Evidence map›Paper›PMID 39534084›Full record

ReviewFrontiers in pharmacology2024

Decoding tumor-fibrosis interplay: mechanisms, impact on progression, and innovative therapeutic strategies.

Huiguang Chen, Xuexin Xu, Jingxian Li, Yu Xue, Xin Li, Kaiyu Zhang, Haihui Jiang, Xiaoliu Liu, Mingzhe Li

Abstract readReview
PubMed Full text at PMC Publisher
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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Review
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  7. 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

9 authors.

Huiguang Chen *Institute of Infection, Immunology, and Tumor Microenvironment, School of Medicine, Wuhan University of Science and Technology, Wuhan, China.
Xuexin Xu *Institute of Infection, Immunology, and Tumor Microenvironment, School of Medicine, Wuhan University of Science and Technology, Wuhan, China.
Jingxian Li *Institute of Infection, Immunology, and Tumor Microenvironment, School of Medicine, Wuhan University of Science and Technology, Wuhan, China.
Yu XueInstitute of Infection, Immunology, and Tumor Microenvironment, School of Medicine, Wuhan University of Science and Technology, Wuhan, China.
Xin LiInstitute of Infection, Immunology, and Tumor Microenvironment, School of Medicine, Wuhan University of Science and Technology, Wuhan, China.
Kaiyu ZhangInstitute of Infection, Immunology, and Tumor Microenvironment, School of Medicine, Wuhan University of Science and Technology, Wuhan, China.
Haihui JiangInstitute of Infection, Immunology, and Tumor Microenvironment, School of Medicine, Wuhan University of Science and Technology, Wuhan, China.
Xiaoliu LiuInstitute of Infection, Immunology, and Tumor Microenvironment, School of Medicine, Wuhan University of Science and Technology, Wuhan, China.
Mingzhe LiDepartment of Anatomy, School of Medicine, Wuhan University of Science and Technology, Wuhan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant tumors are a category of diseases that possess invasive and metastatic capabilities, with global incidence and mortality rates remaining high. In recent years, the pivotal role of fibrosis in tumor progression, drug resistance, and immune evasion has increasingly been acknowledged. Fibrosis enhances the proliferation, migration, and invasion of tumor cells by modifying the composition and structure of the extracellular matrix, thereby offering protection for immune evasion by tumor cells. The activation of cancer-associated fibroblasts (CAFs) plays a significant role in this process, as they further exacerbate the malignant traits of tumors by secreting a variety of cytokines and growth factors. Anti-fibrotic tumor treatment strategies, including the use of anti-fibrotic drugs and inhibition of fibrosis-related signaling pathways such as Transforming Growth Factor-β (TGF-β), have demonstrated potential in delaying tumor progression and improving the effectiveness of chemotherapy, targeted therapy, and immunotherapy. In the future, by developing novel drugs that target the fibrotic microenvironment, new therapeutic options may be available for patients with various refractory tumors.

Indexed as

CAFsEMTfibrosisTGF-βtumor

Identifiers

PMID39534084
PMCPMC11555290

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.