Evidence map›Paper›PMID 27471651›Full record

ArticleOncoimmunology2016

A novel role of breast cancer-derived hyaluronan on inducement of M2-like tumor-associated macrophages formation.

Guoliang Zhang, Lin Guo, Cuixia Yang, Yiwen Liu, Yiqing He, Yan Du, Wenjuan Wang, Feng Gao

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 92 citations in OpenAlex.

  1. NFAT1Cellular & molecular biology letters · 2026
    Article
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  3. Overcoming resistance to anti-PD-1/PD-L1 therapy in cancer.Cancer drug resistance (Alhambra, Calif.) · 2026
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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

8 authors at 3 institutions in 1 country.

Guoliang ZhangDepartment of Molecular Biology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai, P. R. China.
Lin GuoDepartment of clinical Laboratory, Shanghai Oncology Hospital, Shanghai Fudan University School of Medicine , Shanghai, P. R. China.
Cuixia YangDepartment of Molecular Biology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai, P. R. China.
Yiwen LiuDepartment of Molecular Biology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai, P. R. China.
Yiqing HeDepartment of Molecular Biology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai, P. R. China.
Yan DuDepartment of Molecular Biology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai, P. R. China.
Wenjuan WangDepartment of Molecular Biology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai, P. R. China.
Feng GaoDepartment of Molecular Biology and Clinical Laboratory, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai, P. R. China.
Shanghai Sixth People's Hospital · CNShanghai Jiao Tong University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microenvironmental signals determine the differentiation types and distinct functions of macrophages. Tumor-associated macrophages (TAM) constitute major infiltrates around solid tumor cells and accelerate tumor progression due to their immunosuppressive functions. However, the mechanisms through which tumor microenvironment modulates macrophages transition are not completely elucidated. Hyaluronan (HA), a prominent component in tumor microenvironment, is a notable immunoregulator and its high level is often related to poor prognosis. Herein, we found that the number of M2 macrophages was highly correlated with HA expression in tumor tissues from breast cancer patients. Experimental data showed that breast cancer-derived HA stimulated M2-like TAM formation in a mouse model and had multiple effects on macrophages transformation in vitro, including upregulating CD204, CD206, IL-10 and TGF-β, activating STAT3 signal, and suppressing killing capacity. These data indicate that HA derived from breast cancer activates macrophages in an alternative manner. Further mechanism study revealed that HA-CD44-ERK1/2-STAT3 pathway served as an important regulator in M2-like TAM formation. Therefore, targeting TAM by abrogating HA-CD44 interaction may be a potential strategy for breast cancer immunotherapy.

Indexed as

Breast cancerCD44ERK1/2hyaluronanSTAT3tumor-associated macrophages

Identifiers

PMID27471651
PMCPMC4938366
OpenAlexW2343597033

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.