Literature DB >> 26485571

Atypical patterns of segregation of familial enlargement of the vestibular aqueduct.

Julie A Muskett1, Parna Chattaraj1, John F Heneghan2, Fabian R Reimold2, Boris E Shmukler2, Carmen C Brewer1, Kelly A King1, Christopher K Zalewski1, Thomas H Shawker3, John A Butman3, Margaret A Kenna4,5, Wade W Chien6, Seth L Alper2, Andrew J Griffith1.   

Abstract

OBJECTIVES/HYPOTHESIS: Hearing loss and enlarged vestibular aqueduct (EVA) can be inherited as an autosomal recessive trait caused by mutant alleles of the SLC26A4 gene. In some other families, EVA does not segregate in a typical autosomal recessive pattern. The goal of this study was to characterize the SLC26A4 genotypes and phenotypes of extended families with atypical segregation of EVA. STUDY
DESIGN: Prospective study of cohort of families ascertained between 1998 and 2014 at the National Institutes of Health Clinical Center.
METHODS: Study subjects were members of eight families segregating EVA in at least two members who were not related as siblings. Evaluations included pure-tone audiometry, temporal bone imaging, SLC26A4 nucleotide sequence analysis, SLC26A4-linked marker genotype and haplotype analysis, and pedigree analysis.
RESULTS: One family had members with EVA caused by different etiologies, and two families had pseudodominant inheritance of recessive mutations of SLC26A4. In five families, the etiology remained unknown and could include inheritance of mutant alleles at another genetic locus, nongenetic influences, or a combination of these factors.
CONCLUSIONS: Familial EVA can demonstrate a variety of atypical segregation patterns. Pseudodominant inheritance of SLC26A4 mutations or recessive alleles of other hearing loss genes may be more likely to occur in families in which deaf individuals have intermarried. The etiologic basis of atypical segregation of EVA without detectable SLC26A4 mutations remains unknown. Future studies of these families may reveal novel genes for EVA. LEVEL OF EVIDENCE: NA Laryngoscope, 126:E240-E247, 2016.
© 2015 The American Laryngological, Rhinological and Otological Society, Inc.

Entities:  

Keywords:  Assortative mating; SLC26A4; deafness; genetic; hearing loss; pseudodominant

Mesh:

Substances:

Year:  2015        PMID: 26485571      PMCID: PMC4838554          DOI: 10.1002/lary.25737

Source DB:  PubMed          Journal:  Laryngoscope        ISSN: 0023-852X            Impact factor:   3.325


  27 in total

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Authors:  D Shears; H Conlon; T Murakami; K Fukai; R Alles; R Trembath; M Bitner-Glindzicz
Journal:  Clin Genet       Date:  2004-05       Impact factor: 4.438

2.  Investigation of the role of congenital cytomegalovirus infection in the etiology of enlarged vestibular aqueducts.

Authors:  Shannon P Pryor; Gail J Demmler; Anne C Madeo; Yandan Yang; Chris K Zalewski; Carmen C Brewer; John A Butman; Karen B Fowler; Andrew J Griffith
Journal:  Arch Otolaryngol Head Neck Surg       Date:  2005-05

3.  Origins and frequencies of SLC26A4 (PDS) mutations in east and south Asians: global implications for the epidemiology of deafness.

Authors:  H-J Park; S Shaukat; X-Z Liu; S H Hahn; S Naz; M Ghosh; H-N Kim; S-K Moon; S Abe; K Tukamoto; S Riazuddin; M Kabra; R Erdenetungalag; J Radnaabazar; S Khan; A Pandya; S-I Usami; W E Nance; E R Wilcox; S Riazuddin; A J Griffith
Journal:  J Med Genet       Date:  2003-04       Impact factor: 6.318

4.  The large vestibular aqueduct syndrome.

Authors:  G E Valvassori; J D Clemis
Journal:  Laryngoscope       Date:  1978-05       Impact factor: 3.325

5.  Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS).

Authors:  L A Everett; B Glaser; J C Beck; J R Idol; A Buchs; M Heyman; F Adawi; E Hazani; E Nassir; A D Baxevanis; V C Sheffield; E D Green
Journal:  Nat Genet       Date:  1997-12       Impact factor: 38.330

6.  Phenocopies for deafness and goiter development in a large inbred Brazilian kindred with Pendred's syndrome associated with a novel mutation in the PDS gene.

