Evidence map›Paper›PMID 26663681›Full record

ArticleCancer science2016

Role of deltaNp63(pos)CD44v(pos) cells in the development of N-nitroso-tris-chloroethylurea-induced peripheral-type mouse lung squamous cell carcinomas.

Shotaro Yamano, Min Gi, Yoshiyuki Tago, Kenichiro Doi, Satoshi Okada, Yukiyoshi Hirayama, Hirokazu Tachibana, Naomi Ishii, Masaki Fujioka, Kumiko Tatsumi and 1 more

Abstract read
In one paragraph

Article in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

24 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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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.

Shotaro YamanoDepartment of Molecular Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Min GiDepartment of Molecular Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Yoshiyuki TagoDepartment of Molecular Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Kenichiro DoiDepartment of Molecular Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Satoshi OkadaDepartment of Molecular Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Yukiyoshi HirayamaDepartment of Molecular Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Hirokazu TachibanaDepartment of Molecular Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Naomi IshiiDepartment of Molecular Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Masaki FujiokaDepartment of Molecular Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Kumiko TatsumiDepartment of Molecular Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Hideki WanibuchiDepartment of Molecular Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of cells expressing stem cell markers deltaNp63 and CD44v has not yet been elucidated in peripheral-type lung squamous cell carcinoma (pLSCC) carcinogenesis. Female A/J mice were painted topically with N-nitroso-tris-chloroethylurea (NTCU) for induction of pLSCC, and the histopathological and molecular characteristics of NTCU-induced lung lesions were examined. Histopathologically, we found atypical bronchiolar hyperplasia, squamous metaplasia, squamous dysplasia, and pLSCCs in the treated mice. Furthermore, we identified deltaNp63(pos)CD44v(pos)CK5/6(pos)CC10(pos) clara cells as key constituents of early precancerous atypical bronchiolar hyperplasia. In addition, deltaNp63(pos)CD44v(pos) cells existed throughout the atypical bronchiolar hyperplasias, squamous metaplasias, squamous dysplasias, and pLSCCs. Overall, our findings suggest that NTCU induces pLSCC through an atypical bronchiolar hyperplasia-metaplasia-dysplasia-SCC sequence in mouse lung bronchioles. Notably, Ki67-positive deltaNp63(pos)CD44v(pos) cancer cells, cancer cells overexpressing phosphorylated epidermal growth factor receptor and signal transducer and activator of transcription 3, and tumor-associated macrophages were all present in far greater numbers in the peripheral area of the pLSCCs compared with the central area. These findings suggest that deltaNp63(pos)CD44v(pos) clara cells in mouse lung bronchioles might be the origin of the NTCU-induced pLSCCs. Our findings also suggest that tumor-associated macrophages may contribute to creating a tumor microenvironment in the peripheral area of pLSCCs that allows deltaNp63(pos)CD44v(pos) cancer cell expansion through activation of epidermal growth factor receptor signaling, and that exerts an immunosuppressive effect through activation of signal transducer and activator of transcription 3 signaling.

Indexed as

AnimalsCarcinogensCarcinoma, Squamous CellCarmustineDisease Models, AnimalDisease ProgressionFemaleHyaluronan ReceptorsImmune ToleranceImmunohistochemistryLung NeoplasmsMacrophagesMiceNeoplastic Stem CellsPhosphoproteinsPrecancerous ConditionsCarcinogensCarmustineCd44 protein, mouseHyaluronan ReceptorsN-nitroso-tris-chloroethylureaPhosphoproteinsTrans-ActivatorsTrp63 protein, mouseCD44(v9)deltaNp63miceN-nitroso-tris-chloroethylureasquamous cell carcinoma

Identifiers

PMID26663681
PMCPMC4768398

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.