Evidence map›Paper›PMID 25302503›Full record

ArticlePloS one2014

Circulating AIM as an indicator of liver damage and hepatocellular carcinoma in humans.

Tomoko Yamazaki, Mayumi Mori, Satoko Arai, Ryosuke Tateishi, Masanori Abe, Mihoko Ban, Akemi Nishijima, Maki Maeda, Takeharu Asano, Toshihiro Kai and 14 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 50 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

24 authors at 10 institutions in 1 country.

Tomoko YamazakiLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Mayumi MoriLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Satoko AraiLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Ryosuke TateishiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Masanori AbeDepartment of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Ehime, Japan.
Mihoko BanShunkaikai, Inoue Hospital, Nagasaki, Japan.
Akemi NishijimaLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Maki MaedaShunkaikai, Inoue Hospital, Nagasaki, Japan.
Takeharu AsanoDepartment of Gastroenterology, Jichi Medical University, Saitama Medical Center, Omiya, Japan.
Toshihiro KaiLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Kiyohiro IzuminoShunkaikai, Inoue Hospital, Nagasaki, Japan.
Jun TakahashiShunkaikai, Inoue Hospital, Nagasaki, Japan.
Kayo AoyamaLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Sei HaradaDepartment of Preventive Medicine and Public Health, School of Medicine, Keio University, Tokyo, Japan.
Toru TakebayashiDepartment of Preventive Medicine and Public Health, School of Medicine, Keio University, Tokyo, Japan.
Toshiaki GunjiCenter for Preventive Medicine, NTT Medical Center Tokyo, Tokyo, Japan.
Shin OhnishiNational Center for Global Health and Medicine, Tokyo, Japan.
Shinji SetoShunkaikai, Inoue Hospital, Nagasaki, Japan.
Yukio YoshidaDepartment of Gastroenterology, Jichi Medical University, Saitama Medical Center, Omiya, Japan.
Yoichi HiasaDepartment of Gastroenterology and Metabology, Ehime University Graduate School of Medicine, Ehime, Japan.
Kazuhiko KoikeDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Ken-ichi YamamuraCenter for Animal Resources and Development, Kumamoto University, Kumamoto, Japan.
Ken-ichiro InoueShunkaikai, Inoue Hospital, Nagasaki, Japan.
Toru MiyazakiLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, Japan; Max Planck-The University of Tokyo Center for Integrative Inflammology, Tokyo, Japan; CREST, Japan Science and Technology Agency, Tokyo, Japan.
The University of Tokyo · JPInoue Hospital · JPEhime University · JPKeio University · JPJapan Science and Technology Agency · JPJichi Medical University · JPJichi Medical University Saitama Medical Center · JPKumamoto University · JPNational Center for Global Health and Medicine · JPNTT Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC), the fifth most common cancer type and the third highest cause of cancer death worldwide, develops in different types of liver injuries, and is mostly associated with cirrhosis. However, non-alcoholic fatty liver disease often causes HCC with less fibrosis, and the number of patients with this disease is rapidly increasing. The high mortality rate and the pathological complexity of liver diseases and HCC require blood biomarkers that accurately reflect the state of liver damage and presence of HCC. METHODS AND

findingsHere we demonstrate that a circulating protein, apoptosis inhibitor of macrophage (AIM) may meet this requirement. A large-scale analysis of healthy individuals across a wide age range revealed a mean blood AIM of 4.99 ± 1.8 µg/ml in men and 6.06 ± 2.1 µg/ml in women. AIM levels were significantly augmented in the younger generation (20s-40s), particularly in women. Interestingly, AIM levels were markedly higher in patients with advanced liver damage, regardless of disease type, and correlated significantly with multiple parameters representing liver function. In mice, AIM levels increased in response to carbon tetrachloride, confirming that the high AIM observed in humans is the result of liver damage. In addition, carbon tetrachloride caused comparable states of liver damage in AIM-deficient and wild-type mice, indicating no influence of AIM levels on liver injury progression. Intriguingly, certain combinations of AIM indexes normalized to liver marker score significantly distinguished HCC patients from non-HCC patients and thus could be applicable for HCC diagnosis.

conclusionAIM potently reveals both liver damage and HCC. Thus, our results may provide the basis for novel diagnostic strategies for this widespread and fatal disease.

Indexed as

AdultAgedAnimalsApoptosis Regulatory ProteinsBiomarkers, TumorCarcinoma, HepatocellularFemaleHumansLiverLiver NeoplasmsMaleMiceMiddle AgedReceptors, ScavengerYoung AdultApoptosis Regulatory ProteinsBiomarkers, TumorCD5L protein, humanReceptors, Scavenger

Identifiers

PMID25302503
PMCPMC4193837
OpenAlexW2027562875

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.