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Toxicologic Pathology
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Hepatic Temporal Gene Expression Profiling in Helicobacter hepaticus-Infected A/JCr Mice

Samuel R. Boutin

Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA, Division of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA

Arlin B. Rogers

Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA

Zeli Shen

Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA

Rebecca C. Fry

Computational and Systems Biology Initiative, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA

Jennifer A. Love

Whitehead Institute For Biomedical Research, Cambridge, Massachusetts 02139, USA

Prashant R. Nambiar

Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA

Sebastian Suerbaum

Institute of Medical Microbiology and Hospital Epidemiology, Hannover Medical School, Hannover, Germany

James G. Fox

Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA, jgfox@ mit.edu

Helicobacter hepaticus infection of A/JCr mice is a model of infectious liver cancer. We monitored hepatic global gene expression profiles in H. hepaticus infected and control male A/JCr mice at 3 months, 6 months, and 1 year of age using an Affymetrix-based oligonucleotide microarray platform on the premise that a specific genetic expression signature at isolated time points would be indicative of disease status. Model based expression index comparisons generated by dChip yielded consistent profiles of differential gene expression for H. hepaticus infected male mice with progressive liver disease versus uninfected control mice within each age group. Linear discriminant analysis and principal component analysis allowed segregation of mice based on combined age and lesion status, or age alone. Up-regulation of putative tumor markers correlated with advancing hepatocellular dysplasia. Transcriptionally down-regulated genes in mice with liver lesions included those related to peroxisome proliferator, fatty acid, and steroid metabolism pathways. In conclusion, transcriptional profiling of hepatic genes documented gene expression signatures in the livers of H. hepaticus infected male A/JCr mice with chronic progressive hepatitis and preneoplastic liver lesions, complemented the histopathological diagnosis, and suggested molecular targets for the monitoring and intervention of disease progression prior to the onset of hepatocellular neoplasia.

Key Words: Microarray • hepatitis • chronic • carcinoma • hepatocellular • mice • inbred • Helicobacter.

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Toxicologic Pathology, Vol. 32, No. 6, 678-693 (2004)
DOI: 10.1080/01926230490524058
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