| Literature DB >> 29146883 |
Olivier Bluteau1,2,3, Marie Sebert2,3, Thierry Leblanc4, Régis Peffault de Latour2,5,6,7, Samuel Quentin1, Elodie Lainey8, Lucie Hernandez2,3, Jean-Hugues Dalle2,4, Flore Sicre de Fontbrune6, Etienne Lengline9, Raphael Itzykson2,3,5,9, Emmanuelle Clappier1,2,3, Nicolas Boissel2,5,9, Nadia Vasquez1, Mélanie Da Costa1, Julien Masliah-Planchon3, Wendy Cuccuini1, Anna Raimbault1,2,3, Louis De Jaegere3, Lionel Adès2,9, Pierre Fenaux2,9, Sébastien Maury10, Claudine Schmitt11,12, Marc Muller11,12, Carine Domenech13, Nicolas Blin14, Bénédicte Bruno15, Isabelle Pellier16,17, Mathilde Hunault16,17, Stéphane Blanche18,19, Arnaud Petit20, Guy Leverger20, Gérard Michel21,22, Yves Bertrand13, André Baruchel2,4,5, Gérard Socié2,6,7, Jean Soulier1,2,3.
Abstract
Bone marrow (BM) failure (BMF) in children and young adults is often suspected to be inherited, but in many cases diagnosis remains uncertain. We studied a cohort of 179 patients (from 173 families) with BMF of suspected inherited origin but unresolved diagnosis after medical evaluation and Fanconi anemia exclusion. All patients had cytopenias, and 12.0% presented ≥5% BM blast cells. Median age at genetic evaluation was 11 years; 20.7% of patients were aged ≤2 years and 36.9% were ≥18 years. We analyzed genomic DNA from skin fibroblasts using whole-exome sequencing, and were able to assign a causal or likely causal germ line mutation in 86 patients (48.0%), involving a total of 28 genes. These included genes in familial hematopoietic disorders (GATA2, RUNX1), telomeropathies (TERC, TERT, RTEL1), ribosome disorders (SBDS, DNAJC21, RPL5), and DNA repair deficiency (LIG4). Many patients had an atypical presentation, and the mutated gene was often not clinically suspected. We also found mutations in genes seldom reported in inherited BMF (IBMF), such as SAMD9 and SAMD9L (N = 16 of the 86 patients, 18.6%), MECOM/EVI1 (N = 6, 7.0%), and ERCC6L2 (N = 7, 8.1%), each of which was associated with a distinct natural history; SAMD9 and SAMD9L patients often experienced transient aplasia and monosomy 7, whereas MECOM patients presented early-onset severe aplastic anemia, and ERCC6L2 patients, mild pancytopenia with myelodysplasia. This study broadens the molecular and clinical portrait of IBMF syndromes and sheds light on newly recognized disease entities. Using a high-throughput sequencing screen to implement precision medicine at diagnosis can improve patient management and family counseling.Entities:
Mesh:
Year: 2017 PMID: 29146883 DOI: 10.1182/blood-2017-09-806489
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113