Evidence map›Paper›PMID 28359267›Full record

ArticleBMC cancer2017

Aberrant expression of ALK and EZH2 in Merkel cell carcinoma.

Tuukka Veija, Virve Koljonen, Tom Bohling, Mia Kero, Sakari Knuutila, Virinder Kaur Sarhadi

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  9. Article
  10. Merkel Cell Carcinoma from Molecular Pathology to Novel Therapies.International journal of molecular sciences · 2021
    Review
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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

6 authors at 2 institutions in 1 country.

Tuukka VeijaDepartment of Pathology, Faculty of Medicine, University of Helsinki, Haartmaninkatu 3, P.O. Box 21, FI-00014, Helsinki, Finland. tuukka.veija@helsinki.fi.
Virve KoljonenDepartment of Plastic Surgery, University of Helsinki and Helsinki University Hospital, Topeliuksenkatu 5, P.O. Box 266, FI-00029, Helsinki, Finland.
Tom BohlingDepartment of Pathology, University of Helsinki and HUSLAB, Helsinki University Hospital, Haartmaninkatu 3, P.O. Box 21, FI-00014, Helsinki, Finland.
Mia KeroDepartment of Pathology, University of Helsinki and HUSLAB, Helsinki University Hospital, Haartmaninkatu 3, P.O. Box 21, FI-00014, Helsinki, Finland.
Sakari KnuutilaDepartment of Pathology, Faculty of Medicine, University of Helsinki, Haartmaninkatu 3, P.O. Box 21, FI-00014, Helsinki, Finland.
Virinder Kaur SarhadiDepartment of Pathology, Faculty of Medicine, University of Helsinki, Haartmaninkatu 3, P.O. Box 21, FI-00014, Helsinki, Finland.
University of Helsinki · FIHelsinki University Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDistinct characteristic features categorize Merkel cell carcinoma (MCC) into two subgroups according to the Merkel cell polyomavirus infection. Many mutational studies on MCC have been carried out in recent years without identifying a prominent driver mutation. However, there is paucity reporting the expression of cancer genes at the RNA level in MCC tumors. In this study, we studied the RNA expression profiles of 26 MCC tumors, with a goal to identify prospective molecular targets that could improve the treatment strategies of MCC.

methodsRNA expression of 50 cancer-related genes in 26 MCC tumors was analyzed by targeted amplicon based next-generation sequencing using the Ion Torrent technology and the expression compared with that of normal, non-cancerous skin samples. Sequencing data were processed using Torrent Suite™ Software. Expression profiles of MCV-negative and MCV-positive tumors were compared. Fluorescence in situ hybridization was performed to study ALK rearrangements and immunohistochemistry to study ALK expression in tumor tissue.

resultsALK, CDKN2A, EZH2 and ERBB4 were overexpressed, and EGFR, ERBB2, PDGFRA and FGFR1 were underexpressed in MCC tumors compared to normal skin. In the MCV-negative tumors, MET, NOTCH1, FGFR3, and SMO were overexpressed and JAK3 and NPM1 were under-expressed compared to the MCV-positive tumors.

conclusionsHigh expression of ALK, CDKN2A and EZH2 was recorded in MCC tumors. No ALK fusion was seen by FISH analysis. Overexpression of EZH2 suggests its potential as a drug target in MCC.

Indexed as

AgedAged, 80 and overAnaplastic Lymphoma KinaseBiomarkers, TumorCarcinoma, Merkel CellEnhancer of Zeste Homolog 2 ProteinFemaleHigh-Throughput Nucleotide SequencingHumansMaleMiddle AgedNeoplasm StagingNucleophosminPrognosisReceptor Protein-Tyrosine KinasesSkin NeoplasmsALK protein, humanAnaplastic Lymphoma KinaseBiomarkers, TumorEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanNPM1 protein, humanNucleophosminReceptor Protein-Tyrosine KinasesALKEZH2Merkel cell carcinomaNext-generation sequencingRNA

Identifiers

PMID28359267
PMCPMC5374569
OpenAlexW2599563545

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.