骨髓增生异常综合征与双种系RUNX1和DDX41变体:罕见的遗传易感性的情况下。

IF 1.8 4区 医学 Q3 GENETICS & HEREDITY
Virginia Bove, Maria Noel Spangenberg, Carolina Ottati, Lucia Vázquez, Ana I Catalán, Sofía Grille
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引用次数: 0

摘要

RUNX1和DDX41的种系变异是遗传性髓系肿瘤的确定因素,并且越来越多地被认为是发生骨髓增生异常综合征(MDS)和急性髓系白血病(AML)的关键易感因素。本病例报告详细介绍了一名51岁男性被诊断为MDS伴有过量胚细胞-1 (MDS- eb1),其携带RUNX1致病性种系变异的罕见组合和DDX41变异的新型潜在致病性变体,以及DDX41体细胞突变。这些种系变异的共存突出了遗传性髓系肿瘤的遗传复杂性,并加强了全面基因组检测的必要性,以确保准确的诊断和知情的临床管理。RUNX1和DDX41变体之间的相互作用可能驱动白血病发生,种系RUNX1变体可能培育细胞环境,使体细胞DDX41突变获得,导致血液学恶性肿瘤。相反,种系DDX41变异可能会破坏造血功能,当与RUNX1功能障碍结合时,会导致疾病进展。这个病例强调了髓系肿瘤患者中筛选种系变异的重要性。它强调需要确认这些变异在非造血组织(如成纤维细胞(金标准))中的起源,以避免克隆造血引起的误解。需要进一步的研究来阐明RUNX1和DDX41变异之间相互作用的分子机制,以及它们对疾病进展、治疗结果和家族风险的共同影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Myelodysplastic syndrome with dual germline RUNX1 and DDX41 variants: a rare genetic predisposition case.

Germline variants in RUNX1 and DDX41 are well-established contributors to hereditary myeloid neoplasms and are increasingly recognized as critical predisposing factors in the developing myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). This case report details a 51-year-old male diagnosed with MDS with excess blasts-1 (MDS-EB1), who harbored a rare combination of pathogenic germline variants in RUNX1 and a novel potentially pathogenic variant in DDX41 variant, alongside a somatic DDX41 mutation. The coexistence of these germline variants highlights the genetic complexity underlying hereditary myeloid neoplasms and reinforces the necessity of comprehensive genomic testing to ensure accurate diagnosis and informed clinical management. The interplay between RUNX1 and DDX41 variants may drive leukemogenesis, with the germline RUNX1 variant potentially fostering a cellular environment that enables the acquisition of somatic DDX41 mutations, leading to hematological malignancies. Conversely, the germline DDX41 variant may disrupt hematopoiesis and, when combined with RUNX1 dysfunction, contribute to disease progression. This case underscores the importance of screening germline variants in patients with myeloid neoplasms. It emphasizes the need to confirm the origin of these variants in non-hematopoietic tissues, such as fibroblasts (gold standard), to avoid misinterpretation caused by clonal hematopoiesis. Further research is warranted to elucidate the molecular mechanisms driving the interaction between RUNX1 and DDX41 variants and their collective impact on disease progression, treatment outcomes, and familial risk.

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来源期刊
Familial Cancer
Familial Cancer 医学-遗传学
CiteScore
4.10
自引率
4.50%
发文量
36
审稿时长
6-12 weeks
期刊介绍: In recent years clinical cancer genetics has become increasingly important. Several events, in particular the developments in DNA-based technology, have contributed to this evolution. Clinical cancer genetics has now matured to a medical discipline which is truly multidisciplinary in which clinical and molecular geneticists work together with clinical and medical oncologists as well as with psycho-social workers. Due to the multidisciplinary nature of clinical cancer genetics most papers are currently being published in a wide variety of journals on epidemiology, oncology and genetics. Familial Cancer provides a forum bringing these topics together focusing on the interests and needs of the clinician. The journal mainly concentrates on clinical cancer genetics. Most major areas in the field shall be included, such as epidemiology of familial cancer, molecular analysis and diagnosis, clinical expression, treatment and prevention, counselling and the health economics of familial cancer.
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