| Literature DB >> 31050087 |
Alice Fiévet1,2, Dorine Bellanger1, Guillaume Rieunier1, Catherine Dubois d'Enghien2, Julia Sophie3, Patrick Calvas3, Jean-Paul Carriere4, Mathieu Anheim5, Anna Castrioto6, Olivier Flabeau7, Bertrand Degos8, Claire Ewenczyk9, Nizar Mahlaoui10, Fabien Touzot10, Felipe Suarez11, Marie Hully12, Agathe Roubertie13, Nathalie Aladjidi14, François Tison15, Hélène Antoine-Poirel16, Karine Dahan16, Diane Doummar17, Marie-Christine Nougues18, Christine Ioos19, Christelle Rougeot20, Alice Masurel21, Caroline Bourjault22, Emmanuelle Ginglinger23, Fabienne Prieur24, Aurélie Siri25, Pierre Bordigoni26, Karine Nguyen27, Noel Philippe28, Céline Bellesme29, François Demeocq30, Cecilia Altuzarra31, Michèle Mathieu-Dramard32, Fanny Couderc33, Thilo Dörk34, Nathalie Auger35, Béatrice Parfait36, Khadija Abidallah2, Virginie Moncoutier2, Agnès Collet2, Dominique Stoppa-Lyonnet1,2,37, Marc-Henri Stern1,2.
Abstract
Ataxia-telangiectasia (A-T) is a recessive disorder caused by biallelic pathogenic variants of ataxia-telangiectasia mutated (ATM). This disease is characterized by progressive ataxia, telangiectasia, immune deficiency, predisposition to malignancies, and radiosensitivity. However, hypomorphic variants may be discovered associated with very atypical phenotypes, raising the importance of evaluating their pathogenic effects. In this study, multiple functional analyses were performed on lymphoblastoid cell lines from 36 patients, comprising 49 ATM variants, 24 being of uncertain significance. Thirteen patients with atypical phenotype and presumably hypomorphic variants were of particular interest to test strength of functional analyses and to highlight discrepancies with typical patients. Western-blot combined with transcript analyses allowed the identification of one missing variant, confirmed suspected splice defects and revealed unsuspected minor transcripts. Subcellular localization analyses confirmed the low level and abnormal cytoplasmic localization of ATM for most A-T cell lines. Interestingly, atypical patients had lower kinase defect and less altered cell-cycle distribution after genotoxic stress than typical patients. In conclusion, this study demonstrated the pathogenic effects of the 49 variants, highlighted the strength of KAP1 phosphorylation test for pathogenicity assessment and allowed the establishment of the Ataxia-TeLangiectasia Atypical Score to predict atypical phenotype. Altogether, we propose strategies for ATM variant detection and classification.Entities:
Keywords: ataxia-telangiectasia; ataxia-telangiectasia mutated (ATM); checkpoint; mutation; phenotype; splice
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Year: 2019 PMID: 31050087 DOI: 10.1002/humu.23778
Source DB: PubMed Journal: Hum Mutat ISSN: 1059-7794 Impact factor: 4.878