Evidence map›Paper›PMID 40380196›Full record

ReviewJournal of experimental & clinical cancer research : CR2025

Tumor-associated macrophages remodel the suppressive tumor immune microenvironment and targeted therapy for immunotherapy.

Yan Yang, Sijia Li, Kenneth K W To, Shuangli Zhu, Fang Wang, Liwu Fu

Abstract readReview
In one paragraph

Review in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

132 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  6. From signals to phenotype: multifactorial drivers of tumor-associated macrophage polarization in oral cavity squamous cell carcinoma: a narrative review.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026
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  9. Macrophage PABPC4-SPP1 Axis Orchestrates Immunosuppression in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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72 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

6 authors.

Yan YangState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, P. R. China.
Sijia LiState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, P. R. China.
Kenneth K W ToSchool of Pharmacy, The Chinese University of Hong Kong, Hong Kong, 999077, P.R. China.
Shuangli ZhuState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, P. R. China.
Fang WangState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, P. R. China.
Liwu FuState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, P. R. China. fulw@mail.sysu.edu.cn.

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2023B1515130009Key-Area Research and Development Program of Guangdong Province 2023B1111020005National Natural Science Foundation of China U21A20421the Key Project of Science Technology Program of Guangzhou 2023B03J0029
6 · The paper itself

Abstract

Despite the significant advances in the development of immune checkpoint inhibitors (ICI), primary and acquired ICI resistance remains the primary impediment to effective cancer immunotherapy. Residing in the tumor microenvironment (TME), tumor-associated macrophages (TAMs) play a pivotal role in tumor progression by regulating diverse signaling pathways. Notably, accumulating evidence has confirmed that TAMs interplay with various cellular components within the TME directly or indirectly to maintain the dynamic balance of the M1/M2 ratio and shape an immunosuppressive TME, consequently conferring immune evasion and immunotherapy tolerance. Detailed investigation of the communication network around TAMs could provide potential molecular targets and optimize ICI therapies. In this review, we systematically summarize the latest advances in understanding the origin and functional plasticity of TAMs, with a focus on the key signaling pathways driving macrophage polarization and the diverse stimuli that regulate this dynamic process. Moreover, we elaborate on the intricate interplay between TAMs and other cellular constituents within the TME, that is driving tumor initiation, progression and immune evasion, exploring novel targets for cancer immunotherapy. We further discuss current challenges and future research directions, emphasizing the need to decode TAM-TME interactions and translate preclinical findings into clinical breakthroughs. In conclusion, while TAM-targeted therapies hold significant promise for enhancing immunotherapy outcomes, addressing key challenges-such as TAM heterogeneity, context-dependent plasticity, and therapeutic resistance-remains critical to achieving optimal clinical efficacy.

Indexed as

ImmunotherapyNeoplasmsTumor-Associated MacrophagesTumor MicroenvironmentAnimalsHumansMolecular Targeted TherapyImmune checkpoint inhibitorsImmune evasionImmunotherapyTumor-associated macrophagesTumor microenvironment

Identifiers

PMID40380196
PMCPMC12083052

What OpenQuestion holds

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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.