Applied Tumor Genomics Research Program, Research Programs Unit, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Department of Hematology, Helsinki University Hospital Comprehensive Cancer Center, University of Helsinki, Helsinki, Finland.
Blood. 2023 Jun 8;141(23):2853-2866. doi: 10.1182/blood.2022019425.
Biallelic germ line excision repair cross-complementing 6 like 2 (ERCC6L2) variants strongly predispose to bone marrow failure (BMF) and myeloid malignancies, characterized by somatic TP53-mutated clones and erythroid predominance. We present a series of 52 subjects (35 families) with ERCC6L2 biallelic germ line variants collected retrospectively from 11 centers globally, with a follow-up of 1165 person-years. At initial investigations, 32 individuals were diagnosed with BMF and 15 with a hematological malignancy (HM). The subjects presented with 19 different variants of ERCC6L2, and we identified a founder mutation, c.1424delT, in Finnish patients. The median age of the subjects at baseline was 18 years (range, 2-65 years). Changes in the complete blood count were mild despite severe bone marrow (BM) hypoplasia and somatic TP53 mutations, with no significant difference between subjects with or without HMs. Signs of progressive disease included increasing TP53 variant allele frequency, dysplasia in megakaryocytes and/or erythroid lineage, and erythroid predominance in the BM morphology. The median age at the onset of HM was 37.0 years (95% CI, 31.5-42.5; range, 12-65 years). The overall survival (OS) at 3 years was 95% (95% CI, 85-100) and 19% (95% CI, 0-39) for patients with BMF and HM, respectively. Patients with myelodysplastic syndrome or acute myeloid leukemia with mutated TP53 undergoing hematopoietic stem cell transplantation had a poor outcome with a 3-year OS of 28% (95% CI, 0-61). Our results demonstrated the importance of early recognition and active surveillance in patients with biallelic germ line ERCC6L2 variants.
双等位基因胚系切除修复交叉互补基因 6 样 2(ERCC6L2)变异强烈倾向于骨髓衰竭(BMF)和髓系恶性肿瘤,其特征为体细胞 TP53 突变克隆和红系优势。我们报告了一系列 52 名(35 个家系)双等位基因 ERCC6L2 胚系变异患者,这些患者是从全球 11 个中心回顾性收集的,随访时间为 1165 人年。在初始检查时,32 名患者被诊断为 BMF,15 名患者被诊断为血液系统恶性肿瘤(HM)。这些患者携带 19 种不同的 ERCC6L2 变异,我们在芬兰患者中发现了一个启动子突变 c.1424delT。患者的基线中位年龄为 18 岁(范围,2-65 岁)。尽管骨髓(BM)严重发育不良和体细胞 TP53 突变,但全血细胞计数的变化仍然轻微,患有或不患有 HM 的患者之间没有显著差异。疾病进展的迹象包括 TP53 变异等位基因频率增加、巨核细胞和/或红系谱系发育不良以及 BM 形态学中的红系优势。HM 发病的中位年龄为 37.0 岁(95%CI,31.5-42.5;范围,12-65 岁)。患有 BMF 和 HM 的患者的 3 年总生存率(OS)分别为 95%(95%CI,85-100)和 19%(95%CI,0-39)。接受造血干细胞移植的伴突变 TP53 的骨髓增生异常综合征或急性髓系白血病患者的 3 年 OS 为 28%(95%CI,0-61),预后较差。我们的研究结果表明,双等位基因胚系 ERCC6L2 变异患者的早期识别和积极监测非常重要。