Cancer Research  09 AM Call for Abstracts
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, 1052-1057, March 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 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 Pollack, A.
Right arrow Articles by Irvin, G. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pollack, A.
Right arrow Articles by Irvin, G. L., III

Tumor Progression in Serial Passages of the Dunning R3327-G Rat Prostatic Adenocarcinoma: Growth Rate Response to Endocrine Manipulation1

Alan Pollack2, Norman L. Block, Betty J. Stover and George L. Irvin, III

Research Service, Veterans Administration Medical Center [A. P.], and the Departments of Surgery [A. P., G. L. I.], Microbiology [A. P.], and Urology [N. L. B., B. J. S.], University of Miami School of Medicine, Miami, Florida 33125

Serial passages of the poorly differentiated, androgen-sensitive R3327-G prostatic adenocarcinoma were used to study the progressive changes that occur in tumor growth rate and androgen sensitivity. Different in vivo transplant generations (21st to 28th) were compared. The tumor doubling and animal survival times resulting from the implantation of the 21st to 22nd generation (21–22G) tumor cells in intact male rats were significantly greater than those resulting from the implantation of 23–28G tumor cells. The most dramatic difference between early (21–23G) and late (26–28G) tumor generations, however, was in androgen sensitivity. The 26–28G tumors displayed androgen sensitivity only when implanted into animals castrated 2 to 7 days previously. Tumors grown in the pretreated castrates grew at a significantly slower rate than those in intact rats and the pretreated castrates had longer survival times than the intact rats. When 26–28G tumors were allowed to grow in intact rats to approximately 1 cu cm and then the rats were castrated, no significant difference in the growth rate between these tumors and tumors grown in intact rats was observed. In contrast, the androgen sensitivity of 21–23G tumors could be demonstrated, regardless of whether treatment was started before or after implantation. The fact that androgen sensitivity was still evident under certain conditions in late-generation R3327-G tumors demonstrates that the basic mechanism involving androgen response was still present, although functioning at a much reduced level.

1 Supported in part by the Veterans Administration Merit Review (4321-001); Weeks Endowment Fund, Department of Urology, University of Miami School of Medicine; Urology Research Fund, Inc.; and Surgical Scholarship Fund, University of Miami School of Medicine.

2 To whom requests for reprints should be addressed, at Research Service 151, Veterans Administration Medical Center, 1201 N.W. 16 Street, Miami, FL 33125.

Received 8/14/84. Accepted 11/15/84.







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.