Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.


The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Internet Explorer is no longer a supported browser.

This website may not display properly with Internet Explorer. For the best experience, please use a more recent browser such as the latest versions of Google Chrome, Microsoft Edge, and/or Mozilla Firefox. Thank you.

COVID-19 is an emerging, rapidly evolving situation.

Get the latest public health information from CDC. Get the latest research information from NIH.

Your Environment. Your Health.

University of North Carolina-Chapel Hill: Dataset Details, ID=GSE71849

Superfund Research Program

Elucidating Risks: From Exposure and Mechanism to Outcome

Center Director: Rebecca C. Fry
Grant Number: P42ES005948
Funding Period: 1992-2018
View this project in the NIH Research Portfolio Online Reporting Tools (RePORT)

Learn More About the Grantee

Visit the grantee's eNewsletter page Visit the grantee's Twitter page Visit the grantee's Video page

Title: Mouse frozen liver: vehicle-control vs. CCl4+DEN treated

Accession Number: GSE71849

Link to Dataset:

Repository: Gene Expression Omnibus (GEO)

Data Type(s): Gene Expression

Experiment Type(s): Genome variation profiling by genome tiling array

Organism(s): Mus musculus

Summary: Hepatocellular carcinoma (HCC) is a prevalent human cancer with rising incidence worldwide. Human HCC is frequently associated with chronic liver inflammation and cirrhosis, pathophysiological processes that are a consequence of chronic viral infection, disturbances in metabolism, or exposure to chemical toxicants. To better characterize the pathogenesis of HCC, we used a human disease-relevant mouse model of fibrosis-associated hepatocarcinogenesis. In this model, marked liver tumor response caused by a pro-mutagenic chemical N-nitrosodiethylamine in presence of liver fibrosis was associated with epigenetic events indicative of genomic instability. Therefore, we hypothesized that DNA copy number alterations (CNAs), a feature of genomic instability and a common characteristic of cancer, are concordant between human HCC and mouse models of fibrosis-associated hepatocarcinogenesis. We evaluated DNA CNAs and changes in gene expression in the mouse liver (normal, tumor and non-tumor cirrhotic tissues). In addition, we compared our findings to those in human HCC (tumor and non-tumor cirrhotic/fibrotic tissues). We observed that while fibrotic liver tissue is largely devoid of DNA CNAs, highly frequently occurring DNA CNAs are found in mouse tumors, which is indicative of a profound increase in chromosomal instability in HCC. When compared to CNAs in human HCC, we found that 33% of genes in these segments are similarly affected in the mouse tumors. Our results suggest that CNAs most commonly arise in neoplastic tissue rather than in fibrotic liver, and demonstrate the utility of this mouse model in replicating the molecular features of human HCC.

Publication(s) associated with this dataset:
  • Chappell G, Silva GO, Uehara T, Pogribny IP, Rusyn I. 2016. Characterization of copy number alterations in a mouse model of fibrosis-associated hepatocellular carcinoma reveals concordance with human disease. Cancer Med 5(3):574-585. doi:10.1002/cam4.606 PMID:26778414 PMCID:PMC4799957
to Top