spacer gif spacer gif spacer gif spacer gif spacer gif
QUICK SEARCH:   [advanced]


spacer gif
     Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents    

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 Weinberg, W. C.
Right arrow Articles by Iannaccone, P. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Weinberg, W. C.
Right arrow Articles by Iannaccone, P. M.

Journal of Cell Science, Vol 89, Issue 3 423-431, Copyright © 1988 by Company of Biologists

JOURNAL ARTICLES

Clonality of preneoplastic liver lesions: histological analysis in chimeric rats

WC Weinberg and PM Iannaccone
Northwestern University Medical School, Department of Pathology, Northwestern University Cancer Center, Chicago, IL 60611.

The clonality of chemically induced altered hepatocellular foci was examined in rat liver. Chimeric rats composed of two histologically distinguishable cell lineages were placed on an initiation-promotion protocol for liver cancer induction. This resulted in multiple lesions of altered enzyme expression. These altered hepatocellular foci are generally considered to be initiated sites susceptible to cancer formation. The cellular origins of these lesions were determined by aligning sections demonstrating cell lineage with serial sections stained for altered enzyme expression. Analysis included 110 areas of deficient ATPase (EC 3.6.1.3) activity and 59 glucose-6-phosphatase (EC 3.1.3.9; G-6-Pase) deficient lesions, 744 foci of re-expression of gamma-glutamyl transpeptidase (EC 2.3.2.2; gamma-GT), and decreased glycogen mobilization (187 lesions). Of the 1100 focal enzyme alterations, 1054 were shown to be composed entirely of cells from a single lineage of the two lineages present in the mosaic tissue. Multiple alterations occurred within given lesions. Lesions with up to four phenotypic alterations were found to consist of cells of a single lineage. These results suggest that individual enzyme-altered foci are clonal in origin and that phenotypic heterogeneity within altered hepatocellular foci is due to lesion progression within a clonal population and not to a multicellular derivation.




© The Company of Biologists Ltd 1988