Evidence map›Paper›PMID 22681639›Full record

ArticleLiver international : official journal of the International Association for the Study of the Liver2012

Up-regulated aldo-keto reductase family 1 member B10 in chronic hepatitis C: association with serum alpha-fetoprotein and hepatocellular carcinoma.

Shunsuke Sato, Takuya Genda, Katsuharu Hirano, Hironori Tsuzura, Yutaka Narita, Yoshio Kanemitsu, Tetsu Kikuchi, Katsuyori Iijima, Ryo Wada, Takafumi Ichida

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In one paragraph

Article in Liver international : official journal of the International Association for the Study of the Liver, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 28% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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  12. Immunohistochemistry Detects Increased Expression of Aldo-Keto Reductase Family 1 Member B10 (AKR1B10) in Early-Stage Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2018
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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

10 authors at 1 institution in 1 country.

Shunsuke SatoDepartment of Gastroenterology and Hepatology, Juntendo University Shizuoka Hospital, Shizuoka, Japan.
Takuya Genda
Katsuharu Hirano
Hironori Tsuzura
Yutaka Narita
Yoshio Kanemitsu
Tetsu Kikuchi
Katsuyori Iijima
Ryo Wada
Takafumi Ichida
Juntendo University Shizuoka Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundElevated serum alpha-fetoprotein (AFP) is not only a diagnostic marker for hepatocellular carcinoma (HCC), but is also a risk factor for HCC in chronic hepatitis C patients who do not have HCC.

aimThe aim was to analyse the hepatic gene expression signature in chronic hepatitis C patients with elevated AFP, who were at high risk for HCC.

methodsLiver tissue samples from 48 chronic hepatitis C patients were stratified by their serum AFP levels and analysed for gene expression profiles. The association between aldo-keto reductase family 1 member B10 (AKR1B10) expression and serum AFP was confirmed by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) and immunohistochemical analyses. A matched case-control study was performed to evaluate the risk of AKR1B10 expression for HCC development.

resultsDistinct hepatic gene expression patterns were demonstrated in patients with elevated AFP (≥10 ng/mL) and normal AFP (<10 ng/mL). Of the 627 differently expressed genes, the most abundantly expressed gene in patients with elevated AFP was AKR1B10 (fold change, 26.2; P < 0.001), which was originally isolated as an overexpressed gene in human HCC. The qRT-PCR and immunohistochemical studies confirmed a proportional correlation between AKR1B10 expression and serum AFP. A matched case-control study identified that AKR1B10 up-regulation (>6%) was an independent risk factor for HCC development (hazard ratio, 21.4; P = 0.001).

conclusionAKR1B10 was up-regulated in association with serum AFP, and was an independent risk factor for HCC in chronic hepatitis C patients, suggesting its possible involvement at a very early stage of hepatocarcinogenesis.

Indexed as

AdultAgedAldehyde ReductaseAldo-Keto Reductasesalpha-FetoproteinsBiomarkers, TumorCarcinoma, HepatocellularCase-Control StudiesFemaleGene Expression ProfilingGene Expression Regulation, EnzymologicHepatitis C, ChronicHumansImmunohistochemistryLiverLiver NeoplasmsAKR1B10 protein, humanAldehyde ReductaseAldo-Keto Reductasesalpha-FetoproteinsBiomarkers, Tumor

Identifiers

PMID22681639
PMCPMC3466415
OpenAlexW1986622713

What OpenQuestion holds

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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.