María José Ramírez, Roser Pujol, Jordi Minguillón, Massimo Bogliolo, Ilaria Persico, Debora Cavero, Aurora de la Cal, Paula Río, Susana Navarro, José Antonio Casado, Almudena Bailador, Antonio Sanchez de la Fuente, Miguel López de Heredia, Francisco Almazán, M Luisa Antelo, Bienvenida Argilés, Isabel Badell, Marta Baragaño, Cristina Beléndez, Mar Bermúdez, Marta Bernués, María Isabel Buedo, Estela Carrasco, Albert Català, Dolors Costa, Isabel Cuesta, Rafael Fernandez-Delgado, Ana Fernández-Teijeiro, Ángela Figuera, Marta García, Ainhoa Gondra, Macarena González, Soledad González Muñiz, Ines Hernández-Rodríguez, Fátima Ibañez, Nicholas John Kelleher, Francisco Lendínez, Mónica López, Ricardo López-Almaraz, Inmaculada Marchante, Carmen Mendoza, José Nieto, Emilio Ojeda, Salvador Payán-Pernía, Irene Peláez, Inmaculada Pérez de Soto, Raquel Portugal, María A Ramos-Arroyo, Alexandra Regueiro, Ana Rodríguez, Jordi Rosell, Raquel Saez, José Sánchez, Martha Sánchez, MªLeonor Senent, María Tapia, Juan Pablo Trujillo-Quintero, José Manuel Vagace, Jaime Verdú-Amorós, Victória Verdugo, Isabel Vidales, Jasson Villarreal, Cristina Díaz-de-Heredia, Julián Sevilla, Juan Antonio Bueren, Jordi Surrallés
{"title":"范可尼贫血症突变类型和染色体脆性的预后意义。","authors":"María José Ramírez, Roser Pujol, Jordi Minguillón, Massimo Bogliolo, Ilaria Persico, Debora Cavero, Aurora de la Cal, Paula Río, Susana Navarro, José Antonio Casado, Almudena Bailador, Antonio Sanchez de la Fuente, Miguel López de Heredia, Francisco Almazán, M Luisa Antelo, Bienvenida Argilés, Isabel Badell, Marta Baragaño, Cristina Beléndez, Mar Bermúdez, Marta Bernués, María Isabel Buedo, Estela Carrasco, Albert Català, Dolors Costa, Isabel Cuesta, Rafael Fernandez-Delgado, Ana Fernández-Teijeiro, Ángela Figuera, Marta García, Ainhoa Gondra, Macarena González, Soledad González Muñiz, Ines Hernández-Rodríguez, Fátima Ibañez, Nicholas John Kelleher, Francisco Lendínez, Mónica López, Ricardo López-Almaraz, Inmaculada Marchante, Carmen Mendoza, José Nieto, Emilio Ojeda, Salvador Payán-Pernía, Irene Peláez, Inmaculada Pérez de Soto, Raquel Portugal, María A Ramos-Arroyo, Alexandra Regueiro, Ana Rodríguez, Jordi Rosell, Raquel Saez, José Sánchez, Martha Sánchez, MªLeonor Senent, María Tapia, Juan Pablo Trujillo-Quintero, José Manuel Vagace, Jaime Verdú-Amorós, Victória Verdugo, Isabel Vidales, Jasson Villarreal, Cristina Díaz-de-Heredia, Julián Sevilla, Juan Antonio Bueren, Jordi Surrallés","doi":"10.1002/ajh.27520","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":7724,"journal":{"name":"American Journal of Hematology","volume":" ","pages":""},"PeriodicalIF":10.1000,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Prognostic significance of mutation type and chromosome fragility in Fanconi anemia.\",\"authors\":\"María José Ramírez, Roser Pujol, Jordi Minguillón, Massimo Bogliolo, Ilaria Persico, Debora Cavero, Aurora de la Cal, Paula Río, Susana Navarro, José Antonio Casado, Almudena Bailador, Antonio Sanchez de la Fuente, Miguel López de Heredia, Francisco Almazán, M Luisa Antelo, Bienvenida Argilés, Isabel Badell, Marta Baragaño, Cristina Beléndez, Mar Bermúdez, Marta Bernués, María Isabel Buedo, Estela Carrasco, Albert Català, Dolors Costa, Isabel Cuesta, Rafael Fernandez-Delgado, Ana Fernández-Teijeiro, Ángela Figuera, Marta García, Ainhoa Gondra, Macarena González, Soledad González Muñiz, Ines Hernández-Rodríguez, Fátima Ibañez, Nicholas John Kelleher, Francisco Lendínez, Mónica López, Ricardo López-Almaraz, Inmaculada Marchante, Carmen Mendoza, José Nieto, Emilio Ojeda, Salvador Payán-Pernía, Irene Peláez, Inmaculada Pérez de Soto, Raquel Portugal, María A Ramos-Arroyo, Alexandra Regueiro, Ana Rodríguez, Jordi Rosell, Raquel Saez, José Sánchez, Martha Sánchez, MªLeonor Senent, María Tapia, Juan Pablo Trujillo-Quintero, José Manuel Vagace, Jaime Verdú-Amorós, Victória Verdugo, Isabel Vidales, Jasson Villarreal, Cristina Díaz-de-Heredia, Julián Sevilla, Juan Antonio Bueren, Jordi Surrallés\",\"doi\":\"10.1002/ajh.27520\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":7724,\"journal\":{\"name\":\"American Journal of Hematology\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":10.1000,\"publicationDate\":\"2024-11-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American Journal of Hematology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1002/ajh.27520\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"HEMATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American Journal of Hematology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1002/ajh.27520","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"HEMATOLOGY","Score":null,"Total":0}
Prognostic significance of mutation type and chromosome fragility in Fanconi anemia.
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.
期刊介绍:
The American Journal of Hematology offers extensive coverage of experimental and clinical aspects of blood diseases in humans and animal models. The journal publishes original contributions in both non-malignant and malignant hematological diseases, encompassing clinical and basic studies in areas such as hemostasis, thrombosis, immunology, blood banking, and stem cell biology. Clinical translational reports highlighting innovative therapeutic approaches for the diagnosis and treatment of hematological diseases are actively encouraged.The American Journal of Hematology features regular original laboratory and clinical research articles, brief research reports, critical reviews, images in hematology, as well as letters and correspondence.