Evidence map›Paper›PMID 27696251›Full record

ArticleEndocrine2016

Targeted next-generation sequencing for TP53, RAS, BRAF, ALK and NF1 mutations in anaplastic thyroid cancer.

Soeren Latteyer, Vera Tiedje, Katharina König, Saskia Ting, Lukas C Heukamp, Lydia Meder, Kurt Werner Schmid, Dagmar Führer, Lars Christian Moeller

Abstract read
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In one paragraph

Article in Endocrine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
5.4field-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, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.

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  20. Analysis ofMolecular and clinical oncology · 2021
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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

9 authors at 3 institutions in 1 country.

Soeren LatteyerDepartment of Endocrinology and Metabolism, University Hospital Essen, University of Duisburg-Essen, Hufelandstraße 55, Essen, 45122, Germany.
Vera TiedjeDepartment of Endocrinology and Metabolism, University Hospital Essen, University of Duisburg-Essen, Hufelandstraße 55, Essen, 45122, Germany.
Katharina KönigInstitute of Pathology, University Hospital Cologne, Kerpener Straße 62, Cologne, 50935, Germany.
Saskia TingInstitute of Pathology, University Hospital Essen, University of Duisburg-Essen, Hufelandstraße 55, Essen, 45122, Germany.
Lukas C HeukampNEO New Oncology AG, Gottfried-Hagen-Str. 20, Cologne, 51105, Germany.
Lydia MederInstitute of Pathology, University Hospital Cologne, Kerpener Straße 62, Cologne, 50935, Germany.
Kurt Werner SchmidInstitute of Pathology, University Hospital Essen, University of Duisburg-Essen, Hufelandstraße 55, Essen, 45122, Germany.
Dagmar FührerDepartment of Endocrinology and Metabolism, University Hospital Essen, University of Duisburg-Essen, Hufelandstraße 55, Essen, 45122, Germany.
Lars Christian MoellerDepartment of Endocrinology and Metabolism, University Hospital Essen, University of Duisburg-Essen, Hufelandstraße 55, Essen, 45122, Germany. lars.moeller@uk-essen.de.
University of Duisburg-Essen · DEUniversity Hospital Cologne · DEInstitut für Hämatopathologie Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anaplastic thyroid carcinoma (ATC) is the most aggressive thyroid cancer with a median survival of 4-6 months. Identification of mutations contributing to aberrant activation of signaling cascades in ATC may provide novel opportunities for targeted therapy. Thirty-nine ATC samples were studied by next-generation sequencing (NGS) with an established gene panel. High quality readout was obtained in 30/39 ATC. Twenty-eight ATC harbored a mutation in at least one of the studied genes: TP53 (18/30), NF1 (11/30), ALK (6/30), NRAS (4/30), ATRX (3/30), BRAF (2/30), HRAS (2/30), KRAS (1/30). In 17/30 ATC (54 %) mutations were found in two or more genes. Twenty-one of the identified variants are listed in COSMIC as somatic mutations reported in other cancer entities. In three ATC samples no mutations were detected and none of the ATCs was positive for BRAF

Indexed as

AgedAged, 80 and overAnaplastic Lymphoma KinaseDNA Mutational AnalysisFemaleGenes, Neurofibromatosis 1Genes, p53Genes, rasHumansMaleMiddle AgedProto-Oncogene Proteins B-rafReceptor Protein-Tyrosine KinasesThyroid Carcinoma, AnaplasticThyroid NeoplasmsALK protein, humanAnaplastic Lymphoma KinaseProto-Oncogene Proteins B-rafReceptor Protein-Tyrosine KinasesALKAnaplastic thyroid cancerATCATRXBRAFNext-generation sequencingNF1RAS

Identifiers

PMID27696251
OpenAlexW2524754702

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.