Skip to main content
  • AACR Publications
    • Blood Cancer Discovery
    • Cancer Discovery
    • Cancer Epidemiology, Biomarkers & Prevention
    • Cancer Immunology Research
    • Cancer Prevention Research
    • Cancer Research
    • Clinical Cancer Research
    • Molecular Cancer Research
    • Molecular Cancer Therapeutics

AACR logo

  • Register
  • Log in
  • Log out
  • My Cart
Advertisement

Main menu

  • Home
  • About
    • The Journal
    • AACR Journals
    • Subscriptions
    • Permissions and Reprints
    • Reviewing
  • Articles
    • OnlineFirst
    • Current Issue
    • Past Issues
    • Meeting Abstracts
    • Collections
      • COVID-19 & Cancer Resource Center
      • Focus on Computer Resources
      • Highly Cited Collection
      • Editors' Picks
      • "Best of" Collection
  • For Authors
    • Information for Authors
    • Author Services
    • Early Career Award
    • Best of: Author Profiles
    • Submit
  • Alerts
    • Table of Contents
    • Editors' Picks
    • OnlineFirst
    • Citations
    • Author/Keyword
    • RSS Feeds
    • My Alert Summary & Preferences
  • News
    • Cancer Discovery News
  • COVID-19
  • Webinars
  • Search More

    Advanced Search

  • AACR Publications
    • Blood Cancer Discovery
    • Cancer Discovery
    • Cancer Epidemiology, Biomarkers & Prevention
    • Cancer Immunology Research
    • Cancer Prevention Research
    • Cancer Research
    • Clinical Cancer Research
    • Molecular Cancer Research
    • Molecular Cancer Therapeutics

User menu

  • Register
  • Log in
  • Log out
  • My Cart

Search

  • Advanced search
Cancer Research
Cancer Research
  • Home
  • About
    • The Journal
    • AACR Journals
    • Subscriptions
    • Permissions and Reprints
    • Reviewing
  • Articles
    • OnlineFirst
    • Current Issue
    • Past Issues
    • Meeting Abstracts
    • Collections
      • COVID-19 & Cancer Resource Center
      • Focus on Computer Resources
      • Highly Cited Collection
      • Editors' Picks
      • "Best of" Collection
  • For Authors
    • Information for Authors
    • Author Services
    • Early Career Award
    • Best of: Author Profiles
    • Submit
  • Alerts
    • Table of Contents
    • Editors' Picks
    • OnlineFirst
    • Citations
    • Author/Keyword
    • RSS Feeds
    • My Alert Summary & Preferences
  • News
    • Cancer Discovery News
  • COVID-19
  • Webinars
  • Search More

    Advanced Search

Regular Articles

Transgenic Mice Overexpressing a Dominant-negative Mutant Type II Transforming Growth Factor β Receptor Show Enhanced Tumorigenesis in the Mammary Gland and Lung in Response to the Carcinogen 7,12-Dimethylbenz-[a]-anthracene

Erwin P. Böttinger, John L. Jakubczak, Diana C. Haines, Kerri Bagnall and Lalage M. Wakefield
Erwin P. Böttinger
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
John L. Jakubczak
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Diana C. Haines
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Kerri Bagnall
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Lalage M. Wakefield
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
DOI:  Published December 1997
  • Article
  • Info & Metrics
  • PDF
Loading

Abstract

To test the hypothesis that the transforming growth factor-β (TGF-β) system has tumor suppressor activity in the mammary gland, we have generated transgenic mice overexpressing a dominant-negative mutant form of the type II TGF-β receptor, under the control of the mouse mammary tumor virus-long terminal repeat. High-level expression of the transgene was observed in the mammary and salivary glands, with lower expression in the lung, spleen, and testis. Older nulliparous transgenic mice (9–17 months) showed a marked increase in the incidence and degree of lobulo-alveolar side-branching in the mammary glands when compared to wild-type littermates (24.8% of glands examined histologically versus 14.4%; P = 0.004), suggesting a role for endogenous TGF-βs in regulating development or maintenance of mammary alveoli. Spontaneous tumorigenesis was unchanged in the transgenic mice. However, following initiation with the carcinogen 7,12-dimethylbenz[a]anthracene, the transgenic group showed a significant increase in the incidence and multiplicity of mammary tumors when compared with wild-type littermates (40% incidence in transgenic mice versus 22% for wild-type, with 4 of 25 transgenics developing multiple mammary tumors versus 0 of 27 wild-type; P = 0.03). An early increase in the incidence of lung tumors was also observed in transgenic mice, but no difference between genotype groups was seen in the incidence of tumors in tissues in which the transgene is not expressed. The data show that the endogenous TGF-β system has tumor suppressor activity in the mammary gland and lung.

