Evidence map›Paper›PMID 17420988›Full record

ArticleGenes, chromosomes & cancer2007

Allelic imbalances and microdeletions affecting the PTPRD gene in cutaneous squamous cell carcinomas detected using single nucleotide polymorphism microarray analysis.

Karin J Purdie, Sally R Lambert, Muy-Teck Teh, Tracy Chaplin, Gael Molloy, Manoj Raghavan, David P Kelsell, Irene M Leigh, Catherine A Harwood, Charlotte M Proby and 1 more

Open access · greenAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
13.9field-weighted citation impact, top 1% 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

42 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
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  8. Protein Tyrosine Phosphatases as Potential Regulators of STAT3 Signaling.International journal of molecular sciences · 2018
    Review
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  12. Abundant copy-number loss of CYCLOPS and STOP genes in gastric adenocarcinoma.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2016
    Article
  13. 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

11 authors at 3 institutions in 1 country.

Karin J PurdieCancer Research UK Skin Tumour Laboratory, Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, Queen Mary, University of London, London, England, UK. k.purdie@qmul.ac.uk
Sally R Lambert
Muy-Teck Teh
Tracy Chaplin
Gael Molloy
Manoj Raghavan
David P Kelsell
Irene M Leigh
Catherine A Harwood
Charlotte M Proby
Bryan D Young
Queen Mary University of London · GBCancer Research UK · GBNinewells Hospital · GB

Funding

Cancer Research UK A6438Cancer Research UK A6695Cancer Research UK A6789
6 · The paper itself

Abstract

Cutaneous squamous cell carcinomas (SCC) are the second most commonly diagnosed cancers in fair-skinned people; yet the genetic mechanisms involved in SCC tumorigenesis remain poorly understood. We have used single nucleotide polymorphism (SNP) microarray analysis to examine genome-wide allelic imbalance in 16 primary and 2 lymph node metastatic SCC using paired non-tumour samples to counteract normal copy number variation. The most common genetic change was loss of heterozygosity (LOH) on 9p, observed in 13 of 16 primary SCC. Other recurrent events included LOH on 3p (9 tumors), 2q, 8p, and 13 (each in 8 SCC) and allelic gain on 3q and 8q (each in 6 tumors). Copy number-neutral LOH was observed in a proportion of samples, implying that somatic recombination had led to acquired uniparental disomy, an event not previously demonstrated in SCC. As well as recurrent patterns of gross chromosomal changes, SNP microarray analysis revealed, in 2 primary SCC, a homozygous microdeletion on 9p23 within the protein tyrosine phosphatase receptor type D (PTPRD) locus, an emerging frequent target of homozygous deletion in lung cancer and neuroblastoma. A third sample was heterozygously deleted within this locus and PTPRD expression was aberrant. Two of the 3 primary SCC with PTPRD deletion had demonstrated metastatic potential. Our data identify PTPRD as a candidate tumor suppressor gene in cutaneous SCC with a possible association with metastasis.

Indexed as

AllelesOligonucleotide Array Sequence AnalysisPolymorphism, Single NucleotideAgedAged, 80 and overCarcinoma, Squamous CellChromosome AberrationsFemaleHumansLoss of HeterozygosityMaleMiddle AgedProtein Tyrosine PhosphatasesReceptor-Like Protein Tyrosine Phosphatases, Class 2Skin NeoplasmsProtein Tyrosine PhosphatasesPTPRD protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 2

Identifiers

PMID17420988
PMCPMC2426828
OpenAlexW2147158070

What OpenQuestion holds

Textmetadata
LicenceTDM
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.