Ramírez María José, Pujol Roser, Minguillón Jordi, Bogliolo Massimo, Persico Ilaria, Cavero Debora, de la Cal Aurora, Río Paula, Navarro Susana, Casado José Antonio, Bailador Almudena, de la Fuente Antonio Sanchez, de Heredia Miguel López, Almazán Francisco, Antelo M Luisa, Argilés Bienvenida, Badell Isabel, Baragaño Marta, Beléndez Cristina, Bermúdez Mar, Bernués Marta, Buedo María Isabel, Carrasco Estela, Català Albert, Costa Dolors, Cuesta Isabel, Fernandez-Delgado Rafael, Fernández-Teijeiro Ana, Figuera Ángela, García Marta, Gondra Ainhoa, González Macarena, Muñiz Soledad González, Hernández-Rodríguez Ines, Ibañez Fátima, Kelleher Nicholas John, Lendínez Francisco, López Mónica, López-Almaraz Ricardo, Marchante Inmaculada, Mendoza Carmen, Nieto José, Ojeda Emilio, Payán-Pernía Salvador, Peláez Irene, de Soto Inmaculada Pérez, Portugal Raquel, Ramos-Arroyo María A, Regueiro Alexandra, Rodríguez Ana, Rosell Jordi, Saez Raquel, Sánchez José, Sánchez Martha, Senent MªLeonor, Tapia María, Trujillo-Quintero Juan Pablo, Vagace José Manuel, Verdú-Amorós Jaime, Verdugo Victória, Vidales Isabel, Villarreal Jasson, Díaz-de-Heredia Cristina, Sevilla Julián, Bueren Juan Antonio, Surrallés Jordi
Joint Research Unit on Genomic Medicine, Universitat Autònoma de Barcelona (UAB)-IR SANT PAU, Barcelona, Spain.
Centro de Investigación Biomédica en Red de Enfermedades Raras, Instituto de Salud Carlos III (CIBERER, ISCIII), Madrid, Spain.
Am J Hematol. 2025 Feb;100(2):272-284. doi: 10.1002/ajh.27520. Epub 2024 Nov 19.
Fanconi anemia (FA) is a rare genetic disease characterized by high phenotypic and genotypic heterogeneity, and extreme chromosome fragility. To better understand the natural history of FA, identify genetic risk and prognostic factors, and develop novel therapeutic strategies, the Spanish Registry of Patients with FA collects data on clinical features, chromosome fragility, genetic subtypes, and DNA sequencing with informed consent of participating individuals. In this article, we describe the clinical evolution of 227 patients followed up for up to 30 years, for whom our data indicate a cumulative cancer incidence of 86% by age 50. We found that patients with lower chromosome fragility had a milder malformation spectrum and better outcomes in terms of later-onset hematologic impairment, less severe bone marrow failure, and lower cancer risk. We also found that outcomes were better for patients with mutations leading to mutant FANCA protein expression (genetic hypomorphism) than for patients lacking this protein. Likewise, prognosis was consistently better for patients with biallelic mutations in FANCD2 (mainly hypomorphic mutations) than for patients with biallelic mutations in FANCA and FANCG, with the lack of the mutant protein in patients with biallelic mutations in FANCG contributing to their poorer outcomes. Our results regarding the clinical impact of chromosome fragility and genetic hypomorphism suggest that mutant FA proteins retain residual activity. This finding should encourage the development of novel therapeutic strategies aimed at partially or fully enhancing mutant FA function, thereby preventing or delaying bone marrow failure and cancer in patients with FA. Clinical Trial Registration number: NCT06490510.
范可尼贫血(FA)是一种罕见的遗传性疾病,其特点是具有高度的表型和基因型异质性以及极端的染色体脆性。为了更好地了解FA的自然病史,识别遗传风险和预后因素,并开发新的治疗策略,西班牙FA患者登记处收集了参与个体在知情同意下的临床特征、染色体脆性、遗传亚型和DNA测序数据。在本文中,我们描述了227例随访长达30年的患者的临床病程,我们的数据表明,到50岁时,这些患者的累积癌症发病率为86%。我们发现,染色体脆性较低的患者畸形谱较轻,在迟发性血液学损害、较轻的骨髓衰竭和较低的癌症风险方面预后较好。我们还发现,导致突变FANCA蛋白表达(遗传亚效性)的突变患者的预后优于缺乏该蛋白的患者。同样,FANCD2双等位基因突变(主要是亚效性突变)患者的预后始终优于FANCA和FANCG双等位基因突变患者,FANCG双等位基因突变患者缺乏突变蛋白导致其预后较差。我们关于染色体脆性和遗传亚效性临床影响的结果表明,突变的FA蛋白保留了残余活性。这一发现应鼓励开发旨在部分或完全增强突变FA功能的新治疗策略,从而预防或延缓FA患者的骨髓衰竭和癌症。临床试验注册号:NCT06490510。