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Start Over Author "Luchetti, Silvia" Publisher american society of clinical oncology
3 results on '"Luchetti, Silvia"'

1. Clinical effects of driver somatic mutations on the outcomes of patients with myelodysplastic syndromes treated with allogeneic hematopoietic stem-cell transplantation

Author

Della Porta, Matteo G., Galli, Anna Maria, Bacigalupo, Andrea, Zibellini, Silvia, Bernardi, Massimo, Rizzo, Ettore, Allione, Bernardino, Van Lint, Maria Teresa, Pioltelli, Pietro, Marenco, Paola, Bosi, Alberto, Voso, Maria Teresa, Sica, Simona, Cuzzola, Mariella, Angelucci, Emanuele, Rossi, Marianna, Ubezio, Marta, Malovini, Alberto, Limongelli, Ivan, Ferretti, Virginia V., Spinelli, Orietta, Tresoldi, Cristina, Pozzi, Sarah, Luchetti, Silvia, Pezzetti, Laura, Catricalà, Silvia, Milanesi, Chiara, Riva, Alberto, Bruno, Benedetto, Ciceri, Fabio, Bonifazi, Francesca, Bellazzi, Riccardo, Papaemmanuil, Elli, Santoro, Armando, Alessandrino, Emilio P., Rambaldi, Alessandro, Cazzola, Mario, Bacigalupo, Andrea (ORCID:0000-0002-9119-567X), Sica, Simona (ORCID:0000-0003-2426-3465), Della Porta, Matteo G., Galli, Anna Maria, Bacigalupo, Andrea, Zibellini, Silvia, Bernardi, Massimo, Rizzo, Ettore, Allione, Bernardino, Van Lint, Maria Teresa, Pioltelli, Pietro, Marenco, Paola, Bosi, Alberto, Voso, Maria Teresa, Sica, Simona, Cuzzola, Mariella, Angelucci, Emanuele, Rossi, Marianna, Ubezio, Marta, Malovini, Alberto, Limongelli, Ivan, Ferretti, Virginia V., Spinelli, Orietta, Tresoldi, Cristina, Pozzi, Sarah, Luchetti, Silvia, Pezzetti, Laura, Catricalà, Silvia, Milanesi, Chiara, Riva, Alberto, Bruno, Benedetto, Ciceri, Fabio, Bonifazi, Francesca, Bellazzi, Riccardo, Papaemmanuil, Elli, Santoro, Armando, Alessandrino, Emilio P., Rambaldi, Alessandro, Cazzola, Mario, Bacigalupo, Andrea (ORCID:0000-0002-9119-567X), and Sica, Simona (ORCID:0000-0003-2426-3465)

Abstract

Purpose: The genetic basis of myelodysplastic syndromes (MDS) is heterogeneous, and various combinations of somatic mutations are associated with different clinical phenotypes and outcomes. Whether the genetic basis of MDS influences the outcome of allogeneic hematopoietic stem-cell transplantation (HSCT) is unclear. Patients and Methods: We studied 401 patients with MDS or acute myeloid leukemia (AML) evolving from MDS (MDS/AML). We used massively parallel sequencing to examine tumor samples collected before HSCT for somatic mutations in 34 recurrently mutated genes in myeloid neoplasms. We then analyzed the impact of mutations on the outcome of HSCT. Results: Overall, 87% of patients carried one or more oncogenic mutations. Somatic mutations of ASXL1, RUNX1, and TP53 were independent predictors of relapse and overall survival after HSCT in both patients with MDS and patients with MDS/AML (P values ranging from.003 to.035). In patients with MDS/AML, gene ontology (ie, secondary-type AML carrying mutations in genes of RNA splicing machinery, TP53-mutated AML, or de novo AML) was anindependent predictor of posttransplantation outcome (P =.013). The impact of ASXL1, RUNX1, and TP53 mutations on posttransplantation survival was independent of the revised International Prognostic Scoring System (IPSS-R). Combining somatic mutations and IPSS-R risk improved the ability to stratify patients by capturing more prognostic information at an individual level. Accounting for various combinations of IPSS-R risk and somatic mutations, the 5-year probability of survival after HSCT ranged from 0% to 73%. Conclusion: Somatic mutation in ASXL1, RUNX1, or TP53 is independently associated with unfavorable outcomes and shorter survival after allogeneic HSCT for patients with MDS and MDS/AML. Accounting for these genetic lesions may improve the prognostication precision in clinical practice and in designing clinical trials.

