Evidence map›Paper›PMID 40805183›Full record

ReviewCancers2025

Cancer-Associated Fibroblasts: Immunosuppressive Crosstalk with Tumor-Infiltrating Immune Cells and Implications for Therapeutic Resistance.

Jogendra Singh Pawar, Md Abdus Salam, Md Shalman Uddin Dipto, Md Yusuf Al-Amin, Moushumi Tabassoom Salam, Sagnik Sengupta, Smita Kumari, Lohitha Gujjari, Ganesh Yadagiri

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Review
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  5. Overcoming tumour resistance in cancer immunotherapy through predictive and pharmacodynamic biomarkers.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

9 authors.

Jogendra Singh PawarDivision of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, The Ohio State University, Columbus, OH 43210, USA.ORCID 0000-0002-4675-7784
Md Abdus SalamFaculty of Biotechnology & Biomedical Engineering, Rajshahi Medical University, Rajshahi 6100, Bangladesh.ORCID 0000-0001-7424-9237
Md Shalman Uddin DiptoDepartment of Pharmacy, University of Rajshahi, Rajshahi 6205, Bangladesh.ORCID 0009-0001-3466-7239
Md Yusuf Al-AminPurdue University Interdisciplinary Life Sciences Graduate Program, Purdue University, West Lafayette, IN 47907, USA.ORCID 0000-0002-6086-5159
Moushumi Tabassoom SalamDepartment of Pharmacy, University of Rajshahi, Rajshahi 6205, Bangladesh.
Sagnik SenguptaDepartment of Radiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0009-0004-8703-5042
Smita KumariDivision of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, The Ohio State University, Columbus, OH 43210, USA.ORCID 0000-0003-1596-9239
Lohitha GujjariDorothy M. Davis Heart and Lung Research Institute, Division of Pulmonary, Critical Care & Sleep Medicine, Department of Internal Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH 43210, USA.
Ganesh YadagiriDepartment of Obstetrics and Gynecology, College of Medicine, The Ohio State University, Columbus, OH 43210, USA.ORCID 0000-0002-5634-6006

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is no longer considered as an isolated event. Rather, it occurs because of a complex biological drive orchestrating different cell types, growth factors, cytokines, and signaling pathways within the tumor microenvironment (TME). Cancer-associated fibroblasts (CAFs) are the most populous stromal cells within the complex ecosystem of TME, with significant heterogeneity and plasticity in origin and functional phenotypes. Very enigmatic cells, CAFs determine the progress and outcomes of tumors through extensive reciprocal signaling with different tumors infiltrating immune cells in the TME. In their biological drive, CAFs release numerous chemical mediators and utilize various signaling pathways to recruit and modulate tumor-infiltrating immune cells. The CAF-induced secretome and exosomes render immune cells ineffective for their antitumor activities. Moreover, by upregulating immune inhibitory checkpoints, CAFs create an immunosuppressive TME that impedes the susceptibility of tumor cells to tumor-infiltrating lymphocytes (TILs). Further, by depositing and remodeling extracellular matrix (ECM), CAFs reshape the TME, which enhances tumor growth, invasion, metastasis, and chemoresistance. Understanding of CAF biology and its crosstalk with tumor-infiltrating immune cells is crucial not only to gain insight in tumorigenesis but to optimize the potential of novel targeted immunotherapies for cancers. The complex relationships between CAFs and tumor-infiltrating immune cells remain unclear and need further study. Herein, in this narrative review we have focused on updates of CAF biology and its interactions with tumor-infiltrating immune cells in generating immunosuppressive TME and resistance to cell death.

Indexed as

biological crosstalkCAF-induced immunosuppressioncancer-associated fibroblaststumor cell resistancetumor-infiltrating immune cellstumor microenvironment

Identifiers

PMID40805183
PMCPMC12346030

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.