Document Detail


Phenotype diversity in type 1 Gaucher disease: discovering the genetic basis of Gaucher disease/hematologic malignancy phenotype by individual genome analysis.
MedLine Citation:
PMID:  22493294     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Gaucher disease (GD), an inherited macrophage glycosphingolipidosis, manifests with an extraordinary variety of phenotypes that show imperfect correlation with mutations in the GBA gene. In addition to the classic manifestations, patients suffer from increased susceptibility to hematologic and nonhematologic malignancies. The mechanism(s) underlying malignancy in GD is not known, but is postulated to be secondary to macrophage dysfunction and immune dysregulation arising from lysosomal accumulation of glucocerebroside. However, there is weak correlation between GD/cancer phenotype and the systemic burden of glucocerebroside-laden macrophages. Therefore, we hypothesized that genetic modifier(s) may underlie the GD/cancer phenotype. In the present study, the genetic basis of GD/T-cell acute lymphoblastic lymphoma in 2 affected siblings was deciphered through genomic analysis. GBA gene sequencing revealed homozygosity for a novel mutation, D137N. Whole-exome capture and massively parallel sequencing combined with homozygosity mapping identified a homozygous novel mutation in the MSH6 gene that leads to constitutional mismatch repair deficiency syndrome and increased cancer risk. Enzyme studies demonstrated that the D137N mutation in GBA is a pathogenic mutation, and immunohistochemistry confirmed the absence of the MSH6 protein. Therefore, precise phenotype annotation followed by individual genome analysis has the potential to identify genetic modifiers of GD, facilitate personalized management, and provide novel insights into disease pathophysiology.
Authors:
Sarah M Lo; Murim Choi; Jun Liu; Dhanpat Jain; Rolf G Boot; Wouter W Kallemeijn; Johannes M F G Aerts; Farzana Pashankar; Gary M Kupfer; Shrikant Mane; Richard P Lifton; Pramod K Mistry
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Publication Detail:
Type:  Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-04-04
Journal Detail:
Title:  Blood     Volume:  119     ISSN:  1528-0020     ISO Abbreviation:  Blood     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-05-18     Completed Date:  2012-07-16     Revised Date:  2013-05-22    
Medline Journal Info:
Nlm Unique ID:  7603509     Medline TA:  Blood     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4731-40     Citation Subset:  AIM; IM    
Affiliation:
Section of Pediatric Hematology-Oncology, Department of Pediatrics, Yale School of Medicine, 333 Cedar St., New Haven, CT 06520, USA.
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MeSH Terms
Descriptor/Qualifier:
Adult
Child
Child, Preschool
Female
Gaucher Disease / complications,  diagnosis,  genetics*,  pathology
Genome, Human / genetics
Hematologic Neoplasms / complications,  diagnosis,  genetics*,  pathology
Humans
Individuality
Male
Pedigree
Phenotype
Sequence Analysis, DNA*
Siblings
beta-Glucosidase / analysis,  genetics
Grant Support
ID/Acronym/Agency:
K24DK066306/DK/NIDDK NIH HHS; UL1 TR000142/TR/NCATS NIH HHS
Chemical
Reg. No./Substance:
EC 3.2.1.21/beta-Glucosidase
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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