Evidence map›Paper›PMID 35236758›Full record

ArticleLife science alliance2022

Meflin-positive cancer-associated fibroblasts enhance tumor response to immune checkpoint blockade.

Yuki Miyai, Daisuke Sugiyama, Tetsunari Hase, Naoya Asai, Tetsuro Taki, Kazuki Nishida, Takayuki Fukui, Toyofumi Fengshi Chen-Yoshikawa, Hiroki Kobayashi, Shinji Mii and 6 more

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 49 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

16 authors at 2 institutions in 1 country.

Yuki MiyaiDepartment of Pathology, Nagoya University Hospital, Nagoya, Japan.ORCID 0000-0003-0386-1431
Daisuke SugiyamaDepartment of Immunology, Nagoya University Hospital, Nagoya, Japan.
Tetsunari HaseDepartment of Respiratory Medicine, Nagoya University Hospital, Nagoya, Japan.ORCID 0000-0002-9653-8424
Naoya AsaiDepartment of Pathology, Nagoya University Hospital, Nagoya, Japan.
Tetsuro TakiDepartment of Pathology, Nagoya University Hospital, Nagoya, Japan.
Kazuki NishidaCenter for Advanced Medicine and Clinical Research, Nagoya University Hospital, Nagoya, Japan.ORCID 0000-0003-0367-8557
Takayuki FukuiDepartment of Thoracic Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Toyofumi Fengshi Chen-YoshikawaDepartment of Thoracic Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hiroki KobayashiDepartment of Pathology, Nagoya University Hospital, Nagoya, Japan.ORCID 0000-0002-1717-4870
Shinji MiiDepartment of Pathology, Nagoya University Hospital, Nagoya, Japan.
Yukihiro ShirakiDepartment of Pathology, Nagoya University Hospital, Nagoya, Japan.ORCID 0000-0003-3666-0556
Yoshinori HasegawaDepartment of Respiratory Medicine, Nagoya University Hospital, Nagoya, Japan.
Hiroyoshi NishikawaDepartment of Immunology, Nagoya University Hospital, Nagoya, Japan.ORCID 0000-0001-6563-9807
Yuichi AndoDepartment of Clinical Oncology and Chemotherapy, Nagoya University Hospital, Nagoya, Japan.
Masahide TakahashiDepartment of Pathology, Nagoya University Hospital, Nagoya, Japan.
Atsushi EnomotoDepartment of Pathology, Nagoya University Hospital, Nagoya, Japan enomoto@iar.nagoya-u.ac.jp.ORCID 0000-0002-9206-6116
Nagoya University Hospital · JPNagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAFs) are an integral component of the tumor microenvironment (TME). Most CAFs shape the TME toward an immunosuppressive milieu and attenuate the efficacy of immune checkpoint blockade (ICB) therapy. However, the detailed mechanism of how heterogeneous CAFs regulate tumor response to ICB therapy has not been defined. Here, we show that a recently defined CAF subset characterized by the expression of Meflin, a glycosylphosphatidylinositol-anchored protein marker of mesenchymal stromal/stem cells, is associated with survival and favorable therapeutic response to ICB monotherapy in patients with non-small cell lung cancer (NSCLC). The prevalence of Meflin-positive CAFs was positively correlated with CD4-positive T-cell infiltration and vascularization within non-small cell lung cancer tumors. Meflin deficiency and CAF-specific Meflin overexpression resulted in defective and enhanced ICB therapy responses in syngeneic tumors in mice, respectively. These findings suggest the presence of a CAF subset that promotes ICB therapy efficacy, which adds to our understanding of CAF functions and heterogeneity.

Indexed as

Cancer-Associated FibroblastsCarcinoma, Non-Small-Cell LungLung NeoplasmsAnimalsHumansImmune Checkpoint InhibitorsMiceTumor MicroenvironmentImmune Checkpoint Inhibitors

Identifiers

PMID35236758
PMCPMC8897596
OpenAlexW4214934150

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.