Evidence map›Paper›PMID 36672284›Full record

ReviewCancers2023

Therapeutic Targeting of Cancer-Associated Fibroblasts in the Non-Small Cell Lung Cancer Tumor Microenvironment.

Yasushi Shintani, Toru Kimura, Soichiro Funaki, Naoko Ose, Takashi Kanou, Eriko Fukui

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
10.4field-weighted citation impact, top 1% 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

35 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Tumorigenesis and Tumor Microenvironment in Lung Cancer.Current issues in molecular biology · 2026
    Review
  8. Review
  9. Modeling CAF-tumor interactions to overcome therapy resistance.Journal of experimental & clinical cancer research : CR · 2026
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Identification ofCancers · 2025
    Article
  18. Article
  19. Review
  20. Review
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

6 authors at 1 institution in 1 country.

Yasushi ShintaniDepartment of General Thoracic Surgery, Graduate School of Medicine, Osaka University, 2-2-L5, Yamadaoka, Suita, Osaka 565-0871, Japan.ORCID 0000-0002-2540-5288
Toru KimuraDepartment of General Thoracic Surgery, Graduate School of Medicine, Osaka University, 2-2-L5, Yamadaoka, Suita, Osaka 565-0871, Japan.
Soichiro FunakiDepartment of General Thoracic Surgery, Graduate School of Medicine, Osaka University, 2-2-L5, Yamadaoka, Suita, Osaka 565-0871, Japan.
Naoko OseDepartment of General Thoracic Surgery, Graduate School of Medicine, Osaka University, 2-2-L5, Yamadaoka, Suita, Osaka 565-0871, Japan.ORCID 0000-0002-3509-9536
Takashi KanouDepartment of General Thoracic Surgery, Graduate School of Medicine, Osaka University, 2-2-L5, Yamadaoka, Suita, Osaka 565-0871, Japan.
Eriko FukuiDepartment of General Thoracic Surgery, Graduate School of Medicine, Osaka University, 2-2-L5, Yamadaoka, Suita, Osaka 565-0871, Japan.
The University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the most frequently diagnosed cancer and the leading cause of cancer death worldwide. The most common lung cancer is non-small cell lung cancer (NSCLC), with an overall 5-year survival rate of around 20% because NSCLC is a metastatic disease. A better understanding of the mechanism underlying lung cancer metastasis is therefore urgently needed. The tumor microenvironment involves different types of stromal cells and functions as key components in the progression of NSCLC. Through epithelial-mesenchymal transition (EMT), in which epithelial cells lose their polarity and acquire mesenchymal potential, cancer cells acquire metastatic abilities, as well as cancer stem-cell-like potential. We previously reported that cancer-associated fibroblasts (CAFs) interact with lung cancer cells to allow for the acquisition of malignancy and treatment resistance by paracrine loops via EMT signals in the tumor microenvironment. Furthermore, CAFs regulate the cytotoxic activity of immune cells via various cytokines and chemokines, creating a microenvironment of immune tolerance. Regulation of CAFs can therefore affect immune responses. Recent research has shown several roles of CAFs in NSCLC tumorigenesis, owing to their heterogeneity, so molecular markers of CAFs should be elucidated to better classify tumor-promoting subtypes and facilitate the establishment of CAF-specific targeted therapies. CAF-targeted cancer treatments may suppress EMT and regulate the niche of cancer stem cells and the immunosuppressive network and thus may prove useful for NSCLC treatment through multiple mechanisms.

Indexed as

anticancer resistancecancer-associated fibroblastscancer progressionheterogeneitynon-small cell lung cancernovel markerstarget therapytumor microenvironment

Identifiers

PMID36672284
PMCPMC9856659
OpenAlexW4313584627

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.