Document Detail


Genotype-phenotype relationships in hepatocellular tumors from mice and man.
MedLine Citation:
PMID:  15965925     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Experimentally induced liver tumors in mice harbor activating mutations in either Catnb (beta-catenin) or Ha-ras, according to the carcinogenic treatment. We have now investigated by microarray analysis the gene expression profiles in tumors of the two genotypes. In total, 364 genes or expressed sequences with aberrant expression relative to normal liver were identified, but only 30 of these demonstrated unidirectional changes in both tumor types. Several functional clusters were identified that involve changes in amino acid utilization and ammonia disposition in Catnb-mutated tumors as opposed to alterations in lipid and cholesterol metabolism in Ha-ras-mutated tumors. Moreover, several genes coding for inhibitory molecules within the Wnt-signaling pathway were upregulated in Catnb-mutated tumors, suggesting induction of a negative feedback loop, whereas Ha-ras-mutated tumors showed alterations in the expression of several genes functional in monomeric G-protein signaling. We conclude that mouse hepatoma cells adopt different evolutionary strategies that allow for their selective outgrowth under variable environmental conditions. Human hepatocellular cancers (HCC) lack RAS mutations but are frequently mutated in CTNNB1, the human Catnb ortholog. The set of genes aberrantly expressed in Catnb-mutated mouse tumors was used to screen, by expression profiling, for dysregulation of orthologous genes within a panel of 25 HCCs, of which 10 were CTNNB1-mutated. HCCs with activated beta-catenin displayed a gene expression profile that was similar to Catnb-mutated mouse tumors but distinct from the other human HCCs. In conclusion, expression fingerprints may be used for diagnostic purposes and potential new therapeutic intervention strategies. Supplementary material for this article can be found on the HEPATOLOGY website (http://www.interscience.wiley.com/jpages/0270-9139/suppmat/index/html).
Authors:
Sabine Stahl; Carina Ittrich; Philip Marx-Stoelting; Christoph Köhle; Ozge Altug-Teber; Olaf Riess; Michael Bonin; Jürgen Jobst; Stephan Kaiser; Albrecht Buchmann; Michael Schwarz
Related Documents :
20154675 - Germline mutations in tmem127 confer susceptibility to pheochromocytoma.
7923195 - P16 alterations and deletion mapping of 9p21-p22 in malignant mesothelioma.
19909015 - Combined analysis of smoking, tp53, and fgfr3 mutations in tunisian patients with invas...
9592195 - Detection of ras gene mutations in peripheral blood of carcinoma patients using cd45 im...
6088735 - Definition of hepatic tumor microcirculation by single photon emission computerized tom...
20361945 - Notch signaling: emerging molecular targets for cancer therapy.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Hepatology (Baltimore, Md.)     Volume:  42     ISSN:  0270-9139     ISO Abbreviation:  Hepatology     Publication Date:  2005 Aug 
Date Detail:
Created Date:  2005-07-21     Completed Date:  2005-08-18     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8302946     Medline TA:  Hepatology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  353-61     Citation Subset:  IM    
Affiliation:
Institut für Pharmakologie und Toxikologie, Abteilung Toxikologie, Universität Tübingen, Wilhelmstrasse 56, 72074 Tübingen, Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Carcinoma, Hepatocellular / genetics*
Cytoskeletal Proteins / genetics*
Gene Expression Profiling
Genes, ras*
Genotype
Glutamate-Ammonia Ligase / genetics
Humans
Liver Neoplasms / genetics*
Male
Mice
Mice, Inbred C3H
Mutation
Phenotype
Signal Transduction
Trans-Activators / genetics*
beta Catenin
Chemical
Reg. No./Substance:
0/CTNNB1 protein, human; 0/Catnb protein, mouse; 0/Cytoskeletal Proteins; 0/Trans-Activators; 0/beta Catenin; EC 6.3.1.2/Glutamate-Ammonia Ligase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  An education for the future.
Next Document:  The modular microarchitecture of human liver.