| Literature DB >> 26712909 |
Maya Lewinsohn1, Anna L Brown2, Luke M Weinel3, Connie Phung1, George Rafidi1, Ming K Lee4, Andreas W Schreiber5, Jinghua Feng6, Milena Babic7, Chan-Eng Chong8, Young Lee8, Agnes Yong9, Graeme K Suthers10, Nicola Poplawski10, Meryl Altree11, Kerry Phillips11, Louise Jaensch11, Miriam Fine11, Richard J D'Andrea12, Ian D Lewis9, Bruno C Medeiros13, Daniel A Pollyea14, Mary-Claire King4, Tom Walsh4, Siobán Keel15, Akiko Shimamura16, Lucy A Godley1, Christopher N Hahn17, Jane E Churpek1, Hamish S Scott18.
Abstract
Recently our group and others have identified DDX41 mutations both as germ line and acquired somatic mutations in families with multiple cases of late onset myelodysplastic syndrome (MDS) and/or acute myeloid leukemia (AML), suggesting that DDX41 acts as a tumor suppressor. To determine whether novel DDX41 mutations could be identified in families with additional types of hematologic malignancies, our group screened two cohorts of families with a diverse range of hematologic malignancy subtypes. Among 289 families, we identified nine (3%) with DDX41 mutations. As previously observed, MDS and AML were the most common malignancies, often of the erythroblastic subtype, and 1 family displayed early-onset follicular lymphoma. Five novel mutations were identified, including missense mutations within important functional domains and start-loss and splicing mutations predicted to result in truncated proteins. We also show that most asymptomatic mutation carriers have normal blood counts until malignancy develops. This study expands both the mutation and phenotypic spectra observed in families with germ line DDX41 mutations. With an increasing number of both inherited and acquired mutations in this gene being identified, further study of how DDX41 disruption leads to hematologic malignancies is critical.Entities:
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Year: 2015 PMID: 26712909 PMCID: PMC4968341 DOI: 10.1182/blood-2015-10-676098
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113