Evidence map›Paper›PMID 20140953›Full record

ArticleGenes, chromosomes & cancer2010

Deletion at chromosome arm 9p in relation to BRAF/NRAS mutations and prognostic significance for primary melanoma.

Caroline Conway, Samantha Beswick, Faye Elliott, Yu-Mei Chang, Juliette Randerson-Moor, Mark Harland, Paul Affleck, Jerry Marsden, D Scott Sanders, Andy Boon and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
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  4. Review
  5. Article
  6. Emerging Biomarkers in Cutaneous Melanoma.Molecular diagnosis & therapy · 2018
    Review
  7. Article
  8. Article
  9. Article
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  11. Tumor genetic analyses of patients with metastatic melanoma treated with the BRAF inhibitor dabrafenib (GSK2118436).Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    Article
  12. Article
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  16. Article
  17. [Detection of MTAP protein and gene expression in non-small cell lung cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2011
    Article
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 4 institutions in 1 country.

Caroline ConwaySection of Epidemiology and Biostatistics, Leeds Institute of Molecular Medicine, University of Leeds, St. James's University Hospital, Leeds, UK.
Samantha Beswick
Faye Elliott
Yu-Mei Chang
Juliette Randerson-Moor
Mark Harland
Paul Affleck
Jerry Marsden
D Scott Sanders
Andy Boon
Margaret A Knowles
D Timothy Bishop
Julia A Newton-Bishop
University of Leeds · GBLeeds Teaching Hospitals NHS Trust · GBUniversity Hospitals Birmingham NHS Foundation Trust · GBWarwickshire Hospital · GB

Funding

Cancer Research UK 10589
6 · The paper itself

Abstract

We report an investigation of gene dosage at 9p21.3 and mutations in BRAF and NRAS, as predictors of relapse and histological markers of poor melanoma prognosis. Formalin-fixed primary melanomas from 74 relapsed and 42 nonrelapsed patients were sequenced for common BRAF and NRAS mutations (N = 71 results) and gene dosage at 9p21.3 including the genes CDKN2A (which encodes CDKN2A and P14ARF), CDKN2B (CDKN2B), and MTAP was measured using multiplexed ligation-dependant probe amplification (MLPA), (N = 75 results). BRAF/NRAS mutations were detected in 77% of relapsers and 58% of nonrelapsers (Fisher's exact P = 0.17), and did not predict ulceration or mitotic rate. There was no relationship between BRAF/NRAS mutations and gene dosage at 9p21.3. Reduced gene dosage at MTAP showed a borderline association with BRAF mutation (P = 0.04) and reduced gene dosage at the interferon gene cluster was borderline associated with wild type NRAS (P = 0.05). Reduced gene dosage in the CDKN2A regions coding for CDKN2A was associated with an increased risk of relapse (P = 0.03). Reduced gene dosage across 9p21.3 was associated with increased tumor thickness, mitotic rate, and ulceration (P = 0.02, 0.02, and 0.002, respectively), specifically in coding regions impacting on CDKN2B and P14ARF and CDKN2A. Loss at MTAP (P = 0.05) and the interferon gene cluster (P = 0.03) on 9p21 was also associated with tumor ulceration. There was no association between reduced gene dosage at 9p21.3 and subtype or site of tumor. This study presents supportive evidence that CDKN2B, P14ARF, and CDKN2A may all play a tumor suppressor role in melanoma progression.

Indexed as

Chromosomes, Human, Pair 9Gene DeletionGenes, rasChromosome MappingCluster AnalysisCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16DNA Mutational AnalysisGene DosageHistocytochemistryHumansMelanomaNucleic Acid Amplification TechniquesPrognosisProto-Oncogene Proteins B-rafPurine-Nucleoside Phosphorylase5'-methylthioadenosine phosphorylaseCDKN2B protein, humanCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16Proto-Oncogene Proteins B-rafPurine-Nucleoside PhosphorylaseTumor Suppressor Protein p14ARF

Identifiers

PMID20140953
PMCPMC2948432
OpenAlexW2081527075

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.