Evidence map›Paper›PMID 29444910›Full record

ArticleEndocrine-related cancer2018

The neuroendocrine phenotype, genomic profile and therapeutic sensitivity of GEPNET cell lines.

Tobias Hofving, Yvonne Arvidsson, Bilal Almobarak, Linda Inge, Roswitha Pfragner, Marta Persson, Göran Stenman, Erik Kristiansson, Viktor Johanson, Ola Nilsson

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Endocrine-related cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 84 citations in OpenAlex.

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  19. Potential for Increasing Uptake of RadiolabeledCancer biotherapy & radiopharmaceuticals · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Tobias HofvingSahlgrenska Cancer CenterDepartment of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden tobias.hofving@gu.se.
Yvonne ArvidssonSahlgrenska Cancer CenterDepartment of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Bilal AlmobarakSahlgrenska Cancer CenterDepartment of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Linda IngeSahlgrenska Cancer CenterDepartment of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Roswitha PfragnerInstitute of Pathophysiology and ImmunologyCenter for Molecular Medicine, Medical University of Graz, Graz, Austria.
Marta PerssonSahlgrenska Cancer CenterDepartment of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Göran StenmanSahlgrenska Cancer CenterDepartment of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Erik KristianssonDepartment of Mathematical SciencesChalmers University of Technology, Gothenburg, Sweden.
Viktor JohansonDepartment of SurgeryInstitute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Ola NilssonSahlgrenska Cancer CenterDepartment of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
University of Gothenburg · SESahlgrenska University Hospital · SEChalmers University of Technology · SEMedical University of Graz · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Experimental models of neuroendocrine tumour disease are scarce, and no comprehensive characterisation of existing gastroenteropancreatic neuroendocrine tumour (GEPNET) cell lines has been reported. In this study, we aimed to define the molecular characteristics and therapeutic sensitivity of these cell lines. We therefore performed immunophenotyping, copy number profiling, whole-exome sequencing and a large-scale inhibitor screening of seven GEPNET cell lines. Four cell lines, GOT1, P-STS, BON-1 and QGP-1, displayed a neuroendocrine phenotype while three others, KRJ-I, L-STS and H-STS, did not. Instead, these three cell lines were identified as lymphoblastoid. Characterisation of remaining authentic GEPNET cell lines by copy number profiling showed that GOT1, among other chromosomal alterations, harboured losses on chromosome 18 encompassing the

Indexed as

Intestinal NeoplasmsNeuroendocrine TumorsPancreatic NeoplasmsStomach NeoplasmsAntineoplastic AgentsBiomarkers, TumorDNA Copy Number VariationsExome SequencingGenomicsHistone Deacetylase InhibitorsHumansMutationPhenotypeProtein Kinase InhibitorsTumor Cells, CulturedAntineoplastic AgentsBiomarkers, TumorHistone Deacetylase InhibitorsProtein Kinase Inhibitorscell linescopy number alterationsexome sequencingGEPNETimmunophenotypinginhibitor screeningneuroendocrine tumourtrametinibvorinostat

Identifiers

PMID29444910
PMCPMC5827037
OpenAlexW2786723185

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.