Evidence map›Paper›PMID 23914742›Full record

ArticleJournal of translational medicine2013

Identification of prefoldin amplification (1q23.3-q24.1) in bladder cancer using comparative genomic hybridization (CGH) arrays of urinary DNA.

Virginia López, Pilar González-Peramato, Javier Suela, Alvaro Serrano, Ferrán Algaba, Juan C Cigudosa, August Vidal, Joaquim Bellmunt, Oscar Heredero, Marta Sánchez-Carbayo

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Article in Journal of translational medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 30 citations in OpenAlex.

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  8. Review
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  11. Prefoldin Function in Cellular Protein Homeostasis and Human Diseases.Frontiers in cell and developmental biology · 2021
    Review
  12. Article
  13. Review
  14. MCL1 and DEDD Promote Urothelial Carcinoma Progression.Molecular cancer research : MCR · 2019
    Article
  15. Article
  16. Article
  17. 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

10 authors at 8 institutions in 1 country.

Virginia LópezTumor Markers Group, Molecular Pathology Program, Spanish National Cancer Center, Melchor Fernandez Almagro 3, Madrid E-28029, Spain.
Pilar González-Peramato
Javier Suela
Alvaro Serrano
Ferrán Algaba
Juan C Cigudosa
August Vidal
Joaquim Bellmunt
Oscar Heredero
Marta Sánchez-Carbayo
Centre for Biomedical Network Research on Rare Diseases · ESSpanish National Cancer Research Centre · ESBellvitge University Hospital · ESComplejo Hospitalario de Salamanca · ESHospital Del Mar · ESHospital Universitario de Guadalajara · ESHospital Universitario La Paz · ESPuigvert Foundation · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundArray-CGH represents a comprehensive tool to discover genomic disease alterations that could potentially be applied to body fluids. In this report, we aimed at applying array-CGH to urinary samples to characterize bladder cancer.

methodsUrinary DNA from bladder cancer patients and controls were hybridized on 44K oligonucleotide arrays. Validation analyses of identified regions and candidates included fluorescent in situ hybridization (FISH) and immunohistochemistry in an independent set of bladder tumors spotted on custom-made tissue arrays (n = 181).

resultsQuality control of array-CGH provided high reproducibility in dilution experiments and when comparing reference pools. The most frequent genomic alterations (minimal recurrent regions) among bladder cancer urinary specimens included gains at 1q and 5p, and losses at 10p and 11p. Supervised hierarchical clustering identified the gain at 1q23.3-q24.1 significantly correlated to stage (p = 0.011), and grade (p = 0.002). The amplification and overexpression of Prefoldin (PFND2), a selected candidate mapping to 1q23.3-q24.1, correlated to increasing stage and tumor grade by means of custom-designed and optimized FISH (p = 0.013 and p = 0.023, respectively), and immunohistochemistry (p ≤0.0005 and p = 0.011, respectively), in an independent set of bladder tumors included in tissue arrays. Moreover, PFND2 overexpression was significantly associated with poor disease-specific survival (p ≤0.0005). PFND2 was amplified and overexpressed in bladder tumors belonging to patients providing urinary specimens where 1q23.3q24.1 amplification was detected by array-CGH.

conclusionsGenomic profiles of urinary DNA mirrowed bladder tumors. Molecular profiling of urinary DNA using array-CGH contributed to further characterize genomic alterations involved in bladder cancer progression. PFND2 was identified as a tumor stratification and clinical outcome prognostic biomarker for bladder cancer patients.

Indexed as

Comparative Genomic HybridizationGene Expression Regulation, NeoplasticBiomarkersBiomarkers, TumorChromosomes, Human, Pair 1Cluster AnalysisDNAHumansImmunohistochemistryIn Situ Hybridization, FluorescenceMolecular ChaperonesReproducibility of ResultsUrinary Bladder NeoplasmsBiomarkersBiomarkers, TumorDNAMolecular Chaperonesprefoldin

Identifiers

PMID23914742
PMCPMC3750577
OpenAlexW2098190335

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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.