Evidence map›Paper›PMID 26008974›Full record

ArticleOncotarget2015

Identification of deregulation of apoptosis and cell cycle in neuroendocrine tumors of the lung via NanoString nCounter expression analysis.

Robert Fred Henry Walter, Robert Werner, Saskia Ting, Claudia Vollbrecht, Dirk Theegarten, Daniel Christian Christoph, Kurt Werner Schmid, Jeremias Wohlschlaeger, Fabian Dominik Mairinger

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2015. 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
–field-weighted citation impact
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.

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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.

Robert Fred Henry WalterRuhrlandklinik, West German Lung Center, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Robert WernerInstitute of Pathology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Saskia TingInstitute of Pathology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Claudia VollbrechtInstitute of Pathology, University Hospital Cologne, Cologne, Germany.
Dirk TheegartenInstitute of Pathology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Daniel Christian ChristophDepartment of Medical Oncology, West German Cancer Center, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Kurt Werner SchmidInstitute of Pathology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Jeremias WohlschlaegerInstitute of Pathology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Fabian Dominik MairingerInstitute of Pathology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuroendocrine tumors of the lung comprise typical (TC) and atypical carcinoids (AC), large-cell neuroendocrine cancer (LCNEC) and small-cell lung cancer (SCLC). Cell cycle and apoptosis are key pathways of multicellular homeostasis and deregulation of these pathways is associated with cancerogenesis. MATERIALS AND

methodsSixty representative FFPE-specimens (16 TC, 13 AC, 16 LCNEC and 15 SCLC) were used for mRNA expression analysis using the NanoString technique. Eight genes related to apoptosis and ten genes regulating key points of cell cycle were investigated.

resultsASCL1, BCL2, CASP8, CCNE1, CDK1, CDK2, CDKN1A and CDKN2A showed lower expression in carcinoids compared to carcinomas. In contrast, CCNE1 and CDK6 showed elevated expression in carcinoids compared to carcinomas. The calculated BCL2/BAX ratio showed increasing values from TC to SCLC. Between SCLC and LCNEC CDK2, CDKN1B, CDKN2A and PNN expression was significantly different with higher expression in SCLC.

conclusionCarcinoids have increased CDK4/6 and CCND1 expression controlling RB1 phosphorylation via this signaling cascade. CDK2 and CCNE1 were increased in carcinomas showing that these use the opposite way to control RB1. BAX and BCL2 are antagonists in regulating apoptosis. BCL2 expression increased over BAX expression with increasing malignancy of the tumor from TC to SCLC.

Indexed as

ApoptosisApoptosis Regulatory ProteinsBiomarkers, TumorCarcinoid TumorCarcinoma, Large CellCell CycleCell Cycle ProteinsFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHigh-Throughput Nucleotide SequencingHumansLung NeoplasmsMaleNanotechnologyRNA, MessengerApoptosis Regulatory ProteinsBiomarkers, TumorCell Cycle ProteinsRNA, Messengerapoptosiscarcinoidslarge-cell neuroendocrine lung cancerNanoString nCounterPathology Sectionsmall-cell lung cancer

Identifiers

PMID26008974
PMCPMC4694788

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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.