Evidence map›Paper›PMID 27418196›Full record

ArticleCancer science2016

Loss of YAP1 defines neuroendocrine differentiation of lung tumors.

Takeshi Ito, Daisuke Matsubara, Ichidai Tanaka, Kanae Makiya, Zen-Ichi Tanei, Yuki Kumagai, Shu-Jen Shiu, Hiroki J Nakaoka, Shumpei Ishikawa, Takayuki Isagawa and 15 more

Open access · goldAbstract 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 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

65 citing papers in PubMed, 106 citations in OpenAlex.

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  14. Differential NEUROD1, ASCL1, and POU2F3 Expression Defines Molecular Subsets of Bladder Small Cell/Neuroendocrine Carcinoma With Prognostic Implications.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2024
    Article
  15. Article
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  17. EHMT2-mediated transcriptional reprogramming drives neuroendocrine transformation in non-small cell lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  20. Review

5 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

25 authors at 6 institutions in 1 country.

Takeshi ItoMolecular Pathology Laboratory, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Daisuke MatsubaraMolecular Pathology Laboratory, Institute of Medical Science, University of Tokyo, Tokyo, Japan. vzv07574@nifty.com.
Ichidai TanakaDivision of Molecular Oncology, Aichi Cancer Center Research Institute, Aichi, Japan.
Kanae MakiyaMolecular Pathology Laboratory, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Zen-Ichi TaneiMolecular Pathology Laboratory, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Yuki KumagaiMolecular Pathology Laboratory, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Shu-Jen ShiuMolecular Pathology Laboratory, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Hiroki J NakaokaMolecular Pathology Laboratory, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Shumpei IshikawaDepartment of Genomic Pathology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Takayuki IsagawaDepartment of Genomic Pathology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Teppei MorikawaDepartment of Human Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Aya Shinozaki-UshikuDepartment of Human Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Yasushi GotoDepartment of Respiratory Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Tomoyuki NakanoDepartment of Thoracic Surgery, Jichi Medical University, Tochigi, Japan.
Takehiro TsuchiyaDepartment of Thoracic Surgery, University of Tokyo, Tokyo, Japan.
Hiroyoshi TsubochiDepartment of Thoracic Surgery, Jichi Medical University Saitama Medical Center, Saitama, Japan.
Daisuke KomuraDivision of Genome Science, Research Center for Advanced Science and Technology, University of Tokyo, Tokyo, Japan.
Hiroyuki AburataniDivision of Genome Science, Research Center for Advanced Science and Technology, University of Tokyo, Tokyo, Japan.
Yoh DobashiDepartment of Pathology, Jichi Medical University Saitama Medical Center, Saitama, Japan.
Jun NakajimaDepartment of Thoracic Surgery, University of Tokyo, Tokyo, Japan.
Shunsuke EndoDepartment of Thoracic Surgery, Jichi Medical University, Tochigi, Japan.
Masashi FukayamaDepartment of Human Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Yoshitaka SekidoDivision of Molecular Oncology, Aichi Cancer Center Research Institute, Aichi, Japan.
Toshiro NikiDepartment of Integrative Pathology, Jichi Medical University, Tochigi, Japan.
Yoshinori MurakamiMolecular Pathology Laboratory, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
The University of Tokyo · JPTokyo University of Science · JPJichi Medical University · JPAichi Cancer Center · JPTokyo Medical and Dental University · JPJichi Medical University Saitama Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

YAP1, the main Hippo pathway effector, is a potent oncogene and is overexpressed in non-small-cell lung cancer (NSCLC); however, the YAP1 expression pattern in small-cell lung cancer (SCLC) has not yet been elucidated in detail. We report that the loss of YAP1 is a special feature of high-grade neuroendocrine lung tumors. A hierarchical cluster analysis of 15 high-grade neuroendocrine tumor cell lines containing 14 SCLC cell lines that depended on the genes of Hippo pathway molecules and neuroendocrine markers clearly classified these lines into two groups: the YAP1-negative and neuroendocrine marker-positive group (n = 11), and the YAP1-positive and neuroendocrine marker-negative group (n = 4). Among the 41 NSCLC cell lines examined, the loss of YAP1 was only observed in one cell line showing the strong expression of neuroendocrine markers. Immunostaining for YAP1, using the sections of 189 NSCLC, 41 SCLC, and 30 large cell neuroendocrine carcinoma (LCNEC) cases, revealed that the loss of YAP1 was common in SCLC (40/41, 98%) and LCNEC (18/30, 60%), but was rare in NSCLC (6/189, 3%). Among the SCLC and LCNEC cases tested, the loss of YAP1 correlated with the expression of neuroendocrine markers, and a survival analysis revealed that YAP1-negative cases were more chemosensitive than YAP1-positive cases. Chemosensitivity test for cisplatin using YAP1-positive/YAP1-negative SCLC cell lines also showed compatible results. YAP1-sh-mediated knockdown induced the neuroendocrine marker RAB3a, which suggested the possible involvement of YAP1 in the regulation of neuroendocrine differentiation. Thus, we showed that the loss of YAP1 has potential as a clinical marker for predicting neuroendocrine features and chemosensitivity.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntineoplastic AgentsBiomarkers, TumorCell Line, TumorCisplatinCluster AnalysisDisease Models, AnimalDrug Resistance, NeoplasmFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesGenetic Association StudiesHeterograftsHumansAdaptor Proteins, Signal TransducingAntineoplastic AgentsBiomarkers, TumorCisplatinPhosphoproteinsTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinsChemosensitivityHippo pathwayneuroendocrine differentiationsmall-cell lung cancerYAP1

Identifiers

PMID27418196
PMCPMC5084673
OpenAlexW2463239572

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.