Literature DB >> 19716085

Spectrum and prevalence of mutations from the first 2,500 consecutive unrelated patients referred for the FAMILION long QT syndrome genetic test.

Jamie D Kapplinger1, David J Tester, Benjamin A Salisbury, Janet L Carr, Carole Harris-Kerr, Guido D Pollevick, Arthur A M Wilde, Michael J Ackerman.   

Abstract

BACKGROUND: Long QT syndrome (LQTS) is a potentially lethal, highly treatable cardiac channelopathy for which genetic testing has matured from discovery to translation and now clinical implementation.
OBJECTIVES: Here we examine the spectrum and prevalence of mutations found in the first 2,500 unrelated cases referred for the FAMILION LQTS clinical genetic test.
METHODS: Retrospective analysis of the first 2,500 cases (1,515 female patients, average age at testing 23 +/- 17 years, range 0 to 90 years) scanned for mutations in 5 of the LQTS-susceptibility genes: KCNQ1 (LQT1), KCNH2 (LQT2), SCN5A (LQT3), KCNE1 (LQT5), and KCNE2 (LQT6).
RESULTS: Overall, 903 referral cases (36%) hosted a possible LQTS-causing mutation that was absent in >2,600 reference alleles; 821 (91%) of the mutation-positive cases had single genotypes, whereas the remaining 82 patients (9%) had >1 mutation in > or =1 gene, including 52 cases that were compound heterozygous with mutations in >1 gene. Of the 562 distinct mutations, 394 (70%) were missense, 428 (76%) were seen once, and 336 (60%) are novel, including 92 of 199 in KCNQ1, 159 of 226 in KCNH2, and 70 of 110 in SCN5A.
CONCLUSION: This cohort increases the publicly available compendium of putative LQTS-associated mutations by >50%, and approximately one-third of the most recently detected mutations continue to be novel. Although control population data suggest that the great majority of these mutations are pathogenic, expert interpretation of genetic test results will remain critical for effective clinical use of LQTS genetic test results.

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Year:  2009        PMID: 19716085      PMCID: PMC3049907          DOI: 10.1016/j.hrthm.2009.05.021

Source DB:  PubMed          Journal:  Heart Rhythm        ISSN: 1547-5271            Impact factor:   6.343


  34 in total

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2.  Cardiac channelopathies: it's in the genes.

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Journal:  Cell       Date:  2001-05-18       Impact factor: 41.582

5.  Spectrum of mutations in long-QT syndrome genes. KVLQT1, HERG, SCN5A, KCNE1, and KCNE2.

Authors:  I Splawski; J Shen; K W Timothy; M H Lehmann; S Priori; J L Robinson; A J Moss; P J Schwartz; J A Towbin; G M Vincent; M T Keating
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6.  Information theory-based analysis of CYP2C19, CYP2D6 and CYP3A5 splicing mutations.

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10.  Identification of large gene deletions and duplications in KCNQ1 and KCNH2 in patients with long QT syndrome.

Authors:  Carey-Anne Eddy; Judith M MacCormick; Seo-Kyung Chung; Jackie R Crawford; Donald R Love; Mark I Rees; Jonathan R Skinner; Andrew N Shelling
Journal:  Heart Rhythm       Date:  2008-06-04       Impact factor: 6.343

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  156 in total

Review 1.  HERG1 channelopathies.

Authors:  Michael C Sanguinetti
Journal:  Pflugers Arch       Date:  2009-11-22       Impact factor: 3.657

2.  Multiple splicing defects caused by hERG splice site mutation 2592+1G>A associated with long QT syndrome.

Authors:  Matthew R Stump; Qiuming Gong; Zhengfeng Zhou
Journal:  Am J Physiol Heart Circ Physiol       Date:  2010-11-05       Impact factor: 4.733

3.  High-throughput discovery of trafficking-deficient variants in the cardiac potassium channel KV11.1.

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Journal:  Heart Rhythm       Date:  2020-06-06       Impact factor: 6.343

4.  Inhibition of nonsense-mediated mRNA decay by antisense morpholino oligonucleotides restores functional expression of hERG nonsense and frameshift mutations in long-QT syndrome.

Authors:  Qiuming Gong; Matthew R Stump; Zhengfeng Zhou
Journal:  J Mol Cell Cardiol       Date:  2010-10-28       Impact factor: 5.000

5.  Congenital long-QT syndrome in Addison's disease: a novel association.

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6.  Prevalence of HCM and long QT syndrome mutations in young sudden cardiac death-related cases.

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Review 8.  Genetics of sudden cardiac death caused by ventricular arrhythmias.

Authors:  Roos F Marsman; Hanno L Tan; Connie R Bezzina
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9.  High-risk long QT syndrome mutations in the Kv7.1 (KCNQ1) pore disrupt the molecular basis for rapid K(+) permeation.

Authors:  Don E Burgess; Daniel C Bartos; Allison R Reloj; Kenneth S Campbell; Jonathan N Johnson; David J Tester; Michael J Ackerman; Véronique Fressart; Isabelle Denjoy; Pascale Guicheney; Arthur J Moss; Seiko Ohno; Minoru Horie; Brian P Delisle
Journal:  Biochemistry       Date:  2012-11-02       Impact factor: 3.162

Review 10.  From Genotype to Phenotype.

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