Evidence map›Paper›PMID 35884375›Full record

ReviewCancers2022

Good and Bad Stroma in Pancreatic Cancer: Relevance of Functional States of Cancer-Associated Fibroblasts.

Ryota Ando, Akihiro Sakai, Tadashi Iida, Kunio Kataoka, Yasuyuki Mizutani, Atsushi Enomoto

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Ryota AndoDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Akihiro SakaiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Tadashi IidaDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Kunio KataokaDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Yasuyuki MizutaniDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Atsushi EnomotoDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.ORCID 0000-0002-9206-6116
Nagoya University · JP

Funding

Japan Agency for Medical Research and Development 21lm0203005j0005Japan Agency for Medical Research and Development 22ck0106706h0002Japan Agency for Medical Research and Development 22gm1210009s0104Ministry of Education, Culture, Sports, Science and Technology 21K15995
6 · The paper itself

Abstract

A well-known feature of human pancreatic ductal adenocarcinoma (PDAC) is the extensive proliferation of cancer-associated fibroblasts (CAFs) and highly fibrotic stroma. Recent evidence, based mainly on single-cell analyses, has identified various subsets of CAFs in PDAC mouse models. However, we do not know how these CAF subsets are involved in the progression and drug resistance of human PDAC. Additionally, it remains unclear whether these diverse CAFs have distinct origins and are indicators of genuinely distinct CAF lineages or reflect different states of the same CAFs depending on the tumor microenvironment. Interestingly, recent preclinical studies have started to characterize the nature of cancer-restraining CAFs and have identified their markers Meflin and collagen type I alpha 1. These studies have led to the development of strategies to induce changes in CAF phenotypes using chemical reagents or recombinant viruses, and some of them have been tested in clinical studies. These strategies have the unique potential to convert the so-called bad stroma to good stroma and may also have therapeutic implications for non-cancer diseases such as fibrotic diseases. Together with recently developed sophisticated strategies that specifically target distinct CAF subsets via adoptive cell transfer therapy, vaccination, and antibody-drug conjugates, any future findings arising from these clinical efforts may expand our understanding of the significance of CAF diversity in human PDAC.

Indexed as

cancer-associated fibroblastsfibrosisimmunoglobulin superfamily containing leucine-rich repeatMeflinpancreatic cancerstromatumor microenvironment

Identifiers

PMID35884375
PMCPMC9317763
OpenAlexW4284880966

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.