Evidence map›Paper›PMID 22378017›Full record

ReviewHepatology (Baltimore, Md.)2012

Fibrosis-dependent mechanisms of hepatocarcinogenesis.

David Y Zhang, Scott L Friedman

Open access · bronzeAbstract readReview
In one paragraph

Review in Hepatology (Baltimore, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers.

0numbers the graph read from it
0cells of the map it votes in
229citing papers in PubMed
15.2field-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

229 citing papers in PubMed, 442 citations in OpenAlex.

  1. Article
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  4. Review
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  13. Review
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  15. Article
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  17. Observational
  18. Article
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169 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

David Y ZhangDivision of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA.
Scott L Friedman
Icahn School of Medicine at Mount Sinai · US

Funding

MOUNT SINAI MEDICAL SCIENTIST TRAINING PROGRAMT32GM007280 · NIGMS · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BARON, MARGARET H · 1985 to 2021
$22.8M
The Role of KLF6 in Hepatic FibrosisR01DK056621 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI FRIEDMAN, SCOTT L. · 2000 to 2019
$6.2M
THE ROLE OF STELLATE CELLS IN HEPATIC FIBROSISR01DK037340 · NIDDK · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI FRIEDMAN, SCOTT L. · 1987 to 2010
$3.5M
Project 2P20AA017067 · NIAAA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FRIEDMAN, SCOTT L. · 2008 to 2012
$2.5M
Mentoring Junior Faculty in Alcoholic Liver DiseaseK05AA018408 · NIAAA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FRIEDMAN, SCOTT L. · 2009 to 2013
$1.1M
NIAAA NIH HHS K05 AA018408NIAAA NIH HHS K05AA018408NIAAA NIH HHS P20 AA017067NIAAA NIH HHS P20AA017067NIDDK NIH HHS R01 DK037340NIDDK NIH HHS R01 DK056621NIDDK NIH HHS R01DK56621NIGMS NIH HHS T32 GM007280NIGMS NIH HHS T32-GM007280
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a rising worldwide cause of cancer mortality, making the elucidation of its underlying mechanisms an urgent priority. The liver is unique in its response to injury, simultaneously undergoing regeneration and fibrosis. HCC occurs in the context of these two divergent responses, leading to distinctive pathways of carcinogenesis. In this review we highlight pathways of liver tumorigenesis that depend on, or are enhanced by, fibrosis. Activated hepatic stellate cells drive fibrogenesis, changing the composition of the extracellular matrix. Matrix quantity and stiffness also increase, providing a reservoir for bound growth factors. In addition to promoting angiogenesis, these factors may enhance the survival of both preneoplastic hepatocytes and activated hepatic stellate cells. Fibrotic changes also modulate the activity of inflammatory cells in the liver, reducing the activity of natural killer and natural killer T cells that normally contribute to tumor surveillance. These pathways synergize with inflammatory signals, including telomerase reactivation and reactive oxygen species release, ultimately resulting in cancer. Clarifying fibrosis-dependent tumorigenic mechanisms will help rationalize antifibrotic therapies as a strategy to prevent and treat HCC.

Indexed as

AnimalsCarcinoma, HepatocellularHumansLiver CirrhosisLiver Neoplasms

Identifiers

PMID22378017
PMCPMC4087159
OpenAlexW2068149517

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.