Cancer Research Cancer Epigenetics  Genetics and Biology of Brain Cancer
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 45, 4804-4809, October 1, 1985]
© 1985 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 Google Scholar
Google Scholar
Right arrow Articles by Weinroth, S. E.
Right arrow Articles by Hays, E. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Weinroth, S. E.
Right arrow Articles by Hays, E. F.

Genetic Complexity of Glucocorticoid-induced Lysis of Murine T-Lymphoma Cells1

Stephen E. Weinroth, Carol L. MacLeod, Lory Minning and Esther F. Hays2

Laboratory of Biomedical and Environmental Sciences, Los Angeles 90024 [S. E. W., E. F. H.]; Department of Medicine, University of California, Los Angeles, Los Angeles 90024 [E. F. H.]; and Cancer Center, University of California, San Diego, La Jolla 92093 [C. L. M., L. M.], California

Several well characterized murine T-lymphoma cell lines were used in somatic cell hybridization experiments to study the genetic regulation of glucocorticoid-induced lysis. Cell fusions were carried out among the SL 12-derived cloned lines and between the W7 and SAK8 lines all of which have functional hormone receptors. These cell lines differ in their sensitivity to glucocorticoid-induced lysis. The resultant hybrids were characterized by their growth response to 1 µM dexamethasone, their hormone receptor content, their chromosome number, and the expression of surface antigens. Fusion of the hormone-sensitive W7 parent to a number of glucocorticoid-resistant cell lines resulted in hybrids which were of the sensitive phenotype. In contrast the fusion of another hormone-sensitive clone, SL12.4, with glucocorticoid-resistant SL12 clones or with SAK8 always resulted in hybrids resistant to glucocorticoid lysis. These results reveal a complex genetic regulation of the hormone response or the requirement for multiple gene activity in the mechanism for glucocorticoid-induced cell lysis.

1 The Laboratory of Biomedical and Environmental Sciences is operated for the United States Department of Energy by the University of California under Contract DE-AC03-76-SF00012. This article was supported by the Director of the Office of Energy Research, Office of Health and Environmental Research; NIH Research Grants CA 12386 (U.C.L.A.) and CA 37778 (University of CA, San Diego), and the Margaret E. Early Trust grant.

2 To whom requests for reprints should be addressed, at UCLA Warren Hall, 900 Veteran Avenue, Los Angeles, CA 90024.

Received 3/28/85. Revised 6/10/85. Accepted 6/20/85.







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 © 1985 by the American Association for Cancer Research.