Wilhelm Johannsen Centre for Functional Genome Research, Department of Cellular and Molecular Medicine, University of Copenhagen, 2200 Copenhagen N, Denmark.
Department of Epidemiology Research, Statens Serum Institut, 2300 Copenhagen S, Denmark.
Am J Hum Genet. 2018 Jun 7;102(6):1090-1103. doi: 10.1016/j.ajhg.2018.04.005. Epub 2018 May 24.
The 6%-9% risk of an untoward outcome previously established by Warburton for prenatally detected de novo balanced chromosomal rearrangements (BCRs) does not account for long-term morbidity. We performed long-term follow-up (mean 17 years) of a registry-based nationwide cohort of 41 individuals carrying a prenatally detected de novo BCR with normal first trimester screening/ultrasound scan. We observed a significantly higher frequency of neurodevelopmental and/or neuropsychiatric disorders than in a matched control group (19.5% versus 8.3%, p = 0.04), which was increased to 26.8% upon clinical follow-up. Chromosomal microarray of 32 carriers revealed no pathogenic imbalances, illustrating a low prognostic value when fetal ultrasound scan is normal. In contrast, mate-pair sequencing revealed disrupted genes (ARID1B, NPAS3, CELF4), regulatory domains of known developmental genes (ZEB2, HOXC), and complex BCRs associated with adverse outcomes. Seven unmappable autosomal-autosomal BCRs with breakpoints involving pericentromeric/heterochromatic regions may represent a low-risk group. We performed independent phenotype-aware and blinded interpretation, which accurately predicted benign outcomes (specificity = 100%) but demonstrated relatively low sensitivity for prediction of the clinical outcome in affected carriers (sensitivity = 45%-55%). This sensitivity emphasizes the challenges associated with prenatal risk prediction for long-term morbidity in the absence of phenotypic data given the still immature annotation of the morbidity genome and poorly understood long-range regulatory mechanisms. In conclusion, we upwardly revise the previous estimates of Warburton to a morbidity risk of 27% and recommend sequencing of the chromosomal breakpoints as the first-tier diagnostic test in pregnancies with a de novo BCR.
先前由 Warburton 确定的 6%-9%的不良后果风险并未考虑到长期的发病率。我们对一个基于注册的全国性队列进行了长期随访(平均 17 年),该队列由 41 名携带产前检测到的新发平衡染色体重排(BCR)且第一孕期筛查/超声检查正常的个体组成。我们观察到神经发育和/或神经精神障碍的发生频率明显高于匹配对照组(19.5%对 8.3%,p=0.04),在临床随访中增加到 26.8%。32 名携带者的染色体微阵列未发现致病性不平衡,这表明当胎儿超声检查正常时,预后价值较低。相比之下,mate-pair 测序揭示了基因的破坏(ARID1B、NPAS3、CELF4)、已知发育基因的调控域(ZEB2、HOXC)和与不良结果相关的复杂 BCR。7 个无法映射的常染色体-常染色体 BCR,其断点涉及着丝粒/异染色质区域,可能代表一个低风险组。我们进行了独立的表型感知和盲法解释,这准确地预测了良性结果(特异性=100%),但对受影响携带者的临床结果预测的敏感性相对较低(敏感性=45%-55%)。这种敏感性强调了在缺乏表型数据的情况下,产前风险预测对长期发病率的挑战,因为发病率基因组的注释仍不成熟,并且对长距离调控机制的理解也较差。总之,我们将 Warburton 的先前估计向上修正为发病率风险为 27%,并建议在新发 BCR 的妊娠中进行染色体断点测序作为一线诊断测试。