Evidence mapPaperPMID 41704419Full record

ReviewFrontiers in cell and developmental biology2025

Unveiling the tumor microenvironment in colorectal cancer therapeutic resistance.

Jiyu Han, Weitian Liang, Kai Li

Abstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
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

9 citing papers in PubMed.

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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

3 authors.

Jiyu HanEditorial Department of "Progress of Anatomical Sciences", China Medical University Journal Center, Shenyang, China.
Weitian LiangDepartment of Intensive Care Medicine, The First Affiliated Hospital of China Medical University, Shenyang, China.
Kai LiDepartment of Oncology Surgery, The First Affiliated Hospital of China Medical University, Shenyang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Therapeutic resistance remains a major barrier to effective treatment in colorectal cancer (CRC), where the tumor microenvironment (TME) plays a pivotal role in modulating responses to chemotherapy, immunotherapy, and targeted therapies. This review synthesizes current evidence on how cellular and non-cellular TME components contribute to resistance mechanisms in CRC. Key immune cells, including T cells, macrophages, neutrophils, natural killer cells, dendritic cells, and myeloid-derived suppressor cells, orchestrate immunosuppressive networks that impair drug efficacy. For instance, regulatory T cells and M2-polarized macrophages promote chemoresistance via cytokine secretion and metabolic reprogramming, while neutrophils and myeloid-derived suppressor cells hinder immune checkpoint blockade through extracellular trap formation and T-cell exhaustion. Non-cellular elements, such as extracellular matrix remodeling, hypoxia-induced metabolic shifts, and dysregulated cytokines like IL-6 and TGF-β, further exacerbate resistance by fostering epithelial-mesenchymal transition and angiogenesis. Tables highlight specific molecular axes and therapeutic implications. By elucidating these interactions, this article underscores the potential of TME-targeted strategies, such as macrophage reprogramming, cytokine inhibition, and combination therapies, to overcome resistance and improve clinical outcomes in CRC patients. Future research should prioritize integrating TME biomarkers for personalized treatment approaches.

Indexed as

chemotherapycolorectal cancerdrug resistanceimmunotherapytargeted therapyTIMETME

Identifiers

PMID41704419
PMCPMC12907415

What Socratic holds

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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.