JCB logo
amgmicro.com
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
This Article
Right arrow Full Text (PDF, 7559K)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Stocklin, E.
Right arrow Articles by Groner, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Stocklin, E.
Right arrow Articles by Groner, B.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

The Journal of Cell Biology, Vol 122, 199-208, Copyright © 1993 by The Rockefeller University Press

ARTICLES

An activated allele of the c-erbB-2 oncogene impairs kidney and lung function and causes early death of transgenic mice

E Stocklin, F Botteri and B Groner
Friedrich Miescher Institute, Basel, Switzerland.

The pathogenicity of the human c-erbB-2 oncogene was evaluated in transgenic mice. A DNA sequence comprising the promoter-enhancer region of the MMTV LTR and a constitutively activated allele of the human c- erbB-2 growth factor receptor gene was introduced into the germ line of mice. Expression of the transgene was observed in kidney, lung, mammary gland, salivary gland, Harderian gland, and in epithelial cells of the male reproductive tract. All transgenic mice expressing the c-erbB-2 receptor died within four months of birth. Histopathological analysis suggests that preneoplastic lesions in kidney and lung most likely caused organ failure and the early death of the transgenic mice. Focal dilatation and atypical proliferation of the tubular epithelial cells was found in the kidney. These hyperplastic lesions were found adjacent to normal tubules. Immunohistochemistry showed that normal renal structures were completely negative for c-erbB-2 protein expression. Atypical pseudopapillary proliferation of bronchial and bronchiolar epithelial cells narrowed the bronchial lumen in lung. Alveoli appeared normal. The expression of c-erbB-2 protein was strictly limited to the proliferating epithelial cells and not detected in normal tissue. The mammary glands of two parous mice were underdeveloped, lacking lobular- alveolar structures and were lactation deficient. Only a few ducts were interspersed in the fat pad. A virgin mouse developed a focal adenocarcinoma infiltrating the mammary fat pad. Expression of the c- erbB-2 protein was enhanced in the proliferating epithelial cells. Transgenic males were sterile. Epithelial hyperplasia and hypertrophy in the epididymis, vas deferens and seminal vesicles was found. The transgene is not uniformly expressed in the tissues where the MMTV LTR is transcriptionally active. The scattered transgene expression invariably coincides with epithelial hyperplasia.
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents