Evidence map›Paper›PMID 39286635›Full record

ReviewFrontiers in pharmacology2024

Unveiling the contribution of tumor-associated macrophages in driving epithelial-mesenchymal transition: a review of mechanisms and therapeutic Strategies.

Yijia Zhang, Xiaofei Ding, Xue Zhang, Ye Li, Rui Xu, Hai-Jun Li, Daiying Zuo, Guang Chen

Abstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

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

  1. Pooled it
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  3. Platelets as regulators of cancer immunity: mechanisms and therapeutic perspectives.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 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.

Yijia ZhangDepartment of Pharmacy, Taizhou Second People's Hospital (Mental Health Center affiliated to Taizhou University School of Medicine), Taizhou University, Taizhou, Zhejiang, China.
Xiaofei DingDepartment of Pharmacology, Taizhou University, Taizhou, Zhejiang, China.
Xue ZhangDepartment of Pharmacology, Shenyang Pharmaceutical University, Shenyang, China.
Ye LiDepartment of Pharmacology, Shenyang Pharmaceutical University, Shenyang, China.
Rui XuDepartment of Pharmacology, Shenyang Pharmaceutical University, Shenyang, China.
Hai-Jun LiDepartment of Pharmacy, Taizhou Second People's Hospital (Mental Health Center affiliated to Taizhou University School of Medicine), Taizhou University, Taizhou, Zhejiang, China.
Daiying ZuoDepartment of Pharmacology, Shenyang Pharmaceutical University, Shenyang, China.
Guang ChenDepartment of Pharmacy, Taizhou Second People's Hospital (Mental Health Center affiliated to Taizhou University School of Medicine), Taizhou University, Taizhou, Zhejiang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-associated macrophages (TAMs), fundamental constituents of the tumor microenvironment (TME), significantly influence cancer development, primarily by promoting epithelial-mesenchymal transition (EMT). EMT endows cancer cells with increased motility, invasiveness, and resistance to therapies, marking a pivotal juncture in cancer progression. The review begins with a detailed exposition on the origins of TAMs and their functional heterogeneity, providing a foundational understanding of TAM characteristics. Next, it delves into the specific molecular mechanisms through which TAMs induce EMT, including cytokines, chemokines and stromal cross-talking. Following this, the review explores TAM-induced EMT features in select cancer types with notable EMT characteristics, highlighting recent insights and the impact of TAMs on cancer progression. Finally, the review concludes with a discussion of potential therapeutic targets and strategies aimed at mitigating TAM infiltration and disrupting the EMT signaling network, thereby underscoring the potential of emerging treatments to combat TAM-mediated EMT in cancer. This comprehensive analysis reaffirms the necessity for continued exploration into TAMs' regulatory roles within cancer biology to refine therapeutic approaches and improve patient outcomes.

Indexed as

CSF1R, colony-stimulating factor 1 receptorECM, extracellular matrixEMT, epithelialmesenchymal transitionTAM, tumor associated macrophageTME, tumor microenvironment

Identifiers

PMID39286635
PMCPMC11402718

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.