Literature DB >> 29417725

Whole-exome sequencing for mutation detection in pediatric disorders of insulin secretion: Maturity onset diabetes of the young and congenital hyperinsulinism.

S R Johnson1,2,3,4, P J Leo4, A M McInerney-Leo4, L K Anderson4, M Marshall4, I McGown5, F Newell4, M A Brown4, L S Conwell1,3, M Harris1,2,3, E L Duncan3,4,6.   

Abstract

BACKGROUND: To assess the utility of whole-exome sequencing (WES) for mutation detection in maturity-onset diabetes of the young (MODY) and congenital hyperinsulinism (CHI). MODY and CHI are the two commonest monogenic disorders of glucose-regulated insulin secretion in childhood, with 13 causative genes known for MODY and 10 causative genes identified for CHI. The large number of potential genes makes comprehensive screening using traditional methods expensive and time-consuming.
METHODS: Ten subjects with MODY and five with CHI with known mutations underwent WES using two different exome capture kits (Nimblegen SeqCap EZ Human v3.0 Exome Enrichment Kit, Nextera Rapid Capture Exome Kit). Analysis was blinded to previously identified mutations, and included assessment for large deletions. The target capture of five exome capture technologies was also analyzed using sequencing data from >2800 unrelated samples.
RESULTS: Four of five MODY mutations were identified using Nimblegen (including a large deletion in HNF1B). Although targeted, one mutation (in INS) had insufficient coverage for detection. Eleven of eleven mutations (six MODY, five CHI) were identified using Nextera Rapid (including the previously missed mutation). On reconciliation, all mutations concorded with previous data and no additional variants in MODY genes were detected. There were marked differences in the performance of the capture technologies.
CONCLUSIONS: WES can be useful for screening for MODY/CHI mutations, detecting both point mutations and large deletions. However, capture technologies require careful selection.
© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Entities:  

Keywords:  capture technology comparison; congenital hyperinsulinism; massively parallel sequencing; maturity onset diabetes of the young; mutation detection; whole-exome sequencing

Mesh:

Year:  2018        PMID: 29417725     DOI: 10.1111/pedi.12638

Source DB:  PubMed          Journal:  Pediatr Diabetes        ISSN: 1399-543X            Impact factor:   4.866


  7 in total

Review 1.  Genetic characteristics of patients with congenital hyperinsulinism.

Authors:  Mary Ellen Vajravelu; Diva D De León
Journal:  Curr Opin Pediatr       Date:  2018-08       Impact factor: 2.856

2.  MODY10 caused by c.309-314del CCAGCT insGCGC mutation of the insulin gene: a case report.

Authors:  Shu-Qin Lei; Jie-Ying Wang; Rong-Min Li; Jie Chang; Zhen Li; Li Ren; Yan-Mei Sang
Journal:  Am J Transl Res       Date:  2020-10-15       Impact factor: 4.060

3.  Exome sequencing in children with clinically suspected maturity-onset diabetes of the young.

Authors:  Mustafa Tosur; Claudia Soler-Alfonso; Katie M Chan; Michael M Khayat; Shalini N Jhangiani; Qingchang Meng; Ahmad Refaey; Donna Muzny; Richard A Gibbs; David R Murdock; Jennifer E Posey; Ashok Balasubramanyam; Maria J Redondo; Aniko Sabo
Journal:  Pediatr Diabetes       Date:  2021-08-19       Impact factor: 4.866

4.  Frequency and characterization of mutations in genes in a large cohort of patients referred to MODY registry.

Authors:  Emily Breidbart; Liyong Deng; Patricia Lanzano; Xiao Fan; Jiancheng Guo; Rudolph L Leibel; Charles A LeDuc; Wendy K Chung
Journal:  J Pediatr Endocrinol Metab       Date:  2021-04-13       Impact factor: 1.634

5.  Reverse Phenotyping Maternal Cystic Kidney Disease by Diagnosis in a Newborn: Case Report and Literature Review on Neonatal Cystic Kidney Diseases.

Authors:  Dovilė Ruzgienė; Meda Sutkevičiūtė; Birutė Burnytė; Kristina Grigalionienė; Augustina Jankauskienė
Journal:  Acta Med Litu       Date:  2021-08-02

Review 6.  Hyperinsulinemic hypoglycemia in children and adolescents: Recent advances in understanding of pathophysiology and management.

Authors:  Maria Gϋemes; Sofia Asim Rahman; Ritika R Kapoor; Sarah Flanagan; Jayne A L Houghton; Shivani Misra; Nick Oliver; Mehul Tulsidas Dattani; Pratik Shah
Journal:  Rev Endocr Metab Disord       Date:  2020-12       Impact factor: 6.514

7.  A KCNK16 mutation causing TALK-1 gain of function is associated with maturity-onset diabetes of the young.

Authors:  Sarah M Graff; Stephanie R Johnson; Paul J Leo; Prasanna K Dadi; Matthew T Dickerson; Arya Y Nakhe; Aideen M McInerney-Leo; Mhairi Marshall; Karolina E Zaborska; Charles M Schaub; Matthew A Brown; David A Jacobson; Emma L Duncan
Journal:  JCI Insight       Date:  2021-07-08
  7 in total

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