Evidence map›Paper›PMID 31598393›Full record

ReviewAmerican journal of cancer research2019

Therapeutic targeting of the crosstalk between cancer-associated fibroblasts and cancer stem cells.

Tu-Xiong Huang, Xin-Yuan Guan, Li Fu

Abstract readReview
In one paragraph

Review in American journal of cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing 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

66 citing papers in PubMed.

  1. Review
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  8. Understanding and overcoming multidrug resistance in cancer.Nature reviews. Clinical oncology · 2025
    Review
  9. Review
  10. Feasibility and mechanism ofAnnals of nuclear medicine · 2025
    Article
  11. Review
  12. Targeting breast tumor extracellular matrix and stroma utilizing nanoparticles.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  13. State-of-the-Art Liver Cancer Organoids: Modeling Cancer Stem Cell Heterogeneity for Personalized Treatment.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025
    Review
  14. Review
  15. The intellectual base and research fronts of LGR5: a bibliometric analysis.Frontiers in research metrics and analytics · 2025
    Review
  16. Article
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  18. Article
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6 more citing papers are in PubMed but not listed here.

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

3 authors.

Tu-Xiong HuangGuangdong Key Laboratory for Genome Stability & Disease Prevention, Department of Pharmacology and Shenzhen International Cancer Center, Shenzhen University School of Medicine Shenzhen, China.
Xin-Yuan GuanDepartment of Clinical Oncology, The University of Hong Kong Hong Kong.
Li FuGuangdong Key Laboratory for Genome Stability & Disease Prevention, Department of Pharmacology and Shenzhen International Cancer Center, Shenzhen University School of Medicine Shenzhen, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAFs) play critical roles in cancer progression and treatment failure. CAFs display extreme phenotypic heterogeneity and functional diversity. Some subpopulations of CAFs have the ability to reconstitute cancer stemness by promoting the expansion of cancer stem cells (CSCs) or by inducing the generation of CSCs from differentiated cancer cells. CAFs regulate cancer stemness in different types of solid tumors by activating a wide array of CSC-related signaling by secreting proteins and exosomes. As feedback, the CSCs can also induce the proliferation and further activation of CAFs to promote their CSC-supporting activities, thus completing the loop of CAF-CSC crosstalk. Current research on targeting CAF-CSC crosstalk could be classified into (i) specific depletion of CAF subpopulations that have CSC-supporting activities and (ii) targeting molecular signaling in CAF-CSC crosstalk, such as the IL6/STAT3, TGF-β/SDF-1/PI3K, WNT/β-catenin, HGF/cMET and SHH/Hh pathways. Strategies targeting CAF-CSC crosstalk may open new avenues for overcoming cancer progression and therapeutic resistance.

Indexed as

CAFscancer stemnesscancer therapyCSCstherapeutic resistance

Identifiers

PMID31598393
PMCPMC6780671

What OpenQuestion holds

Textmetadata
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.