Rajendra Kurup Akhil, Malcolmson Janet, Villani Anita, Kim Raymond H, Yee Karen Wl
Division of Medical Oncology and Hematology, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Department of Medicine, University of Toronto, Toronto, ON, Canada.
Ann Hematol. 2025 Aug 27. doi: 10.1007/s00277-025-06536-2.
Germline mutations in ETV6 have been associated with thrombocytopenia and predisposition to hematological malignancies. Here, we report a pedigree with a multiple family member with an ETV6 c.1127T > A (p.Leu376Gln) variant, initially classified as a variant of uncertain significance (VUS), found to be segregating with thrombocytopenia and hematological/solid tumor malignancies. The proband, a 63-year-old male with chronic thrombocytopenia and a family history of hematological malignancies, presented with pancytopenia and was diagnosed as myelodysplastic syndrome (MDS). Next generation sequencing (NGS) from the bone marrow revealed the ETV6 c.1127T > A (p.Leu376Gln) variant with a variant allele frequency (VAF) of 46%. Germline testing on skin fibroblasts confirmed the presence of the same ETV6 variant in the proband and two of his siblings: one of them was diagnosed with acute lymphoblastic leukemia (ALL) during childhood and therapy-related MDS during adulthood, and another sibling with chronic isolated thrombocytopenia. The ETV6 c.1127T > A (p.Leu376Gln) variant potentially affects the ETS DNA-binding domain, leading to impaired DNA binding with a preserved dimerization capability, resulting in a dominant negative effect by cytoplasmic sequestration. This ETV6 variant has not been reported in a large population database, hence it has been designated as a VUS. Segregation of this variant with thrombocytopenia and hematological/solid tumor malignancies in the pedigree, alongside supporting evidence from other reported ETV6 variants, suggests its pathogenicity. This report highlights the pathogenicity of ETV6 c.1127T > A (p.Leu376Gln) variant and supports its reclassification from VUS to likely pathogenic, adding to the vast evidence of ETV6-associated thrombocytopenia and leukemia predisposition.
ETV6基因的种系突变与血小板减少症以及血液系统恶性肿瘤的易感性有关。在此,我们报告一个家系,其中多名家庭成员携带ETV6基因c.1127T>A(p.Leu376Gln)变异,该变异最初被分类为意义未明的变异(VUS),现发现其与血小板减少症以及血液系统/实体肿瘤恶性肿瘤共分离。先证者是一名63岁男性,患有慢性血小板减少症且有血液系统恶性肿瘤家族史,表现为全血细胞减少,被诊断为骨髓增生异常综合征(MDS)。对其骨髓进行的二代测序(NGS)显示ETV6基因c.1127T>A(p.Leu376Gln)变异,变异等位基因频率(VAF)为46%。对皮肤成纤维细胞进行的种系检测证实先证者及其两名兄弟姐妹中存在相同的ETV6变异:其中一人在儿童期被诊断为急性淋巴细胞白血病(ALL),成年期被诊断为治疗相关的MDS,另一兄弟姐妹患有慢性孤立性血小板减少症。ETV6基因c.1127T>A(p.Leu376Gln)变异可能影响ETS DNA结合结构域,导致DNA结合受损但二聚化能力保留,通过细胞质隔离产生显性负效应。该ETV6变异在大型人群数据库中尚未见报道,因此被指定为VUS。该变异在该家系中与血小板减少症以及血液系统/实体肿瘤恶性肿瘤共分离,同时有其他报道的ETV变异提供的支持证据,提示其具有致病性。本报告强调了ETV6基因c.1127T>A(p.Leu376Gln)变异的致病性,并支持将其从VUS重新分类为可能致病,为ETV6相关血小板减少症和白血病易感性的大量证据增添了内容。