title: Systems-level analysis of clinically different phenotypes of juvenile nasopharyngeal angiofibromas.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
authors.affiliation: Department of Otorhinolaryngology-Head and Neck Surgery, Haartman Institute and HusLab, Helsinki University Central Hospital and University of Helsinki, Helsinki, Finland. suvi.renkonen@helsinki.fi
authors.forename: Suvi
authors.initials: S
authors.lastname: Renkonen
authors.forename: Matti
authors.initials: M
authors.lastname: Kankainen
authors.forename: Jaana
authors.initials: J
authors.lastname: Hagström
authors.forename: Caj
authors.initials: C
authors.lastname: Haglund
authors.forename: Outi
authors.initials: O
authors.lastname: Monni
authors.forename: Antti A
authors.initials: AA
authors.lastname: Mäkitie
mesh_terms: D000293:Adolescent; D018322:Angiofibroma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D055028:Comparative Genomic Hybridization; D004273:DNA, Neoplasm / Q000235:genetics*; D005260:Female; D005500:Follow-Up Studies; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D009303:Nasopharyngeal Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D010641:Phenotype; D012189:Retrospective Studies; D051746:ZAP-70 Protein-Tyrosine Kinase / Q000096:biosynthesis / Q000235:genetics*
chemical_list: D004273:DNA, Neoplasm; D051746:ZAP-70 Protein-Tyrosine Kinase