Evidence map›Paper›PMID 32060987›Full record

ReviewCancer science2020

Cancer-associated fibroblasts that restrain cancer progression: Hypotheses and perspectives.

Yuki Miyai, Nobutoshi Esaki, Masahide Takahashi, Atsushi Enomoto

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
10.5field-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

114 citing papers in PubMed, 177 citations in OpenAlex.

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54 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

4 authors at 1 institution in 1 country.

Yuki MiyaiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0000-0003-0386-1431
Nobutoshi EsakiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masahide TakahashiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Atsushi EnomotoDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0000-0002-9206-6116
Nagoya University · JP

Funding

Japan Agency for Medical Research and Development, Core Research for Evolutional Science and Technology 19gm0810007h0104Japan Agency for Medical Research and Development, Core Research for Evolutional Science and Technology 19gm1210008s0101Ministry of Education, Culture, Sports, Science and Technology of Japan 18H02638Ministry of Education, Culture, Sports, Science and Technology of Japan 26221304Project for Cancer Research and Therapeutic Evolution (P-CREATE) from AMED 19cm0106332h0002
6 · The paper itself

Abstract

The roles of cancer-associated fibroblasts (CAF) in the progression of various types of cancers are well established. CAF promote cancer progression through pleiotropic mechanisms, including the secretion of soluble factors and extracellular matrix, physical interactions with cancer cells, and the regulation of angiogenesis, immunity and metabolism. Their contribution to therapeutic resistance is also well appreciated. Therefore, CAF have been considered as a therapeutic target in cancer. However, recent studies in autochthonous pancreatic cancer models suggest that specific subset(s) of CAF exhibit cancer-restraining roles, indicating that CAF are functionally and molecularly heterogeneous, which is supported by recent single-cell transcriptome analyses. While cancer-promoting CAF (pCAF) have been extensively studied, the nature and specific marker(s) of cancer-restraining CAF (rCAF) have remained uncharacterized. Interestingly, a recent study provided insight into the nature of rCAF and suggested that they may share molecular properties with pancreatic stellate cells (PSC) and mesenchymal stem/stromal cells (MSC). Complicating this finding is that PSC and MSC have been shown to promote the formation of a tumor-permissive and tumor-promoting environment in xenograft tumor models. However, these cells undergo significant transcriptional and epigenetic changes during ex vivo culture, which confounds the interpretation of experimental results based on the use of cultured cells. In this short review, we describe recent studies and hypotheses on the identity of rCAF and discuss their analogy to fibroblasts that suppress fibrosis in fibrotic diseases. Finally, we discuss how these findings can be exploited to develop novel anticancer therapies in the future.

Indexed as

AnimalsCancer-Associated FibroblastsCell Transformation, NeoplasticDrug Resistance, NeoplasmExtracellular MatrixHeterograftsHumansMesenchymal Stem CellsMiceNeoplasmsNeovascularization, PathologicPancreatic Stellate CellsTumor Microenvironmentcancer-restraining cancer-associated fibroblastsfibrosisMeflinmesenchymal stem/stromal cellstumor microenvironment

Identifiers

PMID32060987
PMCPMC7156845
OpenAlexW3006383935

What OpenQuestion holds

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LicenceCC BY-NC
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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.