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[Cancer Research 52, 4642-4648, September 1, 1992]
© 1992 American Association for Cancer Research

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Down-Regulation of Tenascin Expression by Antiprogestins during Terminal Differentiation of Rat Mammary Tumors

Günter Vollmer1, Horst Michna, Kirsten Ebert and Rudolf Knuppen

Institut für Biochemische Endokrinologie, Medizinische Universität, Ratzeburger Allee 160, D-2400 Lübeck [G. V., K. E., R. K.], and Research Laboratories of Schering AG, Müllerstrasse 170–178, D-1000 Berlin [H. M.], Germany

Studies on tenascin expression in hormonally dependent growing tissues of breast and endometrium suggested that its expression parallels the progression of normal or malignant proliferative alteration of the tissue. With the study presented here we addressed the question of whether antiprogestin-induced terminal differentiation down-regulates tenascin expression. By comparative immunolocalization of tenascin in sections of untreated 7,12-dimethylbenz[{alpha}]anthracene-induced tumors, tumors grown in ovariectomized animals, tamoxifen-treated tumors, and antiprogestin-treated tumors, we obtained the following results. (a) The entire extracellular space of the stromal mesenchyme was filled by tenascin immunoreactivity in cases of untreated control tumors. (b) Both ovariectomy and antiestrogen treatment with tamoxifen did not affect the overall staining pattern and resulted in a slight increase of the arbitrarily judged staining intensity. (c) Within antiprogestin-treated tumors tenascin-like immunoreactivity predominantly was restricted to fiber-like, collagenous connective tissue structures, which appeared in the stromal compartment as a result of the antiprogestin treatment. In large areas of the tumor composed of apparently secretory active tumor cells we failed to immunolcalize tenascin. Our results provide further evidence that expression of tenascin reflects both benign and malignant proliferative alterations of the tissue, whereas its down-regulation is correlated to differentiation of the tissue. Additionally, evidence is provided that the mechanism of tumor growth inhibition by antiprogestins indeed is induction of terminal differentiation of tumor cells.

1 To whom requests for reprints should be addressed.

Received 1/13/92. Accepted 6/16/92.







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 Cell Growth & Differentiation
Copyright © 1992 by the American Association for Cancer Research.