Paternally InheritedIGF2Mutation and Growth Restriction
Author(s) -
Matthias Begemann,
Birgit Zirn,
Gijs W.E. Santen,
Elisa Wirthgen,
Lukas Soellner,
Hans-Martin Büttel,
Roland Schweizer,
Wilbert van Workum,
Gerhard Binder,
Thomas Eggermann
Publication year - 2015
Publication title -
new england journal of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 19.889
H-Index - 1030
eISSN - 1533-4406
pISSN - 0028-4793
DOI - 10.1056/nejmoa1415227
Subject(s) - intrauterine growth restriction , genomic imprinting , imprinting (psychology) , genetics , phenotype , insulin like growth factor 2 , biology , insulin like growth factor 1 receptor , restriction site , mutation , fetal growth , growth restriction , insulin like growth factor 2 receptor , growth factor , gene , medicine , restriction enzyme , pregnancy , fetus , receptor , gene expression , dna methylation
In humans, mutations in IGF1 or IGF1R cause intrauterine and postnatal growth restriction; however, data on mutations in IGF2, encoding insulin-like growth factor (IGF) II, are lacking. We report an IGF2 variant (c.191C→A, p.Ser64Ter) with evidence of pathogenicity in a multigenerational family with four members who have growth restriction. The phenotype affects only family members who have inherited the variant through paternal transmission, a finding that is consistent with the maternal imprinting status of IGF2. The severe growth restriction in affected family members suggests that IGF-II affects postnatal growth in addition to prenatal growth. Furthermore, the dysmorphic features of affected family members are consistent with a role of deficient IGF-II levels in the cause of the Silver-Russell syndrome. (Funded by Bundesministerium für Bildung und Forschung and the European Union.).
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