Background
Sinonasal undifferentiated carcinoma remains a poorly characterized malignancy at both the clinical and molecular level, and consequently the optimal treatment strategy remains undefined.
Methods
We utilized a mass spectroscopy-based approach (Sequenom™) to evaluate 95 hallmark single nucleotide variations within 12 oncogenes or tumor suppressor genes (AKT, BRAF, CDK4, Beta-catenin, EGFR, FBXW7, JAK2, c-KIT, KRAS, PDGFR, PI3K, VEGF) in 13 histologically confirmed SNUC cases.
Results
None of the samples demonstrated activating mutations in any of the 95 SNVs.
Conclusions
Select clinically relevant activating genomic mutations were not identified the 13 patient samples. However, polymorphisms were noted within the promoter region of VEGF. These may merit future study as predictive biomarkers for treatment response or overall survival. Additionally, future studies focusing on larger tumor sets and utilizing whole genome or exome sequencing may help define genetic aberrations in SNUC that can be clinically targeted with available or emerging biological agents.