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.
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1 April 1970
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April 01 1970
GROWTH CHARACTERISTICS OF VIRUS-TRANSFORMED CELLS : MAXIMUM POPULATION DENSITY, INHIBITION BY NORMAL CELLS, SERUM REQUIREMENT, GROWTH IN SOFT AGAR, AND XENOGENEIC TRANSPLANTABILITY
H. Eagle,
H. Eagle
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
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G. E. Foley,
G. E. Foley
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
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H. Koprowski,
H. Koprowski
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
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H. Lazarus,
H. Lazarus
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
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E. M. Levine,
E. M. Levine
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
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R. A. Adams
R. A. Adams
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
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H. Eagle
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
G. E. Foley
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
H. Koprowski
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
H. Lazarus
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
E. M. Levine
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
R. A. Adams
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
Received:
December 04 1969
Online ISSN: 1540-9538
Print ISSN: 0022-1007
Copyright © 1970 by The Rockefeller University Press
1970
J Exp Med (1970) 131 (4): 863–879.
Article history
Received:
December 04 1969
Citation
H. Eagle, G. E. Foley, H. Koprowski, H. Lazarus, E. M. Levine, R. A. Adams; GROWTH CHARACTERISTICS OF VIRUS-TRANSFORMED CELLS : MAXIMUM POPULATION DENSITY, INHIBITION BY NORMAL CELLS, SERUM REQUIREMENT, GROWTH IN SOFT AGAR, AND XENOGENEIC TRANSPLANTABILITY . J Exp Med 1 April 1970; 131 (4): 863–879. doi: https://doi.org/10.1084/jem.131.4.863
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