Footnotes

  • ↵2 To whom requests for reprints should be addressed, at Laboratory of Chemoprevention, Building 41, Room C629, 41 Library Drive, MSC 5055, Bethesda, MD 20892-5055. Phone: (301) 496-8351; Fax: (301) 496-8395; E-mail: wakefiel@dce41.nci.nih.gov.

  • Received July 7, 1997.
  • Accepted October 15, 1997.
  • ©1997 American Association for Cancer Research.
PreviousNext
Back to top
December 1997
Volume 57, Issue 24
  • Table of Contents
  • Table of Contents (PDF)
  • Back Matter (PDF)
  • Editorial Board (PDF)
  • Front Matter (PDF)

Sign up for alerts

Open full page PDF
Article Alerts
Sign In to Email Alerts with your Email Address
Email Article

Thank you for sharing this Cancer Research article.

NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses.

Enter multiple addresses on separate lines or separate them with commas.
Transgenic Mice Overexpressing a Dominant-negative Mutant Type II Transforming Growth Factor β Receptor Show Enhanced Tumorigenesis in the Mammary Gland and Lung in Response to the Carcinogen 7,12-Dimethylbenz-[a]-anthracene
(Your Name) has forwarded a page to you from Cancer Research
(Your Name) thought you would be interested in this article in Cancer Research.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Transgenic Mice Overexpressing a Dominant-negative Mutant Type II Transforming Growth Factor β Receptor Show Enhanced Tumorigenesis in the Mammary Gland and Lung in Response to the Carcinogen 7,12-Dimethylbenz-[a]-anthracene
Erwin P. Böttinger, John L. Jakubczak, Diana C. Haines, Kerri Bagnall and Lalage M. Wakefield
Cancer Res December 15 1997 (57) (24) 5564-5570;

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Share
Transgenic Mice Overexpressing a Dominant-negative Mutant Type II Transforming Growth Factor β Receptor Show Enhanced Tumorigenesis in the Mammary Gland and Lung in Response to the Carcinogen 7,12-Dimethylbenz-[a]-anthracene
Erwin P. Böttinger, John L. Jakubczak, Diana C. Haines, Kerri Bagnall and Lalage M. Wakefield
Cancer Res December 15 1997 (57) (24) 5564-5570;
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
  • Info & Metrics
  • PDF
Advertisement

Related Articles

Cited By...

More in this TOC Section

Regular Articles

  • Ornithine Decarboxylase Induction in Transformation by H-Ras and RhoA
  • Recombinant Humanized Anti-HER2 Antibody (Herceptin™) Enhances the Antitumor Activity of Paclitaxel and Doxorubicin against HER2/neu Overexpressing Human Breast Cancer Xenografts
  • Diosmin and Diosmetin Are Agonists of the Aryl Hydrocarbon Receptor That Differentially Affect Cytochrome P450 1A1 Activity
Show more Regular Articles

Tumor Biology

  • Abstract 6119: RNAi rat models for drug discovery
  • Abstract 2723: XIAOPI formula inhibits breast cancer pre-metastatic niche formation via blocking TAMs/CXCL1 pathway
  • Abstract 3834: Histone methyltransferase SET8 is regulated by miR-192/-215 and induces oncogene-induced senescence via p53-dependent DNA damage in human gastric carcinoma cells
Show more Tumor Biology

Articles

  • Abstract 6119: RNAi rat models for drug discovery
  • Abstract 2723: XIAOPI formula inhibits breast cancer pre-metastatic niche formation via blocking TAMs/CXCL1 pathway
  • Abstract 3834: Histone methyltransferase SET8 is regulated by miR-192/-215 and induces oncogene-induced senescence via p53-dependent DNA damage in human gastric carcinoma cells
Show more Articles
  • Home
  • Alerts
  • Feedback
  • Privacy Policy
Facebook  Twitter  LinkedIn  YouTube  RSS

Articles

  • Online First
  • Current Issue
  • Past Issues
  • Meeting Abstracts

Info for

  • Authors
  • Subscribers
  • Advertisers
  • Librarians

About Cancer Research

  • About the Journal
  • Editorial Board
  • Permissions
  • Submit a Manuscript
AACR logo

Copyright © 2021 by the American Association for Cancer Research.

Cancer Research Online ISSN: 1538-7445
Cancer Research Print ISSN: 0008-5472
Journal of Cancer Research ISSN: 0099-7013
American Journal of Cancer ISSN: 0099-7374

Advertisement