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Cited by 351

The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.

Epidermal growth factor receptor inhibition attenuates liver fibrosis and development of hepatocellular carcinoma

Open access
Fuchs, Bryan C., Hoshida, Yujin, Fujii, Tsutomu, Wei, Lan, Yamada, Suguru, Lauwers, Gregory Y., McGinn, Christopher M., DePeralta, Danielle K., Chen, Xintong, Kuroda, Toshihiko, Lanuti, Michael, Schmitt, Anthony D., Gupta, Supriya, Crenshaw, Andrew, Onofrio, Robert, Taylor, Bradley, Winckler, Wendy, Bardeesy, Nabeel, Caravan, Peter, Golub, Todd R., Tanabe, Kenneth K.·2014·Hepatology

Abstract

Hepatocellular carcinoma (HCC) is the most rapidly increasing cause of cancer-related mortality in the United States. Because of the lack of viable treatment options for HCC, prevention in high-risk patients has been proposed as an alternative strategy. The main risk factor for HCC is cirrhosis and several lines of evidence implicate epidermal growth factor (EGF) in the progression of cirrhosis and development of HCC. We therefore examined the effects of the EGF receptor (EGFR) inhibitor erlotinib on liver fibrogenesis and hepatocellular transformation in three different animal models of progressive cirrhosis: a rat model induced by repeated, low-dose injections of diethylnitrosamine (DEN), a mouse model induced by carbon tetrachloride (CCl 4), and a rat model induced by bile duct ligation (BDL). Erlotinib reduced EGFR phosphorylation in hepatic stellate cells (HSC) and reduced the total number of activated HSC. Erlotinib also decreased hepatocyte proliferation and liver injury. Consistent with all these findings, pharmacological inhibition of EGFR signaling effectively prevented the progression of cirrhosis and regressed fibrosis in some animals. Moreover, by alleviating the underlying liver disease, erlotinib blocked the development of HCC and its therapeutic efficacy could be monitored with a previously reported gene expression signature predictive of HCC risk in human cirrhosis patients. Conclusion: These data suggest that EGFR inhibition using Food and Drug Administration-approved inhibitors provides a promising therapeutic approach for reduction of fibrogenesis and prevention of HCC in high-risk cirrhosis patients who can be identified and monitored by gene expression signatures. (HEPATOLOGY 2014;59:1577-1590)

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Metadata

Authors
Fuchs, B. C., Hoshida, Y., Fujii, T., Wei, L., Yamada, S., Lauwers, G. Y., McGinn, C. M., DePeralta, D. K., Chen, X., Kuroda, T., Lanuti, M., Schmitt, A. D., Gupta, S., Crenshaw, A., Onofrio, R., Taylor, B., Winckler, W., Bardeesy, N., Caravan, P., Golub, T. R., & Tanabe, K. K.
Venue
Hepatology
Published
2014-04
Volume
59
Issue
4
Pages
1577-1590
ISSN
0270-9139 (ISSN-L)
OpenAlex
W2069076782
Cited by
351
References
37
FWCI
15.23
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Epidermal growth factor receptor inhibition attenuates liver fibrosis and development of hepatocellular carcinoma. https://app.cochat.ai/papers/10.1002/hep.26898
The paper
Fuchs, B. C., Hoshida, Y., Fujii, T., Wei, L., Yamada, S., Lauwers, G. Y., McGinn, C. M., DePeralta, D. K., Chen, X., Kuroda, T., Lanuti, M., Schmitt, A. D., Gupta, S., Crenshaw, A., Onofrio, R., Taylor, B., Winckler, W., Bardeesy, N., Caravan, P., . . . Tanabe, K. K. (2014). Epidermal growth factor receptor inhibition attenuates liver fibrosis and development of hepatocellular carcinoma. Hepatology. https://doi.org/10.1002/hep.26898

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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