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Tumor microenvironmental genomic alterations in juvenile nasopharyngeal angiofibroma

Authors

  • Sara Martoreli Silveira MSc,

    1. NeoGene Laboratory, Cancer and Treatment Research Center, Antonio Prudente Foundation, AC Camargo Hospital, São Paulo, SP, Brazil
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  • Maria Aparecida Custódio Domingues PhD,

    1. Department of Pathology, FMB, UNESP, São Paulo State University, Botucatu SP, Brazil
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  • Ossamu Butugan PhD,

    1. Department of Otorhinolaryngology, FMUSP, University of São Paulo, São Paulo, SP, Brazil
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  • Maria Mitzi Brentani PhD,

    1. Department of Radiology, FMUSP, University of São Paulo, São Paulo, SP, Brazil (LIM24)
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  • Silvia Regina Rogatto PhD

    Corresponding author
    1. NeoGene Laboratory, Cancer and Treatment Research Center, Antonio Prudente Foundation, AC Camargo Hospital, São Paulo, SP, Brazil
    2. Department of Urology, FMB, UNESP, São Paulo State University, Botucatu SP, Brazil
    • NeoGene Laboratory, Cancer and Treatment Research Center, Antonio Prudente Foundation, AC Camargo Hospital, São Paulo, SP, Brazil
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Abstract

Background

To better characterize the pathophysiology of juvenile nasopharyngeal angiofibroma (JNA), endothelial and stromal cells were evaluated by genomic imbalances in association with transcript expression levels of genes mapped on these altered regions.

Methods

High-resolution comparative genomic hybridization (HR-CGH) was used in laser-captured endothelial and stromal cells from 9 JNAs. Ten genes were evaluated by quantitative real-timereverse transcription polymerase chain reaction (qRT-PCR) in 15 cases.

Results

Although gains were more frequently detected in endothelial cells, 57% of chromosomal alterations were common by both components. Gene expression analyses revealed a positive correlation between endothelial and stromal components for ASPM, CDH1, CTNNB1, FGF18, and SUPT16H. A significant difference was found for FGF18 and AURKB overexpression in stromal cells and AR down-expression in endothelial cells.

Conclusions

A similar pattern of gene expression and chromosomal imbalances in both exponents would suggest a common mechanism of functional regulation. AURKB, FGF18, and SUPT16H were identified as potential molecular markers in JNA. © 2011 Wiley Periodicals, Inc. Head Neck, 2012

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