Evidence map›Paper›PMID 25940505›Full record

ArticleCancer science2015

Chemokine (C-C motif) ligand 3 detection in the serum of persons exposed to asbestos: A patient-based study.

Jiegou Xu, David B Alexander, Masaaki Iigo, Hirokazu Hamano, Satoru Takahashi, Takako Yokoyama, Munehiro Kato, Ikuji Usami, Takeshi Tokuyama, Masahiro Tsutsumi and 17 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 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

27 authors at 11 institutions in 2 countries.

Jiegou XuNanotoxicology Project, Nagoya City University, Nagoya, Japan.
David B AlexanderNanotoxicology Project, Nagoya City University, Nagoya, Japan.
Masaaki IigoNanotoxicology Project, Nagoya City University, Nagoya, Japan.
Hirokazu HamanoNutritional Science Institute, Morinaga Milk Industry Co., Ltd., Zama, Japan.
Satoru TakahashiDepartment of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Takako YokoyamaDepartment of Respiratory Medicine, Asahi Rosai Hospital, Owariasahi, Japan.
Munehiro KatoDepartment of Respiratory Medicine, Asahi Rosai Hospital, Owariasahi, Japan.
Ikuji UsamiDepartment of Respiratory Medicine, Asahi Rosai Hospital, Owariasahi, Japan.
Takeshi TokuyamaDepartment of Internal Medicine, Saiseikai Chuwa Hospital, Sakura, Japan.
Masahiro TsutsumiDepartment of Pathology, Saiseikai Chuwa Hospital, Sakura, Japan.
Mouka TamuraDepartment of Internal Medicine, Nara Medical Center, National Hospital Organization, Nara, Japan.
Tetsuya OguriDiivision of Respiratory Medicine, Allergy and Rheumatology, Nagoya City University Hospital, Nagoya, Japan.
Akio NiimiDiivision of Respiratory Medicine, Allergy and Rheumatology, Nagoya City University Hospital, Nagoya, Japan.
Yoshimitsu HayashiDepartment of Medicine, Nagoya-Shi Koseiin Medical Welfare Center, Nagoya, Japan.
Yoshifumi YokoyamaDepartment of Medicine, Nagoya-Shi Koseiin Medical Welfare Center, Nagoya, Japan.
Ken TonegawaDepartment of Physical Medicine and Rehabilitation, Nagoya-Shi Koseiin Medical Welfare Center, Nagoya, Japan.
Katsumi FukamachiDepartment of Molecular Toxicology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Mitsuru FutakuchiDepartment of Molecular Toxicology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Yuto SakaiDepartment of Molecular Toxicology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Masumi SuzuiDepartment of Molecular Toxicology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Michihiro KamijimaDepartment of Occupational and Environmental Health, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Naomi HisanagaCenter for Campus Health and Environment, Aichi University of Education, Kariya, Japan.
Toyonori OmoriDepartment of Health Care Policy and Management, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Dai NakaeDepartment of Nutritional Science and Food Safety, Faculty of Applied Biosciences, Tokyo University of Agriculture, Tokyo, Japan.
Akihiko HiroseDivision of Risk Assessment, Biological Safety Research Center, Biological Safety Research Center, National Institute of Health Sciences, Tokyo, Japan.
Jun KannoDivision of Cellular and Molecular Toxicology, Biological Safety Research Center, National Institute of Health Sciences, Tokyo, Japan.
Hiroyuki TsudaNanotoxicology Project, Nagoya City University, Nagoya, Japan.
Nagoya City University · JPJapan Organization of Occupational Health and Safety · JPNagoya Medical Center · JPJikei University Kashiwa hospital · JPNational Institute of Health Sciences · JPAichi University of Education · JPAnhui Medical University · CNMegmilk Snow Brand (Japan) · JPNagoya City University Hospital · JPNational Hospital Organization · JPTokyo University of Agriculture · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure to asbestos results in serious risk of developing lung and mesothelial diseases. Currently, there are no biomarkers that can be used to diagnose asbestos exposure. The purpose of the present study was to determine whether the levels or detection rate of chemokine (C-C motif) ligand 3 (CCL3) in the serum are elevated in persons exposed to asbestos. The primary study group consisted of 76 healthy subjects not exposed to asbestos and 172 healthy subjects possibly exposed to asbestos. The secondary study group consisted of 535 subjects possibly exposed to asbestos and diagnosed with pleural plaque (412), benign hydrothorax (10), asbestosis (86), lung cancer (17), and malignant mesothelioma (10). All study subjects who were possibly exposed to asbestos had a certificate of asbestos exposure issued by the Japanese Ministry of Health, Labour and Welfare. For the primary study group, levels of serum CCL3 did not differ between the two groups. However, the detection rate of CCL3 in the serum of healthy subjects possibly exposed to asbestos (30.2%) was significantly higher (P < 0.001) than for the control group (6.6%). The pleural plaque, benign hydrothorax, asbestosis, and lung cancer groups had serum CCL3 levels and detection rates similar to that of healthy subjects possibly exposed to asbestos. The CCL3 chemokine was detected in the serum of 9 of the 10 patients diagnosed with malignant mesothelioma. Three of the patients with malignant mesothelioma had exceptionally high CCL3 levels. Malignant mesothelioma cells from four biopsy cases and an autopsy case were positive for CCL3, possibly identifying the source of the CCL3 in the three malignant mesothelioma patients with exceptionally high serum CCL3 levels. In conclusion, a significantly higher percentage of healthy persons possibly exposed to asbestos had detectable levels of serum CCL3 compared to healthy unexposed control subjects.

Indexed as

Environmental ExposureAdultAgedAsbestosBiomarkers, TumorCarcinogensCase-Control StudiesChemokine CCL3FemaleHumansLung NeoplasmsMaleMesotheliomaMesothelioma, MalignantMiddle AgedAsbestosBiomarkers, TumorCarcinogensCCL3 protein, humanChemokine CCL3Asbestosbiological markerschemokine CCL3Environmental carcinogensmesothelioma

Identifiers

PMID25940505
PMCPMC4520633
OpenAlexW1974000304

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Registered trials

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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.