Evidence map›Paper›PMID 41444607›Full record

ReviewCell communication and signaling : CCS2025

Cancer-associated fibroblasts: central players in cancer hallmarks and therapeutic resistance.

Yuanjun Lu, Ya Wu, Xiaoyu Xu, Yibin Feng, Ning Wang

Abstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
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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

5 authors.

Yuanjun LuSichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, University of Electronic Science and Technology of China, Chengdu, China.
Ya WuSichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, University of Electronic Science and Technology of China, Chengdu, China.
Xiaoyu XuSchool of Chinese Medicine, the University of Hong Kong, Hong Kong S.A.R, China.
Yibin FengSchool of Chinese Medicine, the University of Hong Kong, Hong Kong S.A.R, China.
Ning WangSchool of Chinese Medicine, the University of Hong Kong, Hong Kong S.A.R, China. ckwang@hku.hk.

Funding

Outstanding youth fund of Sichuan Cancer Hospital YB2024011Sichuan Science and Technology Program 2024YFHZ0366
6 · The paper itself

Abstract

The tumour microenvironment (TME) is now recognized as pivotal to cancer progression and treatment outcomes, alongside cancer cell-intrinsic factors. Among TME constitute, cancer-associated fibroblasts (CAFs) are abundant and actively shape tumour biology. They are heterogenous population arising from multiple origins, and engage in dynamic crosstalk with cancer cells and immune infiltrates to promote virtually all the hallmarks of cancer. By influencing and reinforcement of cancer hallmark traits, CAFs create a pro-tumorigenic niche that also protects cancer cells from therapy, in this way, conferring resistance to conventional therapy. Consequently, CAFs have emerged as central players linking cancer hallmarks to therapeutic resistance. This review discusses the origins and phenotypic diversity of CAFs, the mechanisms of their communication with tumour and immune cells, and how these interactions enforce hallmark capabilities of cancer that underlie treatment resistance. We also highlight preclinical and clinical evidence for CAF-driven drug resistance and examine current strategies to target CAFs or their effects. A deeper understanding of CAF heterogeneity and function could pave the way for novel combination therapies that dismantle the tumour-CAF alliance and improve patient outcomes.

Indexed as

Cancer-Associated FibroblastsDrug Resistance, NeoplasmNeoplasmsAnimalsCell CommunicationHumansTumor MicroenvironmentCancer-associated fibroblastCancer hallmarksTherapeutic resistanceTumour heterogenicityTumour microenvironment

Identifiers

PMID41444607
PMCPMC12729356

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.