Hyperproliferation in Nasal Polyposis Tissues Is Not Associated with Somatic Genomic Instability

Background: Nasal polyps (NPs) are abnormal lesions that arise from any portion of the nasal mucosa or paranasal sinuses within the nasal cavities. They are characterized by the formation of inflammatory swellings of unstable respiratory mucosa, which protrude into the nasal cavity. The causes and the pathogenesis of NP development are not well understood. The current and principal hypothesis is that NPs result from allergy and inflammation, which cause an unstable respiratory mucosa with increased epithelial cell proliferation and epithelial morphologic changes. Objective: To understand if epithelial cell hyperproliferation can lead to acquired genomic instability and if nasal polyposis is a consequence of acquired chromosomal alterations in hyperproliferative nasal epithelia. Materials and Methods: To test this hypothesis and to perform a survey of chromosomal aberrations in nasal polyps, we applied array comparative genome hybridization (aCGH; 1 Mb resolution, made of 2464 bacterial artificial chromosome (BAC), P1 derived artificial chromosome (PAC), and P1 clones spanning the whole human genome) to deoxyribonucleic acid (DNA) obtained from the NPs of nine patients. The patients recruited in this study had been analyzed for Ki-67 expression using the MIB-1 antibody as a marker of proliferation and were chosen to represent a wide range of hyperproliferative status. Results: After data analysis, no chromosomal aberrations were detected by aCGH. Conclusions: Our data do not support the hypothesis that nasal polyposis is a consequence of acquired chromosomal alterations in hyperproliferative nasal epithelia.