Eugene Chang

Eugene Chang

Associate Professor, Otolaryngology
Vice Chair, Academic Affairs - Otolaryngology
Associate Professor, Clinical Translational Sciences
Associate Professor, Neurosurgery
Member of the Graduate Faculty
Associate Professor, BIO5 Institute
Primary Department
Department Affiliations
Contact
(520) 626-6673

Research Interest

Dr. Chang’s research is divided into three areas.Cystic fibrosis (CF) research: Dr. Chang is investigating the role of the cystic fibrosis transmembrane conductance regulator (CFTR) gene in the pathogenesis of chronic sinusitis. He published the first animal model of CF sinus disease, and has characterized novel therapies including gene therapy vectors and CFTR potentiators in improving CF sinus disease in both animals and humans.Sinus microbiome research: the “microbiome” is the microbial community that is present in the human body. The sinonasal cavities have traditionally been thought to be sterile cavities, but new research is beginning to elucidate the vast number of microbial communities that populate our sinus. With this knowledge, we are investigating how our current therapies can influence this microbial population and prevent sinus disease.Impact of the upper and lower airway: as otolaryngologists, our focus has been in the airway of the head and neck. Dr. Chang has been investigating how the upper airway can influence disease of the lower airway, and vice versa. This research can influence the understanding of common diseases of the lower airway, such as asthma and chronic obstructive pulmonary disease (COPD).Dr. Chang receives active funding research support from the NIH, and the Cystic Fibrosis Foundation.

Publications

Chang, E. H., Menezes, M., Meyer, N. C., Cucci, R. A., Vervoort, V. S., Schwartz, C. E., & Smith, R. J. (2004). Branchio-oto-renal syndrome: the mutation spectrum in EYA1 and its phenotypic consequences. Human mutation, 23(6), 582-9.

EYA1 mutations cause branchio-oto-renal (BOR) syndrome. These mutations include single nucleotide transitions and transversions, small duplications and deletions, and complex genomic rearrangements. The last cannot be detected by coding sequence analysis of EYA1. We sought to refine the clinical diagnosis of BOR syndrome by analyzing phenotypic data from families segregating EYA1 disease-causing mutations. Based on genotype-phenotype analyses, we propose new criteria for the clinical diagnosis of BOR syndrome. We found that in approximately 40% of persons meeting our criteria, EYA1 mutations were identified. Of these mutations, 80% were coding sequence variants identified by SSCP, and 20% were complex genomic rearrangements identified by a semiquantitative PCR-based screen. We conclude that genetic testing of EYA1 should include analysis of the coding sequence and a screen for complex rearrangements.

Kopelovich, J. C., Baker, M. S., Potash, A., Desai, L., Allen, R. C., & Chang, E. H. (2014). The hybrid lid crease approach to address lateral frontal sinus disease with orbital extension. The Annals of otology, rhinology, and laryngology, 123(12), 826-30.

This study aimed to describe the hybrid lid crease approach in conjunction with functional endoscopic sinus surgery (FESS) for lateral frontal sinus disease with orbital extension.