Published
2016

2. Clinical effects of driver somatic mutations on the outcomes of patients with myelodysplastic syndromes treated with allogeneic hematopoietic stem-cell transplantation

Author

Cristina Tresoldi, Mariella Cuzzola, Orietta Spinelli, Mario Cazzola, Andrea Bacigalupo, Silvia Luchetti, Ettore Rizzo, Silvia Zibellini, Laura Pezzetti, Silvia Catricalà, Benedetto Bruno, Marianna Rossi, Marta Ubezio, Simona Sica, Chiara Milanesi, Maria Teresa Voso, Emilio Paolo Alessandrino, Riccardo Bellazzi, Anna Gallì, Sarah Pozzi, Armando Santoro, Virginia Valeria Ferretti, Massimo Bernardi, Emanuele Angelucci, Alessandro Rambaldi, Alberto Bosi, Pietro Pioltelli, Paola Marenco, Ivan Limongelli, Fabio Ciceri, Matteo G. Della Porta, Alberto Malovini, Elli Papaemmanuil, Maria Teresa Van Lint, Francesca Bonifazi, Bernardino Allione, Alberto Riva, Della Porta, Matteo G., Gallì, Anna, Bacigalupo, Andrea, Zibellini, Silvia, Bernardi, Massimo, Rizzo, Ettore, Allione, Bernardino, Van Lint, Maria Teresa, Pioltelli, Pietro, Marenco, Paola, Bosi, Alberto, Voso, Maria Teresa, Sica, Simona, Cuzzola, Mariella, Angelucci, Emanuele, Rossi, Marianna, Ubezio, Marta, Malovini, Alberto, Limongelli, Ivan, Ferretti, Virginia V., Spinelli, Orietta, Tresoldi, Cristina, Pozzi, Sarah, Luchetti, Silvia, Pezzetti, Laura, Catricalà, Silvia, Milanesi, Chiara, Riva, Alberto, Bruno, Benedetto, Ciceri, Fabio, Bonifazi, Francesca, Bellazzi, Riccardo, Papaemmanuil, Elli, Santoro, Armando, Alessandrino, Emilio P., Rambaldi, Alessandro, and Cazzola, Mario

Subjects
Oncology, medicine.medical_specialty, Cancer Research, Myeloid, Somatic cell, medicine.medical_treatment, Hematopoietic stem cell transplantation, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, hemic and lymphatic diseases, Internal medicine, medicine, business.industry, Myelodysplastic syndromes, Myeloid leukemia, ORIGINAL REPORTS, medicine.disease, Transplantation, Haematopoiesis, Settore MED/15 - MALATTIE DEL SANGUE, medicine.anatomical_structure, RUNX1, chemistry, 030220 oncology & carcinogenesis, Immunology, business, 030215 immunology
Abstract

