Copyright
©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Aug 16, 2014; 2(8): 395-397
Published online Aug 16, 2014. doi: 10.12998/wjcc.v2.i8.395
Published online Aug 16, 2014. doi: 10.12998/wjcc.v2.i8.395
Rare large homozygous CFTR gene deletion in an Iranian patient with cystic fibrosis
Shirin Farjadian, Department of Immunology, Allergy Research Center, Shiraz University of Medical Sciences, 71348-45794 Shiraz, Iran
Mozhgan Moghtaderi, Allergy Research Center, Shiraz University of Medical Sciences, 71348-45794 Shiraz, Iran
Roberta Zuntini, Simona Ferrari, Unità Operativa di Genetica Medica, Dipartimento di Scienze Mediche e Chirurgiche Policlinico Sant’Orsola-Malpighi, 40138 Bologna, Italy
Author contributions: Farjadian S designed, organized, and carried out the molecular genetic studies and drafted the manuscript; Moghtaderi M collected the medical data on the patient and reviewed the manuscript; Zuntini R and Ferrari S carried out some molecular tests and reviewed the manuscript; all authors read and approved the final manuscript.
Supported by Shiraz University of Medical Sciences, Shiraz, Iran and Bologna University, Bologna, Italy
Correspondence to: Shirin Farjadian, PhD, Department of Immunology, Allergy Research Center, Shiraz University of Medical Sciences, Zand Avenue, 71348-45794 Shiraz, Iran. farjadsh@sums.ac.ir
Telephone: +98-711-2351575 Fax: +98-711-2351575
Received: April 9, 2014
Revised: May 11, 2014
Accepted: June 10, 2014
Published online: August 16, 2014
Processing time: 147 Days and 17.8 Hours
Revised: May 11, 2014
Accepted: June 10, 2014
Published online: August 16, 2014
Processing time: 147 Days and 17.8 Hours
Core Tip
Core tip: Genetic analysis of the transmembrane conductance regulatory (CFTR) gene is helpful to characterize patients with cystic fibrosis, but sequencing and multiplex ligation-dependent probe amplification-based testing are only done to diagnose rare or unknown variants. Here we report a 16-year-old boy, the son of consanguineous healthy parents, who lacked both the normal and mutant forms of the ∆F508 alleles in initial molecular tests. Further analysis disclosed a rare large homozygous CFTR gene deletion in this patient.