Evidence map›Paper›PMID 40707476›Full record

ReviewCell death discovery2025

Cancer-associated fibroblasts in cancer drug resistance and cancer progression: a review.

Hideyuki Masuda

Abstract readReview
In one paragraph

Review in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing 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

50 citing papers in PubMed.

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  4. Engineering the next generation of cellular therapies for solid tumors: multi-specific armored CARs and TME reprogramming strategies.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

1 author.

Hideyuki MasudaResearch Institute of Pharmaceutical Sciences, Faculty of Pharmacy, Musashino University, Tokyo, Japan. h-masuda@musashino-u.ac.jp.ORCID http://orcid.org/0009-0006-5335-6205

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although cancer treatment saves many lives, some types of cancer, such as pancreatic ductal adenocarcinoma (PDAC), exhibit therapeutic resistance and continue to show high mortality. Tumors in cancers such as PDAC contain a substantial amount of cancer-associated fibroblast (CAF)-secreted collagen and other extracellular matrix (ECM) components, which significantly contribute to cancer therapeutic resistance. In the tumor microenvironment, CAFs stabilize the tissue by producing ECM components, remodel ECM through degradation, induce metastasis through epithelial-mesenchymal transition, and suppress cancer immune responses. Recent advances in single-cell analysis have gradually elucidated the subtypes of CAFs and their functions, leading to the emergence of CAF-targeting therapeutic strategies. In this review, I provide an overview of CAFs, their functions and classifications, the mechanisms underlying their role in therapeutic resistance, and the current status of CAF-targeting therapeutic strategies. Moreover, I explored how we can advance cancer treatment by leveraging our understanding of CAFs.

Identifiers

PMID40707476
PMCPMC12289933

What OpenQuestion 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 OpenQuestion graph.