Systems-level analysis of clinically different phenotypes of juvenile nasopharyngeal angiofibromas†
Corresponding Author
Suvi Renkonen MD
Department of Otorhinolaryngology–Head and Neck Surgery, Haartman Institute and HusLab, Helsinki University Central Hospital and University of Helsinki, Helsinki, Finland
Department of Otorhinolaryngology, Haartman Institute, PO Box 21, FIN-00014 University of Helsinki, Helsinki, FinlandSearch for more papers by this authorMatti Kankainen MSc
Biomedicum Functional Genomics Unit, Biomedicum HelsinkiGenome-Scale Biology Research Program, University of Helsinki, Helsinki, Finland
Search for more papers by this authorJaana Hagström MD
Department of Pathology, Haartman Institute and HusLab, Helsinki University Central Hospital and University of Helsinki, Helsinki, Finland
Department of Oral PathologyGenome-Scale Biology Research Program, University of Helsinki, Helsinki, Finland
Search for more papers by this authorCaj Haglund MD
Department of Pathology, Haartman Institute and HusLab, Helsinki University Central Hospital and University of Helsinki, Helsinki, Finland
Department of SurgeryGenome-Scale Biology Research Program, University of Helsinki, Helsinki, Finland
Search for more papers by this authorOuti Monni PhD
Institute of Biomedicine, Medical Biochemistry and Developmental Biology, Genome-Scale Biology Research Program, University of Helsinki, Helsinki, Finland
Outi Monni, MD, and Antti A. Mäkitie, MD, contributed equally to this work.
Search for more papers by this authorAntti A. Mäkitie MD
Department of Otorhinolaryngology–Head and Neck Surgery, Haartman Institute and HusLab, Helsinki University Central Hospital and University of Helsinki, Helsinki, Finland
Outi Monni, MD, and Antti A. Mäkitie, MD, contributed equally to this work.
Search for more papers by this authorCorresponding Author
Suvi Renkonen MD
Department of Otorhinolaryngology–Head and Neck Surgery, Haartman Institute and HusLab, Helsinki University Central Hospital and University of Helsinki, Helsinki, Finland
Department of Otorhinolaryngology, Haartman Institute, PO Box 21, FIN-00014 University of Helsinki, Helsinki, FinlandSearch for more papers by this authorMatti Kankainen MSc
Biomedicum Functional Genomics Unit, Biomedicum HelsinkiGenome-Scale Biology Research Program, University of Helsinki, Helsinki, Finland
Search for more papers by this authorJaana Hagström MD
Department of Pathology, Haartman Institute and HusLab, Helsinki University Central Hospital and University of Helsinki, Helsinki, Finland
Department of Oral PathologyGenome-Scale Biology Research Program, University of Helsinki, Helsinki, Finland
Search for more papers by this authorCaj Haglund MD
Department of Pathology, Haartman Institute and HusLab, Helsinki University Central Hospital and University of Helsinki, Helsinki, Finland
Department of SurgeryGenome-Scale Biology Research Program, University of Helsinki, Helsinki, Finland
Search for more papers by this authorOuti Monni PhD
Institute of Biomedicine, Medical Biochemistry and Developmental Biology, Genome-Scale Biology Research Program, University of Helsinki, Helsinki, Finland
Outi Monni, MD, and Antti A. Mäkitie, MD, contributed equally to this work.
Search for more papers by this authorAntti A. Mäkitie MD
Department of Otorhinolaryngology–Head and Neck Surgery, Haartman Institute and HusLab, Helsinki University Central Hospital and University of Helsinki, Helsinki, Finland
Outi Monni, MD, and Antti A. Mäkitie, MD, contributed equally to this work.
Search for more papers by this authorThe authors have no other funding, financial relationships, or conflicts of interest to disclose.
Abstract
Objectives/Hypothesis:
To explore the molecular genetic background of juvenile nasopharyngeal angiofibromas and to identify biological processes and putative factors determining the different growth patterns of these tumors.
Study Design:
By comparing copy number and gene expression level changes of two clinically different phenotypes of juvenile nasopharyngeal angiofibromas, we aimed to find processes essential in the growth and development of these tumors. Based on the results and prior knowledge of the proteins significance for growth, we studied the expression of tyrosine kinase SYK in 27 tumor samples.
Methods:
Comparative genomic hybridization and gene expression analyses were performed for the two tumor samples, and protein expression of SYK was studied in 27 samples by immunohistochemical staining.
Results:
Between low- and high-stage juvenile nasopharyngeal angiofibromas, 1,245 genes showed at least a two-fold change in expression. The corresponding proteins of these transcripts were enriched in different biological processes. Protein kinase SYK was expressed in all 27 samples, and its intensity significantly correlated with tumor stage.
Conclusions:
Because the molecular genetic background of juvenile nasopharyngeal angiofibroma is unknown, our aim was to investigate genomic alterations that could associate to low- and high-stage tumors. We were able to identify gene expression changes that relate to particular biological processes, but assessing clinically relevant molecular profiles still requires further characterization. Due to the low incidence of juvenile angiofibroma, in the future a combination of molecular profiling data from several studies would be useful in understanding the molecular background of the disease. Laryngoscope, 2012
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