Evidence map›Paper›PMID 35411036›Full record

ArticleOncogene2022

Novel TENM3-ALK fusion is an alternate mechanism for ALK activation in neuroblastoma.

Mitsuteru Hiwatari, Masafumi Seki, Ryosuke Matsuno, Kenichi Yoshida, Takeshi Nagasawa, Aiko Sato-Otsubo, Shohei Yamamoto, Motohiro Kato, Kentaro Watanabe, Masahiro Sekiguchi and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 11 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

13 authors at 6 institutions in 2 countries.

Mitsuteru HiwatariDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. mhiwatari-tky@umin.ac.jp.ORCID http://orcid.org/0000-0003-3683-4472
Masafumi SekiDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-4671-7026
Ryosuke MatsunoDepartment of Pediatrics, Kansai Medical University, Osaka, Japan.ORCID http://orcid.org/0000-0003-3231-4760
Kenichi YoshidaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Yoshidakonoecho, Sakyo-ku, Kyoto, Japan.ORCID http://orcid.org/0000-0003-4612-2778
Takeshi NagasawaDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-1552-3619
Aiko Sato-OtsuboDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-2528-0702
Shohei YamamotoDepartment of Pediatrics, Tokai University School of Medicine, Isehara, Kanagawa, Japan.ORCID http://orcid.org/0000-0003-1582-7062
Motohiro KatoDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0001-5145-1774
Kentaro WatanabeDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-0868-5289
Masahiro SekiguchiDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-7941-9319
Satoru MiyanoMedical and Dental Data Science Center, Tokyo Medical and Dental University, Tokyo, Japan.ORCID http://orcid.org/0000-0002-1753-6616
Seishi OgawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Yoshidakonoecho, Sakyo-ku, Kyoto, Japan.ORCID http://orcid.org/0000-0002-7778-5374
Junko TakitaDepartment of Pediatrics, Kyoto University, Yoshidakonoecho, Sakyo-ku, Kyoto, Japan.ORCID http://orcid.org/0000-0002-2452-6520
The University of Tokyo · JPKyoto University · JPKansai Medical University · JPTokai University · JPTokyo Medical and Dental University · JPUniversity of Tokyo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The identification of molecular events underlying the pathogenesis of neuroblastoma can likely result in improved clinical outcomes for this disease. In this study, a translocation within chromosome 2p and 4q was found to bring about the formation of an in-frame fusion gene that was composed of portions of the teneurin transmembrane protein 3 (TENM3, also known as ODZ3) gene and the anaplastic lymphoma kinase (ALK) gene in tumor cells from patients with neuroblastoma. Expression of the full length TENM3-ALK cDNA in NIH-3T3 cells led to the formation of a fusion protein that: (1) possesses constitutive tyrosine kinase activity, (2) induces strong activation of the downstream targets of extracellular signal-regulated kinase (ERK), protein kinase B (a.k.a. AKT), and signal transducer and activator of transcription 3 (STAT3), (3) provokes oncogenic transformation in NOD.Cg-Prkdc

Indexed as

Anaplastic Lymphoma KinaseNeuroblastomaOncogene Proteins, FusionReceptor Protein-Tyrosine KinasesAnimalsCell Line, TumorCell ProliferationCell Transformation, NeoplasticHumansMembrane ProteinsMiceMice, Inbred NODNerve Tissue ProteinsNIH 3T3 CellsTranslocation, GeneticAnaplastic Lymphoma KinaseMembrane ProteinsNerve Tissue ProteinsOncogene Proteins, FusionReceptor Protein-Tyrosine KinasesTENM3 protein, human

Identifiers

PMID35411036
OpenAlexW4223411730

What OpenQuestion holds

Textmetadata
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.