Evidence map›Paper›PMID 34858425›Full record

ReviewFrontiers in immunology2021

Exploiting the STAT3 Nexus in Cancer-Associated Fibroblasts to Improve Cancer Therapy.

Amr Allam, Marina Yakou, Lokman Pang, Matthias Ernst, Jennifer Huynh

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 12% of its field
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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. rs762855 single nucleotide polymorphism modulates the risk for diffuse-type gastric cancer in females: a genome-wide association study in the Korean population.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025
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  13. STAT3 axis in cancer and cancer stem cells: From oncogenesis to targeted therapies.Biochimica et biophysica acta. Reviews on cancer · 2025
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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 at 2 institutions in 1 country.

Amr AllamOlivia Newton-John Cancer Research Institute and La Trobe University School of Cancer Medicine, Heidelberg, VIC, Australia.
Marina YakouOlivia Newton-John Cancer Research Institute and La Trobe University School of Cancer Medicine, Heidelberg, VIC, Australia.
Lokman PangOlivia Newton-John Cancer Research Institute and La Trobe University School of Cancer Medicine, Heidelberg, VIC, Australia.
Matthias ErnstOlivia Newton-John Cancer Research Institute and La Trobe University School of Cancer Medicine, Heidelberg, VIC, Australia.
Jennifer HuynhOlivia Newton-John Cancer Research Institute and La Trobe University School of Cancer Medicine, Heidelberg, VIC, Australia.
La Trobe University · AUOlivia Newton-John Cancer Wellness & Research Centre · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor microenvironment (TME) is composed of a heterogenous population of cells that exist alongside the extracellular matrix and soluble components. These components can shape an environment that is conducive to tumor growth and metastatic spread. It is well-established that stromal cancer-associated fibroblasts (CAFs) in the TME play a pivotal role in creating and maintaining a growth-permissive environment for tumor cells. A growing body of work has uncovered that tumor cells recruit and educate CAFs to remodel the TME, however, the mechanisms by which this occurs remain incompletely understood. Recent studies suggest that the signal transducer and activator of transcription 3 (STAT3) is a key transcription factor that regulates the function of CAFs, and their crosstalk with tumor and immune cells within the TME. CAF-intrinsic STAT3 activity within the TME correlates with tumor progression, immune suppression and eventually the establishment of metastases. In this review, we will focus on the roles of STAT3 in regulating CAF function and their crosstalk with other cells constituting the TME and discuss the utility of targeting STAT3 within the TME for therapeutic benefit.

Indexed as

Cancer-Associated FibroblastsCell CommunicationDisease ProgressionHumansJanus KinasesNeoplasmsPhosphorylationSignal TransductionSTAT3 Transcription FactorTumor MicroenvironmentJanus KinasesSTAT3 protein, humanSTAT3 Transcription Factorcancer associated fibroblasts (CAF)cytokinesSTAT (signal transducer and activator of transcription)tumor developmenttumor microenvironment

Identifiers

PMID34858425
PMCPMC8632218
OpenAlexW3214017138

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.