Evidence for pathogenicity of variant ATM Val1729Leu in a family with ataxia telangiectasia

Neurogenetics - Tập 22 - Trang 143-147 - 2021
Ali S. Shalash1, Thomas W. Rösler2,3, Mohamed Salama4,5, Manuela Pendziwiat6,7, Stefanie H. Müller8, Franziska Hopfner9, Günter U. Höglinger2,3,9, Gregor Kuhlenbäumer10
1Department of Neurology, Faculty of Medicine, Ain Shams University, Cairo, Egypt
2Department of Neurology, School of Medicine, Technical University of Munich, Munich, Germany
3Department of Translational Neurodegeneration, German Center for Neurodegenerative Diseases (DZNE), Munich, Germany
4Institute of Global Health and Human Ecology, American University in Cairo (AUC), Cairo, Egypt
5Faculty of Medicine, Mansoura University, Mansoura, Egypt
6Institute of Clinical Molecular Biology, University of Kiel, Kiel, Germany
7Department of Neuropediatrics, University Medical Center Schleswig-Holstein, University of Kiel, Kiel, Germany
8Institute of Health Informatics, UCL, London, UK
9Department of Neurology, Hannover Medical School, Hannover, Germany
10Department of Neurology, University of Kiel, Kiel, Germany

Tóm tắt

Ataxia telangiectasia is a rare autosomal recessive multisystem disorder caused by mutations in the gene of ATM serine/threonine kinase. It is characterized by neurodegeneration, leading to severe ataxia, immunodeficiency, increased cancer susceptibility, and telangiectasia. Here, we discovered a co-segregation of two ATM gene variants with ataxia telangiectasia in an Egyptian family. While one of these variants (NM_000051.4(ATM_i001):p.(Val128*)) has previously been reported as pathogenic, the other one (NM_000051.4(ATM_i001):p.(Val1729Leu)) is regarded as a variant of uncertain significance. Our findings in this family provide additional evidence for causality of the second variant and argue that its status should be changed to pathogenic.

Tài liệu tham khảo

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