Evidence map›Paper›PMID 20545696›Full record

ArticleCancer science2010

Significance of alternatively activated macrophages in patients with intrahepatic cholangiocarcinoma.

Horlad Hasita, Yoshihiro Komohara, Hirohisa Okabe, Toshiro Masuda, Koji Ohnishi, Xiao F Lei, Toru Beppu, Hideo Baba, Motohiro Takeya

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

158 citing papers in PubMed, 1 synthesis or guideline pooled it, 271 citations in OpenAlex.

  1. Pooled it
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98 more citing papers are in PubMed but not listed here.

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 2 countries.

Horlad HasitaDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Yoshihiro Komohara
Hirohisa Okabe
Toshiro Masuda
Koji Ohnishi
Xiao F Lei
Toru Beppu
Hideo Baba
Motohiro Takeya
Kumamoto University · JPInstitute of Pathology Celle · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many studies have shown that tumor-associated macrophages (TAMs) contribute to tumor development and poor prognosis in various cancers. In this study, we investigated the macrophage populations and phenotypes, and their correlation to angiogenesis, immunosuppression, and clinical prognosis in intrahepatic cholangiocarcinoma (ICC). CD68 (+) and CD163 (+) macrophage infiltration was analyzed in paraffin-embedded tissue samples from 39 patients. CD163 is used as a marker of M2 macrophages. Neovascularization and infiltration of forkhead box P3 (FOXP3) (+) regulatory T cells were also evaluated. The number of CD68 (+) and CD163 (+) macrophages was positively correlated with the numbers of vessels and regulatory T cells. The number of CD163 (+) cells was more closely associated with them. Intrahepatic cholangiocarcinoma (ICC) patients with high counts of CD163 (+) macrophages showed poor disease-free survival (P = 0.0426). The macrophage density was not correlated with overall survival. In an in vitro study using ICC cell lines (HuCCT1, RBE, and MEC) and human macrophages, tumor cell supernatant (TCS) from cell lines induced an activation of signal transducers and activators of transcription-3 (Stat3) and macrophage polarization toward the M2 phenotype. Tumor cell supernatant (TCS) from HuCCT1 most strongly induced Stat3 activation and production of cytokines and other bioactive molecules such as interleukin (IL)-10, vascular endothelial growth factor (VEGF)-A, transforming growth factor (TGF)-beta, and matrix metalloproteinase (MMP)-2. Down-regulation of Stat3 by siRNA significantly suppressed the production of IL-10 and VEGF-A. These results provide suggestive evidence that TAMs contribute to cancer progression via Stat3 activation, and CD163 is useful for evaluating M2 TAMs and predicting the clinical prognosis of ICC patients.

Indexed as

Bile Ducts, IntrahepaticAntigens, CDAntigens, Differentiation, MyelomonocyticBile Duct NeoplasmsCD163 AntigenCD68 MoleculeCell Line, TumorCholangiocarcinomaHumansInterleukin-6Macrophage ActivationMacrophagesPrognosisReceptors, Cell SurfaceSignal TransductionSTAT3 Transcription FactorAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenCD68 antigen, humanCD68 MoleculeInterleukin-6Receptors, Cell SurfaceSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID20545696
PMCPMC11158749
OpenAlexW2003935854

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.