Division of Hematology/Oncology, The Manton Center for Orphan Disease Research, Boston Children's Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA; Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Program in Biological and Biomedical Sciences, Harvard Medical School, Boston, MA 02115, USA.
Division of Hematology/Oncology, The Manton Center for Orphan Disease Research, Boston Children's Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA; Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Am J Hum Genet. 2018 Dec 6;103(6):930-947. doi: 10.1016/j.ajhg.2018.10.027. Epub 2018 Nov 29.
Diamond-Blackfan anemia (DBA) is a rare bone marrow failure disorder that affects 7 out of 1,000,000 live births and has been associated with mutations in components of the ribosome. In order to characterize the genetic landscape of this heterogeneous disorder, we recruited a cohort of 472 individuals with a clinical diagnosis of DBA and performed whole-exome sequencing (WES). We identified relevant rare and predicted damaging mutations for 78% of individuals. The majority of mutations were singletons, absent from population databases, predicted to cause loss of function, and located in 1 of 19 previously reported ribosomal protein (RP)-encoding genes. Using exon coverage estimates, we identified and validated 31 deletions in RP genes. We also observed an enrichment for extended splice site mutations and validated their diverse effects using RNA sequencing in cell lines obtained from individuals with DBA. Leveraging the size of our cohort, we observed robust genotype-phenotype associations with congenital abnormalities and treatment outcomes. We further identified rare mutations in seven previously unreported RP genes that may cause DBA, as well as several distinct disorders that appear to phenocopy DBA, including nine individuals with biallelic CECR1 mutations that result in deficiency of ADA2. However, no new genes were identified at exome-wide significance, suggesting that there are no unidentified genes containing mutations readily identified by WES that explain >5% of DBA-affected case subjects. Overall, this report should inform not only clinical practice for DBA-affected individuals, but also the design and analysis of rare variant studies for heterogeneous Mendelian disorders.
先天性单纯红细胞再生障碍性贫血(DBA)是一种罕见的骨髓衰竭疾病,每 100 万活产儿中有 7 例发病,与核糖体成分的突变有关。为了描述这种异质性疾病的遗传图谱,我们招募了一组 472 名临床诊断为 DBA 的个体,并进行了全外显子组测序(WES)。我们鉴定了 78%个体的相关罕见和预测有害突变。大多数突变是单核苷酸变异,不存在于人群数据库中,预测会导致功能丧失,并且位于 19 个先前报道的核糖体蛋白(RP)编码基因中的 1 个中。使用外显子覆盖估计值,我们鉴定并验证了 31 个 RP 基因缺失。我们还观察到扩展剪接位点突变富集,并使用来自 DBA 个体的细胞系中的 RNA 测序验证了其多样化的效应。利用我们队列的规模,我们观察到与先天性异常和治疗结果的稳健基因型-表型关联。我们还在七个以前未报道的 RP 基因中发现了罕见突变,这些突变可能导致 DBA,以及几种似乎表型模拟 DBA 的不同疾病,包括 9 名个体存在双等位 CECR1 突变,导致 ADA2 缺乏。然而,在全外显子组范围内未发现新基因,这表明没有新基因包含 WES 容易识别的突变,这些突变可解释>5%的 DBA 受影响病例。总的来说,本报告不仅应该为 DBA 受影响个体的临床实践提供信息,而且还应该为异质性孟德尔疾病的罕见变异研究的设计和分析提供信息。