Skip Navigation

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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (7)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Patel, V.
Right arrow Articles by Prime, S.S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Patel, V.
Right arrow Articles by Prime, S.S.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1995 Oxford University Press

research-article

Loss of expression of basement membrane proteins reflects anomalies of chromosomes 3 and 12 in the rat 4-nitroquinoline-N-oxide model of oral carcinogenesis

V. Patel, A.K. Poulopoulos, G. Levan 1, S.M. Game, J.W. Eveson and S.S. Prime 2

Division of Oral Medicine, Pathology and Microbiology, Department of Oral and Dental Science, University of Bristol UK and Bristol BS1 2LY
1Lundberg Laboratory, Department of Genetics, Göteborg University Sweden

2To whom correspondence should be addressed

This study examined the cytogenetic characteristics of keratinocyte cell lines derived from rat oral tissues treated in vivo with the carcinogen 4-nitroquinoline-N-oxide. A parent tumour with a spectrum of differentiation was used to establish clonal subpopulations that formed differentiated (squamous cell carcinomas; SCCs) and undifferentiated (spindle cell phenotype) tumours following transplantation to athymic mice. By contrast to spindle cell tumours, SCCs elaborated basement membrane proteins (laminin and collagen TV). Both diploid and tetraploid subpopulations formed either SCCs or spindle cell tumours. An unbalanced 10q+ translocation was common to all cell lines. Anomalies of chromosomes 3 and 12 (gain, loss, deletions, translocations) were present only in cell lines that formed spindle cell tumours and were absent in keratinocytes forming SCCs. The results suggest that proto-oncogenes and/or tumour suppression genes located to rat chromosomes 3 and 12 may control tumour cell differentiation.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.