Authors:  P Kopp; O K Arseven; L Sabacan; T Kotlar; J Dupuis; H Cavaliere; C L Santos; J L Jameson; G Medeiros-Neto
Journal:  J Clin Endocrinol Metab       Date:  1999-01       Impact factor: 5.958

7.  A comparative analysis of the genetic epidemiology of deafness in the United States in two sets of pedigrees collected more than a century apart.

Authors:  Kathleen S Arnos; Katherine O Welch; Mustafa Tekin; Virginia W Norris; Susan H Blanton; Arti Pandya; Walter E Nance
Journal:  Am J Hum Genet       Date:  2008-07-24       Impact factor: 11.025

8.  The large vestibular aqueduct: a new definition based on audiologic and computed tomography correlation.

Authors:  Mark Boston; Mark Halsted; Jareen Meinzen-Derr; Judy Bean; Shyan Vijayasekaran; Ellis Arjmand; Daniel Choo; Corning Benton; John Greinwald
Journal:  Otolaryngol Head Neck Surg       Date:  2007-06       Impact factor: 3.497

9.  Mutation analysis of the SLC26A4, FOXI1 and KCNJ10 genes in individuals with congenital hearing loss.

Authors:  Lynn M Pique; Marie-Luise Brennan; Colin J Davidson; Frederick Schaefer; John Greinwald; Iris Schrijver
Journal:  PeerJ       Date:  2014-05-08       Impact factor: 2.984

10.  Challenges and solutions for gene identification in the presence of familial locus heterogeneity.

Authors:  Atteeq U Rehman; Regie Lyn P Santos-Cortez; Meghan C Drummond; Mohsin Shahzad; Kwanghyuk Lee; Robert J Morell; Muhammad Ansar; Abid Jan; Xin Wang; Abdul Aziz; Saima Riazuddin; Joshua D Smith; Gao T Wang; Zubair M Ahmed; Khitab Gul; A Eliot Shearer; Richard J H Smith; Jay Shendure; Michael J Bamshad; Deborah A Nickerson; John Hinnant; Shaheen N Khan; Rachel A Fisher; Wasim Ahmad; Karen H Friderici; Sheikh Riazuddin; Thomas B Friedman; Ellen S Wilch; Suzanne M Leal
Journal:  Eur J Hum Genet       Date:  2014-12-10       Impact factor: 4.246

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  5 in total

1.  Hearing loss associated with enlarged vestibular aqueduct and zero or one mutant allele of SLC26A4.

Authors:  Jane Rose; Julie A Muskett; Kelly A King; Christopher K Zalewski; Parna Chattaraj; John A Butman; Margaret A Kenna; Wade W Chien; Carmen C Brewer; Andrew J Griffith
Journal:  Laryngoscope       Date:  2016-11-15       Impact factor: 3.325

2.  A common SLC26A4-linked haplotype underlying non-syndromic hearing loss with enlargement of the vestibular aqueduct.

Authors:  Parna Chattaraj; Tina Munjal; Keiji Honda; Nanna D Rendtorff; Jessica S Ratay; Julie A Muskett; Davide S Risso; Isabelle Roux; E Michael Gertz; Alejandro A Schäffer; Thomas B Friedman; Robert J Morell; Lisbeth Tranebjærg; Andrew J Griffith
Journal:  J Med Genet       Date:  2017-08-05       Impact factor: 6.318

3.  Systematic quantification of the anion transport function of pendrin (SLC26A4) and its disease-associated variants.

Authors:  Koichiro Wasano; Satoe Takahashi; Samuel K Rosenberg; Takashi Kojima; Hideki Mutai; Tatsuo Matsunaga; Kaoru Ogawa; Kazuaki Homma
Journal:  Hum Mutat       Date:  2019-10-26       Impact factor: 4.878

4.  Functional Testing of SLC26A4 Variants-Clinical and Molecular Analysis of a Cohort with Enlarged Vestibular Aqueduct from Austria.

Authors:  Sebastian Roesch; Emanuele Bernardinelli; Charity Nofziger; Miklós Tóth; Wolfgang Patsch; Gerd Rasp; Markus Paulmichl; Silvia Dossena
Journal:  Int J Mol Sci       Date:  2018-01-10       Impact factor: 5.923

5.  SLC26A4-linked CEVA haplotype correlates with phenotype in patients with enlargement of the vestibular aqueduct.

Authors:  Janet R Chao; Parna Chattaraj; Tina Munjal; Keiji Honda; Kelly A King; Christopher K Zalewski; Wade W Chien; Carmen C Brewer; Andrew J Griffith
Journal:  BMC Med Genet       Date:  2019-07-02       Impact factor: 2.103

  5 in total

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