Evidence map›Paper›PMID 25294808›Full record

ArticleOncotarget2014

Epigenetic signatures of alcohol abuse and hepatitis infection during human hepatocarcinogenesis.

Ryan A Hlady, Rochelle L Tiedemann, William Puszyk, Ivan Zendejas, Lewis R Roberts, Jeong-Hyeon Choi, Chen Liu, Keith D Robertson

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.7field-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

51 citing papers in PubMed, 97 citations in OpenAlex.

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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

8 authors at 4 institutions in 1 country.

Ryan A HladyDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA.
Rochelle L TiedemannDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA. Cancer Center, Georgia Regents University, Augusta, GA, USA.
William PuszykDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL, USA.
Ivan ZendejasDepartment of Surgery, University of Florida, Gainesville, FL, USA.
Lewis R RobertsDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA.
Jeong-Hyeon ChoiCancer Center, Georgia Regents University, Augusta, GA, USA.
Chen LiuDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL, USA.
Keith D RobertsonDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA.
University of Florida · USAugusta University · USMayo Clinic · USMayo Clinic in Arizona · US

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI Felicity Enders · 1985 to 2026
$151.3M
Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
Developmental pathways, environmental agents, and epigenetics in liver diseaseR01AA019976 · NIAAA · MAYO CLINIC ROCHESTER · PI LIU, CHEN, ROBERTSON, KEITH D · 2011 to 2015
$3.0M
NIAAA NIH HHS R01 AA019976NIAAA NIH HHS R01 AA19976
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is the second most common cause of cancer deaths worldwide. Deregulated DNA methylation landscapes are ubiquitous in human cancers. Interpretation of epigenetic aberrations in HCC is confounded by multiple etiologic drivers and underlying cirrhosis. We globally profiled the DNA methylome of 34 normal and 122 liver disease tissues arising in settings of hepatitis B (HBV) or C (HCV) viral infection, alcoholism (EtOH), and other causes to examine how these environmental agents impact DNA methylation in a manner that contributes to liver disease. Our results demonstrate that each 'exposure' leaves unique and overlapping signatures on the methylome. CpGs aberrantly methylated in cirrhosis-HCV and conserved in HCC were enriched for cancer driver genes, suggesting a pathogenic role for HCV-induced methylation changes. Additionally, large genomic regions displaying stepwise hypermethylation or hypomethylation during disease progression were identified. HCC-HCV/EtOH methylomes overlap highly with cryptogenic HCC, suggesting shared epigenetically deregulated pathways for hepatocarcinogenesis. Finally, overlapping methylation abnormalities between primary and cultured tumors unveil conserved epigenetic signatures in HCC. Taken together, this study reveals profound epigenome deregulation in HCC beginning during cirrhosis and influenced by common environmental agents. These results lay the foundation for defining epigenetic drivers and clinically useful methylation markers for HCC.

Indexed as

AlcoholismCarcinogenesisCarcinoma, HepatocellularCell Line, TumorDNA MethylationEpigenesis, GeneticFemaleHepatitisHepatitis BHepatitis CHumansLiverLiver CirrhosisLiver NeoplasmsMale

Identifiers

PMID25294808
PMCPMC4253444
OpenAlexW1529159877

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.