Evidence map›Paper›PMID 27197745›Full record

ArticleThe British journal of radiology2016

Hepatocyte nuclear factor 1α-inactivated hepatocellular adenomas exhibit high (18)F-fludeoxyglucose uptake associated with glucose-6-phosphate transporter inactivation.

Kumi Ozaki, Kenichi Harada, Noboru Terayama, Osamu Matsui, Satoshi Saitoh, Yoshito Tomimaru, Takeshi Fujii, Toshifumi Gabata

Open access · greenAbstract read
In one paragraph

Article in The British journal of radiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
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.

Kumi Ozaki1 Department of Radiology, Takaoka City Hospital, Takaoka, Japan.
Kenichi HaradaDepartment of Human Pathology, Kanazawa University Graduate School of Medicine, Kanazawa, Japan.
Noboru Terayama1 Department of Radiology, Takaoka City Hospital, Takaoka, Japan.
Osamu MatsuiDepartment of Radiology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Satoshi SaitohDepartment of Hepatology, Toranomon Hospital, Tokyo, Japan.
Yoshito TomimaruDepartment of Surgery, Toyonaka Municipal Hospital, Toyonaka, Japan.
Takeshi FujiiDepartment of Pathology, Toranomon Hospital, Tokyo, Japan.
Toshifumi GabataDepartment of Radiology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Kanazawa University · JPToranomon Hospital · JPKouseiren Takaoka Hospital · JPToyonaka Municipal Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis immunohistochemical study aimed to elucidate the molecular mechanism underlying the increased fluorine-18 fludeoxyglucose (FDG) uptake in hepatocyte nuclear factor 1α (HNF1α)-inactivated hepatocellular adenomas (H-HCAs).

methodsThree resected H-HCAs were studied using FDG positron emission tomography. Each maximum standardized uptake value (SUVmax) was determined. Resected samples were subjected to immunohistochemical staining for the following glucose metabolism-related proteins: glucose transporter 1 (GLUT1) and glucose transporter 2 (GLUT2), indicative of uptake and transport of glucose into cellular cytoplasm; hexokinase 2 (HK2) and hexokinase 4 (HK4), glucose phosphorylation; glucose-6-phosphate transporter 1 (G6PT1), uptake and transport of glucose-6-phosphate into endoplasmic reticulum; and glucose-6-phosphatase (G6Pase), dephosphorylation.

resultsAll three H-HCAs exhibited increased FDG intake, with an average SUVmax of 6.6 (range: 5.2-8.2). No sample expressed GLUT1 and HK2; all the samples exhibited equivalent GLUT2 and HK4 expression, equivalent or slightly increased G6Pase expression and significantly decreased G6PT1 expression relative to the non-neoplastic hepatocytes of background liver.

conclusionThe increased FDG uptake observed in H-HCAs is associated with GLUT2 and HK4 expression and G6PT1 inactivation. ADVANCES IN KNOWLEDGE: H-HCA exhibits a high FDG uptake owing to the inactivation of G6PT1, which is transcriptionally regulated by HNF1α.

Indexed as

Positron-Emission TomographyAdenoma, Liver CellAdultAntiportersFemaleFluorodeoxyglucose F18Hepatocyte Nuclear Factor 1-alphaHumansLiver NeoplasmsMiddle AgedMonosaccharide Transport ProteinsRadiopharmaceuticalsRetrospective StudiesAntiportersFluorodeoxyglucose F18glucose 6-phosphate(transporter)Hepatocyte Nuclear Factor 1-alphaMonosaccharide Transport ProteinsRadiopharmaceuticals

Identifiers

PMID27197745
PMCPMC5257333
OpenAlexW2404756104

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.