Evidence map›Paper›PMID 29967776›Full record

ReviewBioMed research international2018

Metabolic Reprogramming of Cancer Associated Fibroblasts: The Slavery of Stromal Fibroblasts.

Angelica Avagliano, Giuseppina Granato, Maria Rosaria Ruocco, Veronica Romano, Immacolata Belviso, Antonia Carfora, Stefania Montagnani, Alessandro Arcucci

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 2% 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

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Targeting CAF-specific metabolic pathways in breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article

30 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

8 authors at 1 institution in 1 country.

Angelica AvaglianoDepartment of Public Health, University of Naples Federico II, 80131 Naples, Italy.
Giuseppina GranatoDepartment of Public Health, University of Naples Federico II, 80131 Naples, Italy.
Maria Rosaria RuoccoDepartment of Molecular Medicine and Medical Biotechnology, University of Naples Federico II, 80131 Naples, Italy.
Veronica RomanoDepartment of Public Health, University of Naples Federico II, 80131 Naples, Italy.
Immacolata BelvisoDepartment of Molecular Medicine and Medical Biotechnology, University of Naples Federico II, 80131 Naples, Italy.
Antonia CarforaDepartment of Public Health, University of Naples Federico II, 80131 Naples, Italy.
Stefania MontagnaniDepartment of Public Health, University of Naples Federico II, 80131 Naples, Italy.ORCID 0000-0002-7420-372X
Alessandro ArcucciDepartment of Public Health, University of Naples Federico II, 80131 Naples, Italy.ORCID 0000-0001-9324-4511
University of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer associated fibroblasts (CAFs) are the main stromal cell type of solid tumour microenvironment and undergo an activation process associated with secretion of growth factors, cytokines, and paracrine interactions. One of the important features of solid tumours is the metabolic reprogramming that leads to changes of bioenergetics and biosynthesis in both tumour cells and CAFs. In particular, CAFs follow the evolution of tumour disease and acquire a catabolic phenotype: in tumour tissues, cancer cells and tumour microenvironment form a network where the crosstalk between cancer cells and CAFs is associated with cell metabolic reprogramming that contributes to CAFs activation, cancer growth, and progression and evasion from cancer therapies. In this regard, the study of CAFs metabolic reprogramming could contribute to better understand their activation process, the interaction between stroma, and cancer cells and could offer innovative tools for the development of new therapeutic strategies able to eradicate the protumorigenic activity of CAFs. Therefore, this review focuses on CAFs metabolic reprogramming associated with both differentiation process and cancer and stromal cells crosstalk. Finally, therapeutic responses and potential anticancer strategies targeting CAFs metabolic reprogramming are reviewed.

Indexed as

Tumor MicroenvironmentCancer-Associated FibroblastsFibroblastsStromal Cells

Identifiers

PMID29967776
PMCPMC6008683
OpenAlexW2807211990

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.