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Genetic heterogeneity in LEOPARD syndrome: two families with no mutations in PTPN11

Authors :
Amisha Patel
Lynn Greenhalgh
Michael A. Patton
Kamini Kalidas
Steve Jeffery
Andrew H. Crosby
Isabel K. Temple
Ruth Newbury-Ecob
Adam Shaw
Caroline J Law
Source :
Journal of Human Genetics. 50:21-25
Publication Year :
2004
Publisher :
Springer Science and Business Media LLC, 2004.

Abstract

LEOPARD syndrome (lentigines, electrocardiographic conduction abnormalities, ocular hypertelorism, pulmonary stenosis, abnormal genitalia, retardation of growth, and sensorineural deafness) is an autosomal dominant condition. The main clinical features include multiple lentigines, cardiovascular defects, and facial anomalies, some of which are shared with Noonan syndrome (NS). Recent reports have shown that LEOPARD syndrome can be caused by mutations in PTPN11, the gene in which mutations can produce NS. Here we report the findings of mutation screening and linkage analysis of PTPN11 in three families with LEOPARD syndrome. We identified a novel mutation in one family. The mutation (1529A>C) substitutes proline for glutamine at amino acid 510 (Gln510Pro). No variations in sequence were observed in the other two families, and negative LOD scores excluded linkage to the PTPN11 locus, showing that LEOPARD syndrome is genetically heterogeneous.

Details

ISSN :
1435232X and 14345161
Volume :
50
Database :
OpenAIRE
Journal :
Journal of Human Genetics
Accession number :
edsair.doi.dedup.....1bce0bc3c9d9da559ef97ceb4b0babf9