Lewinsohn Maya, Brown Anna L, Weinel Luke M, Phung Connie, Rafidi George, Lee Ming K, Schreiber Andreas W, Feng Jinghua, Babic Milena, Chong Chan-Eng, Lee Young, Yong Agnes, Suthers Graeme K, Poplawski Nicola, Altree Meryl, Phillips Kerry, Jaensch Louise, Fine Miriam, D'Andrea Richard J, Lewis Ian D, Medeiros Bruno C, Pollyea Daniel A, King Mary-Claire, Walsh Tom, Keel Siobán, Shimamura Akiko, Godley Lucy A, Hahn Christopher N, Churpek Jane E, Scott Hamish S
Section of Hematology/Oncology, Department of Medicine and Center for Clinical Cancer Genetics, and The University of Chicago Comprehensive Cancer Center, The University of Chicago, Chicago, IL;
Department of Genetics and Molecular Pathology, Centre for Cancer Biology, SA Pathology, Adelaide, SA, Australia; School of Pharmacy and Medical Sciences, Division of Health Sciences, University of South Australia, Adelaide, SA, Australia;
Blood. 2016 Feb 25;127(8):1017-23. doi: 10.1182/blood-2015-10-676098. Epub 2015 Dec 28.
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.
最近,我们团队及其他研究团队在多例迟发性骨髓增生异常综合征(MDS)和/或急性髓系白血病(AML)患者的家族中,发现了DDX41突变,这些突变既包括种系突变,也包括获得性体细胞突变,这表明DDX41起着肿瘤抑制基因的作用。为了确定在患有其他类型血液系统恶性肿瘤的家族中是否能发现新的DDX41突变,我们团队对两组患有多种血液系统恶性肿瘤亚型的家族进行了筛查。在289个家族中,我们发现了9个(3%)携带DDX41突变的家族。如之前所观察到的,MDS和AML是最常见的恶性肿瘤,通常为成红细胞亚型,还有1个家族表现为早发性滤泡性淋巴瘤。我们鉴定出了5个新突变,包括重要功能域内的错义突变以及预计会导致蛋白质截短的起始密码子丢失突变和剪接突变。我们还表明,大多数无症状的突变携带者在恶性肿瘤发生之前血常规计数正常。这项研究扩展了在携带种系DDX41突变的家族中观察到的突变和表型谱。随着该基因中越来越多的遗传突变和获得性突变被发现,进一步研究DDX41功能破坏如何导致血液系统恶性肿瘤至关重要。