Evidence map›Paper›PMID 29744335›Full record

ArticleHepatobiliary surgery and nutrition2018

Detection of a lipid peroxidation-induced DNA adduct across liver disease stages.

Heidi Coia, Ning Ma, Aiwu Ruth He, Bhaskar Kallakury, Deborah L Berry, Eva Permaul, Kepher H Makambi, Ying Fu, Fung-Lung Chung

Open access · hybridAbstract read
In one paragraph

Article in Hepatobiliary surgery and nutrition, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed, 14 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

9 authors at 2 institutions in 1 country.

Heidi CoiaDepartment of Biochemistry & Molecular Biology, Georgetown University Medical Center, Washington, DC, USA.
Ning MaDepartment of Biochemistry & Molecular Biology, Georgetown University Medical Center, Washington, DC, USA.
Aiwu Ruth HeDepartment of Oncology, Bioinformatics, and Biomathematics, Georgetown University, Washington, DC, USA.
Bhaskar KallakuryDepartment of Pathology, Lombardi Comprehensive Cancer Center, Bioinformatics, and Biomathematics, Georgetown University, Washington, DC, USA.
Deborah L BerryDepartment of Oncology, Bioinformatics, and Biomathematics, Georgetown University, Washington, DC, USA.
Eva PermaulDepartment of Oncology, Bioinformatics, and Biomathematics, Georgetown University, Washington, DC, USA.
Kepher H MakambiDepartment of Biostatistics, Bioinformatics, and Biomathematics, Georgetown University, Washington, DC, USA.
Ying FuDepartment of Oncology, Bioinformatics, and Biomathematics, Georgetown University, Washington, DC, USA.
Fung-Lung ChungDepartment of Biochemistry & Molecular Biology, Georgetown University Medical Center, Washington, DC, USA.
Georgetown University · USGeorgetown University Medical Center · US

Funding

Mechanisms of obesity-induced hepatocarcinogenesisR01CA190678 · NCI · GEORGETOWN UNIVERSITY · PI CHUNG, FUNG-LUNG, TANG, ERIC MOON-SHONG M. · 2015 to 2019
$1.8M
NCI NIH HHS R01 CA190678
6 · The paper itself

Abstract

backgroundOxidative stress and chronic inflammation can increase cellular levels of reactive oxygen species and lipid peroxidation (LPO) when associated with the pathogenesis of hepatocellular carcinoma (HCC), which can develop following the progression of steatosis, fibrosis and cirrhosis. Using a monoclonal antibody for cyclic γ-hydroxy-1,

methodsFormalin-fixed paraffin embedded (FFPE) liver tissue samples from 49 patients representing normal, steatosis, fibrosis, cirrhosis and HCC were stained for γ-OHPdG and 8-hydroxydeoxyguanosine (8-oxo-dG), an oxidative damage biomarker. Quantification of immunohistochemical (IHC) staining was performed using histological scoring of intensity and distribution. Using primary human hepatocytes (HH) and a stellate cell (SC) co-culture, immunocytochemical staining of γ-OHPdG and Nile Red was performed to determine if the formation of γ-OHPdG was consistent between the clinical sample disease stages and the

resultsγ-OHPdG levels varied significantly between the stages of normal and steatosis, steatosis and fibrosis, and steatosis and cirrhosis (P≤0.005). There was a trend, although not significant, of increased levels of γ-OHPdG in HCC compared to the other groups. A strong correlation was observed (Pearson's, R

conclusionsγ-OHPdG was detected in FFPE liver tissues of patients with different stages of liver disease and

Indexed as

cirrhosisfibrosishepatocellular carcinoma (HCC)N2-propanodeoxyguanosine (γ-OHPdG)steatosisγ-hydroxy-1

Identifiers

PMID29744335
PMCPMC5934137
OpenAlexW2747395172

What OpenQuestion holds

Textmetadata
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.