Evidence map›Paper›PMID 36535346›Full record

ReviewPharmacology & therapeutics2023

DNA methylation in cell plasticity and malignant transformation in liver diseases.

Minwook Kim, Evan Delgado, Sungjin Ko

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Acetaminophen-induced acute liver injury abrogates the cytosine methylation pathway.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Article
  2. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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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 1 institution in 1 country.

Minwook KimDepartment of Developmental Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States of America.
Evan DelgadoDepartment of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States of America; Pittsburgh Liver Research Center, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States of America.
Sungjin KoDepartment of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States of America; Pittsburgh Liver Research Center, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States of America. Electronic address: sungjin@pitt.edu.
University of Pittsburgh · US

Funding

Pittsburgh Liver Research CenterP30DK120531 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Shuchang Silvia Liu · 2019 to 2026
$10.9M
Identifying therapeutic options for intrahepatic cholangiocarcinomaR01CA258449 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KO, SUNGJIN · 2021 to 2025
$1.6M
NCI NIH HHS R01 CA258449NIDDK NIH HHS P30 DK120531
6 · The paper itself

Abstract

The liver possesses extraordinary regenerative capacity mainly attributable to the ability of hepatocytes (HCs) and biliary epithelial cells (BECs) to self-replicate. This ability is left over from their bipotent parent cell, the hepatoblast, during development. When this innate regeneration is compromised due to the absence of proliferative parenchymal cells, such as during cirrhosis, HCs and BEC can transdifferentiate; thus, adding another layer of complexity to the process of liver repair. In addition, dysregulated lineage maintenance in these two cell populations has been shown to promote malignant growth in experimental conditions. Here, malignant transformation, driven in part by insufficient maintenance of lineage reprogramming, contributes to end-stage liver disease. Epigenetic changes are key drivers for cell fate decisions as well as transformation by finetuning overall transcription and gene expression. In this review, we address how altered DNA methylation contributes to the initiation and progression of hepatic cell fate conversion and cancer formation. We also discussed the diagnostic and therapeutic potential of targeting DNA methylation in liver cancer, its current limitations, and what future research is necessary to facilitate its contribution to clinical translation.

Indexed as

Cell PlasticityLiver NeoplasmsCell ProliferationDNA MethylationHumansLiverCellular reprogrammingCholangiocarcinomaEpigeneticsHepatocellular carcinomaLiver progenitor cellTransdifferentiation

Identifiers

PMID36535346
PMCPMC9841769
OpenAlexW4313479829

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.