Literature DB >> 23715653

A familial WT1 mutation associated with incomplete Denys-Drash syndrome.

Chunhua Zhu1, Fei Zhao, Weizhen Zhang, Hongmei Wu, Ying Chen, Guixia Ding, Aihua Zhang, Songming Huang.   

Abstract

UNLABELLED: Denys-Drash syndrome (DDS) is a rare disorder characterized by nephropathy, male pseudohermaphroditism, and wilms tumor. Cases are thought to arise sporadically through a de novo mutation in the wilms tumor suppressor gene (WT1), which encodes a zinc finger protein that not only acts as a tumor suppressor but is essential for normal gonadogenesis, nephrogenesis, and development of the urogenital tract. In this report, we describe a family with the well-known missense mutation in exon 9 of the WT1 gene, 1180C>T (R394W), causing incomplete DDS and no symptoms in their father. The proband, a boy with 46, XY karyotype, was born with ambiguous genitalia, penoscrotal hypospadias, and bilateral inguinal hernias. At 2 years of age, he has proteinuria and diffuse mesangial sclerosis, but no wilms tumor has been detected. The elder sister of the proband, at 3 years of age, has normal genitalia, proteinuria, focal mesangial sclerosis but no wilms tumor. The WT1 mutation was detected in both patients, who have suspected DDS, and their father, who is phenotypically normal.
CONCLUSION: This case is unusual in that the 1180C>T mutation, which has been found in approximately 50 % of patients with complete DDS, has been inherited and is causing mild or no symptoms of DDS.

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Year:  2013        PMID: 23715653     DOI: 10.1007/s00431-013-2004-9

Source DB:  PubMed          Journal:  Eur J Pediatr        ISSN: 0340-6199            Impact factor:   3.183


  28 in total

1.  Discordant expression of a new WT1 gene mutation in a family with monozygotic twins presenting with congenital nephrotic syndrome.

Authors:  Filip Fencl; Michal Malina; Veronika Stará; Jakub Zieg; Dana Mixová; Tomáš Seeman; Květa Bláhová
Journal:  Eur J Pediatr       Date:  2011-05-26       Impact factor: 3.183

2.  Mother-to-child transmitted WT1 splice-site mutation is responsible for distinct glomerular diseases.

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Journal:  J Am Soc Nephrol       Date:  1999-10       Impact factor: 10.121

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Authors:  A Drash; F Sherman; W H Hartmann; R M Blizzard
Journal:  J Pediatr       Date:  1970-04       Impact factor: 4.406

4.  Familial Wilms tumour resulting from WT1 mutation: intronic polymorphism causing artefactual constitutional homozygosity.

Authors:  K Pritchard-Jones; N Rahman; M Gerrard; D Variend; L King-Underwood
Journal:  J Med Genet       Date:  2000-05       Impact factor: 6.318

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Journal:  J Med Genet       Date:  1994-06       Impact factor: 6.318

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Journal:  Clin Nephrol       Date:  1985-12       Impact factor: 0.975

Review 7.  A clinical overview of WT1 gene mutations.

Authors:  M Little; C Wells
Journal:  Hum Mutat       Date:  1997       Impact factor: 4.878

Review 8.  A review of the phenotypic variation due to the Denys-Drash syndrome-associated germline WT1 mutation R362X.

Authors:  Rosemary W Heathcott; Ian M Morison; Marie Claire Gubler; Robin Corbett; Anthony E Reeve
Journal:  Hum Mutat       Date:  2002-04       Impact factor: 4.878

9.  Identification of constitutional WT1 mutations, in patients with isolated diffuse mesangial sclerosis, and analysis of genotype/phenotype correlations by use of a computerized mutation database.

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Journal:  Am J Hum Genet       Date:  1998-04       Impact factor: 11.025

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Authors:  P N Baird; A Santos; N Groves; L Jadresic; J K Cowell
Journal:  Hum Mol Genet       Date:  1992-08       Impact factor: 6.150

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