Evidence map›Paper›PMID 35243280›Full record

ReviewJHEP reports : innovation in hepatology2022

Cellular origins of regenerating liver and hepatocellular carcinoma.

Ágnes Holczbauer, Kirk J Wangensteen, Soona Shin

Open access · goldAbstract readReview
In one paragraph

Review in JHEP reports : innovation in hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 42 citations in OpenAlex.

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  11. Targeting Metabolism: Innovative Therapies for MASLD Unveiled.International journal of molecular sciences · 2025
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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

3 authors at 2 institutions in 1 country.

Ágnes HolczbauerDivision of Gastroenterology and Hepatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Kirk J WangensteenDivision of Gastroenterology and Hepatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Soona ShinLiver Tumor Program, Division of Pediatric General and Thoracic Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
University of Pennsylvania · USCincinnati Children's Hospital Medical Center · US

Funding

Pathogenic Role of Foxl1+ Hepatic Progenitor Cells in Fibrotic Liver DiseaseR37CA225807 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI SHIN, SOONA · 2019 to 2025
$2.5M
Elucidation of TNFR pathway components that regulate liver repopulationR03DK123543 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI WANGENSTEEN, KIRK J · 2020 to 2021
$243k
NCI NIH HHS R37 CA225807NIDDK NIH HHS R03 DK123543
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is the predominant primary cancer arising from the liver and is one of the major causes of cancer-related mortality worldwide. The cellular origin of HCC has been a topic of great interest due to conflicting findings regarding whether it originates in hepatocytes, biliary cells, or facultative stem cells. These cell types all undergo changes during liver injury, and there is controversy about their contribution to regenerative responses in the liver. Most HCCs emerge in the setting of chronic liver injury from viral hepatitis, fatty liver disease, alcohol, and environmental exposures. The injuries are marked by liver parenchymal changes such as hepatocyte regenerative nodules, biliary duct cellular changes, expansion of myofibroblasts that cause fibrosis and cirrhosis, and inflammatory cell infiltration, all of which may contribute to carcinogenesis. Addressing the cellular origin of HCC is the key to identifying the earliest events that trigger it. Herein, we review data on the cells of origin in regenerating liver and HCC and the implications of these findings for prevention and treatment. We also review the origins of childhood liver cancer and other rare cancers of the liver.

Indexed as

BEC, biliary epithelial cellcarcinogenesisCCl4, carbon tetrachlorideCDE, choline-deficient, ethionine-supplementedDDC, 3,5-diethoxicarbonyl-1,4-dihydrocollidineDEN, diethylnitrosamineEpCAM, epithelial cell adhesion moleculeFah, fumarylacetoacetate hydrolaseFLC, fibrolamellar carcinomaFoxl1, forkhead box L1HB, hepatoblastomaHBV, hepatitis B virusHCA, hepatocellular adenomaHCC, hepatocellular carcinomaHCV, hepatitis C virusHDTVI, hydrodynamic tail vein injectionHepatocellular carcinomahepatocyteHNF, hepatocyte nuclear factorHPC, hepatic progenitor cellHybHP, hybrid hepatocyteICC, intrahepatic cholangiocarcinomaKrt19, cytokeratin 19lineage tracingNASH, non-alcoholic steatohepatitisOPN, osteopontinPH, partial hepatectomyprogenitor cellSox9, SRY-box 9TAA, thioacetamide

Identifiers

PMID35243280
PMCPMC8873941
OpenAlexW4200254979

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.