Savage Sharon A, Dufour Carlo
Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA.
Haematology Unit, Istituto Giannina Gaslini, Genoa, Italy.
Semin Hematol. 2017 Apr;54(2):105-114. doi: 10.1053/j.seminhematol.2017.04.004. Epub 2017 Apr 7.
The inherited marrow failure syndromes (IBMFS) are a heterogeneous group of diseases characterized by failure in the production of one or more blood lineage. The clinical manifestations of the IBMFS vary according to the type and number of blood cell lines involved, including different combinations of anemia, leukopenia, and thrombocytopenia. In some IBMFS, systemic non-hematologic manifestations, including congenital malformations, mucocutaneous abnormalities, developmental delay, and other medical complications, may be present. Fanconi anemia (FA), caused by germline pathogenic variants in the DNA repair genes comprising the FA/BRCA pathway is associated with congenital anomalies, bone marrow failure, and increased risk of myelodysplastic syndrome (MDS), acute myelogenous leukemia (AML), and solid tumors. Dyskeratosis congenita (DC) is a telomere biology disorder (TBD) caused by aberrations in key telomere biology genes. In addition to mucocutaneous manifestations, patients with DC are at increased risk of marrow failure, MDS, AML, pulmonary fibrosis, and other complications. Ribosomal biology defects are the primary causes of Diamond Blackfan anemia (DBA) and Shwachman Diamond syndrome (SDS). In addition to pure red blood cell aplasia, DBA is associated with elevated risk of solid tumors, AML, and MDS. Patients with SDS have pancreatic insufficiency, neutropenia, as well as MDS and AML risks. Patients with severe congenital neutropenia (SCN), caused by pathogenic variants in genes essential in myeloid development, have profound neutropenia and high risk of MDS and AML. Herein we review the genetic causes, clinical features, diagnostic modalities, predisposition to malignancies with focus on leukemogenic markers whenever available, and approaches to treatments of the classical IBMFS: FA, DC, SDS, DBA, and SCN.
遗传性骨髓衰竭综合征(IBMFS)是一组异质性疾病,其特征是一种或多种血细胞系生成失败。IBMFS的临床表现因受累血细胞系的类型和数量而异,包括贫血、白细胞减少和血小板减少的不同组合。在某些IBMFS中,可能会出现全身性非血液学表现,包括先天性畸形、皮肤黏膜异常、发育迟缓及其他医学并发症。范可尼贫血(FA)由构成FA/BRCA通路的DNA修复基因中的种系致病变异引起,与先天性异常、骨髓衰竭以及骨髓增生异常综合征(MDS)、急性髓系白血病(AML)和实体瘤的风险增加相关。先天性角化不良(DC)是一种由关键端粒生物学基因异常引起的端粒生物学障碍(TBD)。除皮肤黏膜表现外,DC患者发生骨髓衰竭、MDS、AML、肺纤维化及其他并发症的风险增加。核糖体生物学缺陷是先天性纯红细胞再生障碍性贫血(DBA)和施-戴二氏综合征(SDS)的主要病因。除纯红细胞再生障碍外,DBA还与实体瘤、AML和MDS的风险升高相关。SDS患者有胰腺功能不全、中性粒细胞减少,以及发生MDS和AML的风险。严重先天性中性粒细胞减少症(SCN)由髓系发育必需基因的致病变异引起,患者有严重的中性粒细胞减少,以及发生MDS和AML的高风险。在此,我们综述经典IBMFS(FA、DC、SDS、DBA和SCN)的遗传病因、临床特征、诊断方法、发生恶性肿瘤的倾向(如有可用的致白血病标志物则重点阐述)以及治疗方法。