Evidence map›Paper›PMID 24677197›Full record

ArticleHepatology (Baltimore, Md.)2014

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

Bryan C Fuchs, Yujin Hoshida, Tsutomu Fujii, Lan Wei, Suguru Yamada, Gregory Y Lauwers, Christopher M McGinn, Danielle K DePeralta, Xintong Chen, Toshihiko Kuroda and 11 more

Open access · hybridAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 papers.

0numbers the graph read from it
0cells of the map it votes in
219citing papers in PubMed
12.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

219 citing papers in PubMed, 358 citations in OpenAlex.

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  11. Chemoprevention of hepatocellular carcinoma.Hepatology communications · 2025
    Review
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  19. Role of PNPLA3 in Hepatic Stellate Cells and Hepatic Cellular Crosstalk.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Review
  20. Article

159 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 4 institutions in 1 country.

Bryan C FuchsDivision of Surgical Oncology, Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA.
Yujin Hoshida
Tsutomu Fujii
Lan Wei
Suguru Yamada
Gregory Y Lauwers
Christopher M McGinn
Danielle K DePeralta
Xintong Chen
Toshihiko Kuroda
Michael Lanuti
Anthony D Schmitt
Supriya Gupta
Andrew Crenshaw
Robert Onofrio
Bradley Taylor
Wendy Winckler
Nabeel Bardeesy
Peter Caravan
Todd R Golub
Kenneth K Tanabe
Massachusetts General Hospital · USHarvard University · USBroad Institute · USIcahn School of Medicine at Mount Sinai · US

Funding

TARGETTING DIFFUSE LIVER METASTASES WITH HERPES VIRUSR01CA076183 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI TANABE, KENNETH K · 2000 to 2010
$3.0M
Molecular Prognostic Indicators in Liver Cirrhosis and CancerR01DK099558 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HOSHIDA, YUJIN · 2013 to 2016
$2.6M
The Role of EGF in Human Hepatocellular TransformationK01CA140861 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI FUCHS, BRYAN CHRISTOPHER · 2009 to 2013
$710k
Howard Hughes Medical InstituteNCI NIH HHS K01 CA140861NCI NIH HHS R01 CA076183NIDDK NIH HHS R01 DK099558
6 · The paper itself

Abstract

unlabelledHepatocellular 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 (CCl4 ), 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.

conclusionThese 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.

Indexed as

Disease ProgressionAnimalsBile DuctsCarbon TetrachlorideCarcinoma, HepatocellularCell ProliferationCells, CulturedDiethylnitrosamineDisease Models, AnimalErbB ReceptorsErlotinib HydrochlorideHepatic Stellate CellsHepatocytesHumansLigationLiver CirrhosisCarbon TetrachlorideDiethylnitrosamineErbB ReceptorsErlotinib HydrochlorideQuinazolines

Identifiers

PMID24677197
PMCPMC4086837
OpenAlexW2069076782

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.