Evidence map›Paper›PMID 34289987›Full record

ArticleCancer research2021

TGFβ Signaling Activated by Cancer-Associated Fibroblasts Determines the Histological Signature of Lung Adenocarcinoma.

Ryo Sato, Kosuke Imamura, Takashi Semba, Yusuke Tomita, Sho Saeki, Koei Ikeda, Yoshihiro Komohara, Makoto Suzuki, Takuro Sakagami, Hideyuki Saya and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.6field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 66 citations in OpenAlex.

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  3. mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

11 authors at 3 institutions in 2 countries.

Ryo Sato *Division of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.
Kosuke Imamura *Department of Respiratory Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Takashi SembaDivision of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0002-1987-1645
Yusuke TomitaDepartment of Respiratory Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID 0000-0002-9680-7559
Sho SaekiDepartment of Respiratory Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Koei IkedaDepartment of Thoracic Surgery, Graduate School of Medical Sciences, Kumamoto University Hospital, Kumamoto, Japan.
Yoshihiro KomoharaDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University Hospital, Kumamoto, Japan.
Makoto SuzukiDepartment of Thoracic Surgery, Graduate School of Medical Sciences, Kumamoto University Hospital, Kumamoto, Japan.
Takuro SakagamiDepartment of Respiratory Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID 0000-0002-9057-1127
Hideyuki SayaDivision of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0001-6610-1902
Yoshimi ArimaDivision of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan. arima@z7.keio.jp.
Institute for Advanced Medical Research · USKumamoto University · JPKumamoto University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Invasive lung adenocarcinoma (LADC) can be classified histologically as lepidic, acinar, papillary, micropapillary, or solid. Most LADC tumors manifest several of these histological subtypes, with heterogeneity being related to therapeutic resistance. We report here that in immunodeficient mice, human LADC cells form tumors with distinct histological features, MUC5AC-expressing solid-type or cytokeratin 7 (CK7)-expressing acinar-type tumors, depending on the site of development, and that a solid-to-acinar transition (SAT) could be induced by the tumor microenvironment. The TGFβ-Smad signaling pathway was activated in both tumor and stromal cells of acinar-type tumors. Immortalized cancer-associated fibroblasts (CAF) derived from acinar-type tumors induced SAT in 3D cocultures with LADC cells. Exogenous TGFβ1 or overexpression of an active form of TGFβ1 increased CK7 expression and reduced MUC5AC expression in LADC cells, and knockdown of

Indexed as

Signal TransductionTumor MicroenvironmentAdenocarcinoma of LungAnimalsCancer-Associated FibroblastsCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalFemaleFluorescent Antibody TechniqueHeterograftsHumansImmunohistochemistryInterleukin-8MiceModels, BiologicalInterleukin-8Transforming Growth Factor beta

Identifiers

PMID34289987
PMCPMC9397619
OpenAlexW3184201660

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.