Cancer Research AACR Legacy  EMT and Cancer Progression and Treatment
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

[Cancer Research 48, 5747-5753, October 15, 1988]
© 1988 American Association for Cancer Research

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Miller, B. E.
Right arrow Articles by Heppner, G. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Miller, B. E.
Right arrow Articles by Heppner, G. H.

Dominance of a Tumor Subpopulation Line in Mixed Heterogeneous Mouse Mammary Tumors1

Bonnie E. Miller2, Fred R. Miller, David Wilburn and Gloria H. Heppner

E. Walter Albachten Department of Immunology, Michigan Cancer Foundation, Detroit, Michigan 48201

When mixtures of cell lines 168 and 4T07, both derived from the same mouse mammary tumor, were injected into syngeneic mice, the resulting tumors, analyzed over a large size range by colony-forming assays in selective media, consisted primarily of line 4T07, even when the ratio injected was 100:1 or greater in favor of line 168. This result indicated a suppression of growth of line 168, since the volume-doubling time of line 168 tumors in the absence of line 4T07 was one-half that of line 4T07 tumors. That growth suppression was not due to inhibition of line 168 by immunity induced to line 4T07 was shown in two ways: (a) line 168 tumors grew almost as well in mice preimmunized with line 4T07 as in controls, whereas line 4T07 tumor growth was strongly inhibited in preimmunized mice; and (b) the final composition (favoring line 4T07) in mixed tumors was similar in tumors grown in mice immunosuppressed by irradiation to that in nonirradiated controls. The strong suppression of line 168 did not occur when the two cell lines were injected simultaneously at different s.c. sites, nor did it occur when line 168 cells were injected in mixtures with lethally irradiated line 4T07 cells.

Line 4T07 cells also suppressed the growth of line 168 cells in monolayer cultures. It was not likely that suppression was due to competition for growth factors, since the effect required cell contact. Suppression probably was not mediated through junctional communication, since these cells do not engage in metabolic cooperation. We suggest that a growth-inhibitory factor produced by line 4T07 mediates the suppression of 168 cells.

1 Supported by USPHS Grant CA27419 awarded by the National Cancer Institute, Department of Health and Human Services.

2 To whom requests for reprints should be addressed, at Michigan Cancer Foundation, 110 E. Warren Ave., Detroit, MI 48201.

Received 2/23/88. Revised 7/12/88. Accepted 7/15/88.




This article has been cited by other articles:


Home page
ScienceHome page
L. A. Johnston
Competitive Interactions Between Cells: Death, Growth, and Geography
Science, June 26, 2009; 324(5935): 1679 - 1682.
[Abstract] [Full Text] [PDF]


Home page
Cell Growth Differ.Home page
J. M. Jones, X.-S. Cui, D. Medina, and L. A. Donehower
Heterozygosity of p21WAF1/CIP1 Enhances Tumor Cell Proliferation and Cyclin D1-associated Kinase Activity in a Murine Mammary Cancer Model
Cell Growth Differ., April 1, 1999; 10(4): 213 - 222.
[Abstract] [Full Text]


Home page
Toxicol PatholHome page
C. D. Albright, R. T. Jones, P. M. Grimley, and J. H. Resau
Intercellular Communication in Bronchial Epithelial Cells: Review of Evidence for a Possible Role in Lung Carcinogenesis
Toxicol Pathol, February 1, 1990; 18(2): 324 - 343.
[Abstract] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1988 by the American Association for Cancer Research.