| Literature DB >> 21765025 |
Rachel Emma Dickinson1, Helen Griffin, Venetia Bigley, Louise N Reynard, Rafiqul Hussain, Muzlifah Haniffa, Jeremy H Lakey, Thahira Rahman, Xiao-Nong Wang, Naomi McGovern, Sarah Pagan, Sharon Cookson, David McDonald, Ignatius Chua, Jonathan Wallis, Andrew Cant, Michael Wright, Bernard Keavney, Patrick F Chinnery, John Loughlin, Sophie Hambleton, Mauro Santibanez-Koref, Matthew Collin.
Abstract
The human syndrome of dendritic cell, monocyte, B and natural killer lymphoid deficiency presents as a sporadic or autosomal dominant trait causing susceptibility to mycobacterial and other infections, predisposition to myelodysplasia and leukemia, and, in some cases, pulmonary alveolar proteinosis. Seeking a genetic cause, we sequenced the exomes of 4 unrelated persons, 3 with sporadic disease, looking for novel, heterozygous, and probably deleterious variants. A number of genes harbored novel variants in person, but only one gene, GATA2, was mutated in all 4 persons. Each person harbored a different mutation, but all were predicted to be highly deleterious and to cause loss or mutation of the C-terminal zinc finger domain. Because GATA2 is the only common mutated gene in 4 unrelated persons, it is highly probable to be the cause of dendritic cell, monocyte, B, and natural killer lymphoid deficiency. This disorder therefore constitutes a new genetic form of heritable immunodeficiency and leukemic transformation.Entities:
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Year: 2011 PMID: 21765025 PMCID: PMC5137783 DOI: 10.1182/blood-2011-06-360313
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113