, and the Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, and The Wistar Institute, Philadelphia, Pennsylvania 19104

Virus transformants (like cancer cells, cells transformed by X-ray or carcinogens, or those which have transformed spontaneously) exhibit a number of phenotypic changes which are usually associated, and which may be lost concurrently. That association is, however, not invariable. More particularly, the altered characteristics here studied (escape from contact inhibition of growth and susceptibility to inhibition by other cells, decreased serum requirement, and ability to grow in soft agar) do not, in and of themselves, endow the cell with the capacity to produce a tumor, at least as judged by the methods of assay here used. Although the question as to whether the tumorigenicity of virus transformants is causally linked to any of these associated changes cannot be answered definitively, the evidence suggests a close linkage, rather than identity, between the determinants of oncogenicity and the other properties here studied.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

• Eagle, H. (1971). Buffer Combinations for Mammalian Cell Culture. Science 174: 500-503 [Abstract]  

Home | Help | Feedback | Subscriptions | Archive | Search

TABLE OF CONTENTS