Purpose The genetic basis of myelodysplastic syndromes (MDS) is heterogeneous, and various combinations of somatic mutations are associated with different clinical phenotypes and outcomes. Whether the genetic basis of MDS influences the outcome of allogeneic hematopoietic stem-cell transplantation (HSCT) is unclear. Patients and Methods We studied 401 patients with MDS or acute myeloid leukemia (AML) evolving from MDS (MDS/AML). We used massively parallel sequencing to examine tumor samples collected before HSCT for somatic mutations in 34 recurrently mutated genes in myeloid neoplasms. We then analyzed the impact of mutations on the outcome of HSCT. Results Overall, 87% of patients carried one or more oncogenic mutations. Somatic mutations of ASXL1, RUNX1, and TP53 were independent predictors of relapse and overall survival after HSCT in both patients with MDS and patients with MDS/AML (P values ranging from .003 to .035). In patients with MDS/AML, gene ontology (ie, secondary-type AML carrying mutations in genes of RNA splicing machinery, TP53-mutated AML, or de novo AML) was an independent predictor of posttransplantation outcome (P = .013). The impact of ASXL1, RUNX1, and TP53 mutations on posttransplantation survival was independent of the revised International Prognostic Scoring System (IPSS-R). Combining somatic mutations and IPSS-R risk improved the ability to stratify patients by capturing more prognostic information at an individual level. Accounting for various combinations of IPSS-R risk and somatic mutations, the 5-year probability of survival after HSCT ranged from 0% to 73%. Conclusion Somatic mutation in ASXL1, RUNX1, or TP53 is independently associated with unfavorable outcomes and shorter survival after allogeneic HSCT for patients with MDS and MDS/AML. Accounting for these genetic lesions may improve the prognostication precision in clinical practice and in designing clinical trials.

Published
2016

3. Clinical Effects of Driver Somatic Mutations on the Outcomes of Patients With Myelodysplastic Syndromes Treated With Allogeneic Hematopoietic Stem-Cell Transplantation.

Author

Della Porta MG, Gallì A, Bacigalupo A, Zibellini S, Bernardi M, Rizzo E, Allione B, van Lint MT, Pioltelli P, Marenco P, Bosi A, Voso MT, Sica S, Cuzzola M, Angelucci E, Rossi M, Ubezio M, Malovini A, Limongelli I, Ferretti VV, Spinelli O, Tresoldi C, Pozzi S, Luchetti S, Pezzetti L, Catricalà S, Milanesi C, Riva A, Bruno B, Ciceri F, Bonifazi F, Bellazzi R, Papaemmanuil E, Santoro A, Alessandrino EP, Rambaldi A, and Cazzola M

Abstract

Purpose: The genetic basis of myelodysplastic syndromes (MDS) is heterogeneous, and various combinations of somatic mutations are associated with different clinical phenotypes and outcomes. Whether the genetic basis of MDS influences the outcome of allogeneic hematopoietic stem-cell transplantation (HSCT) is unclear., Patients and Methods: We studied 401 patients with MDS or acute myeloid leukemia (AML) evolving from MDS (MDS/AML). We used massively parallel sequencing to examine tumor samples collected before HSCT for somatic mutations in 34 recurrently mutated genes in myeloid neoplasms. We then analyzed the impact of mutations on the outcome of HSCT., Results: Overall, 87% of patients carried one or more oncogenic mutations. Somatic mutations of ASXL1, RUNX1, and TP53 were independent predictors of relapse and overall survival after HSCT in both patients with MDS and patients with MDS/AML (P values ranging from .003 to .035). In patients with MDS/AML, gene ontology (ie, secondary-type AML carrying mutations in genes of RNA splicing machinery, TP53-mutated AML, or de novo AML) was an independent predictor of posttransplantation outcome (P = .013). The impact of ASXL1, RUNX1, and TP53 mutations on posttransplantation survival was independent of the revised International Prognostic Scoring System (IPSS-R). Combining somatic mutations and IPSS-R risk improved the ability to stratify patients by capturing more prognostic information at an individual level. Accounting for various combinations of IPSS-R risk and somatic mutations, the 5-year probability of survival after HSCT ranged from 0% to 73%., Conclusion: Somatic mutation in ASXL1, RUNX1, or TP53 is independently associated with unfavorable outcomes and shorter survival after allogeneic HSCT for patients with MDS and MDS/AML. Accounting for these genetic lesions may improve the prognostication precision in clinical practice and in designing clinical trials.

Published
2016
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