Evidence map›Paper›PMID 41088408›Full record

ArticleBreast cancer research : BCR2025

Carcinomas exhibiting epithelial-mesenchymal transition manifest an M2 macrophage-enriched tumor immune microenvironment.

Huang-Chun Lien, Yu-Chia Li, Ruby Yun-Ju Huang, Ko-Chen Chen, Tom Wei-Wu Chen, I-Chun Chen, Li-Ping Hsiao, Ling-Chun Yeh, Yen-Shen Lu

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Article in Breast cancer research : BCR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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3citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Huang-Chun LienDepartment of Pathology, National Taiwan University Hospital, Taipei, Taiwan.
Yu-Chia LiGraduate Institute of Pathology, National Taiwan University, Taipei, Taiwan.
Ruby Yun-Ju HuangSchool of Medicine, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Ko-Chen ChenSchool of Medicine, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Tom Wei-Wu ChenDepartment of Oncology, National Taiwan University Hospital, Taipei, Taiwan.
I-Chun ChenDepartment of Medical Oncology, National Taiwan University Cancer Center Hospital, Taipei, Taiwan.
Li-Ping HsiaoDepartment of Oncology, National Taiwan University Hospital, Taipei, Taiwan.
Ling-Chun YehDepartment of Oncology, National Taiwan University Hospital, Taipei, Taiwan.
Yen-Shen LuDepartment of Oncology, National Taiwan University Hospital, Taipei, Taiwan. yslu@ntu.edu.tw.

Funding

Excellent Translational Medicine Research Projects of National Taiwan University College of Medicine and National Taiwan University Hospital 110C101-034 and 111C101-24National Science and Technology Council of Taiwan MOST 109-2320-B-002-036-MY2 and 110-2314-B-002-218
6 · The paper itself

Abstract

backgroundEpithelial-mesenchymal transition (EMT) is linked to an immunosuppressive tumor microenvironment (TME). However, direct comparisons of the TME in paired tumor regions with and without EMT in primary tumors-essential for elucidating EMT's impact on the TME-are still lacking.

methodsUsing Digital Spatial Profiler (DSP) assay and NanoString nCounter Digital Profiling, we analyzed immune-oncology-related markers in the TME of no special type (NST) and paired spindle carcinomatous (SPS) components, the later considered the EMT counterpart of the former, in nine cases of metaplastic breast carcinoma, a type of mammary carcinosarcoma.

resultsWe identified macrophage markers as consistently and significantly enriched immune-oncology-related proteins within the TME profiles of SPS components compared to their paired NST counterparts. Additionally, we observed notable enrichment of macrophage-related signatures, M2 macrophage phenotypes, M2 macrophage-inducing cytokines, and M2 macrophage-related genes, as key distinctions in the TME profiles of SPS components relative to NST counterparts. Immunohistochemistry and multiplex immunofluorescence confirmed the presence of M2 macrophages, predominantly characterized by CD14

conclusionsGiven the immunosuppressive role of M2 macrophages, our findings suggest that an EMT-driven, M2 macrophage-enriched TME-a consistent phenomenon across organs-can contribute to immune suppression. This underscores the therapeutic potential of macrophage-targeting strategies and immune checkpoint inhibition in treating aggressive carcinosarcomas characterized by EMT-mediated, M2 macrophage-rich TMEs.

Indexed as

Breast NeoplasmsEpithelial-Mesenchymal TransitionMacrophagesTumor-Associated MacrophagesTumor MicroenvironmentAnimalsBiomarkers, TumorFemaleGene Expression Regulation, NeoplasticHumansMiceBiomarkers, Tumor

Identifiers

PMID41088408
PMCPMC12522275

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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.