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Your search keyword '"Di Bona, E"' showing total 4 results
Start Over Author "Di Bona, E" Topic myelodysplastic syndromes Language english
4 results on '"Di Bona, E"'

1. Real-world efficacy and safety of luspatercept and predictive factors of response in patients with lower risk myelodysplastic syndromes with ring sideroblasts.

Author

Lanino L, Restuccia F, Perego A, Ubezio M, Fattizzo B, Riva M, Consagra A, Musto P, Cilloni D, Oliva EN, Palmieri R, Poloni A, Califano C, Capodanno I, Itri F, Elena C, Fozza C, Pane F, Pelizzari AM, Breccia M, Di Bassiano F, Crisà E, Ferrero D, Giai V, Barraco D, Vaccarino A, Griguolo D, Minetto P, Quintini M, Paolini S, Sanpaolo G, Sessa M, Bocchia M, Di Renzo N, Diral E, Leuzzi L, Genua A, Guarini A, Molteni A, Nicolino B, Occhini U, Rivoli G, Bono R, Calvisi A, Castelli A, Di Bona E, Di Veroli A, Ferrara F, Fianchi L, Galimberti S, Grimaldi D, Marchetti M, Norata M, Frigeni M, Sancetta R, Selleri C, Tanasi I, Tosi P, Turrini M, Giordano L, Finelli C, Pasini P, Naldi I, Santini V, and Della Porta MG

Subjects
Humans, Activin Receptors, Type II, Immunoglobulin Fc Fragments, Myelodysplastic Syndromes drug therapy, Anemia, Sideroblastic drug therapy
Published
2023
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2. Genomic gain at 6p21: a new cryptic molecular rearrangement in secondary myelodysplastic syndrome and acute myeloid leukemia.

Author

La Starza R, Aventin A, Matteucci C, Crescenzi B, Romoli S, Testoni N, Pierini V, Ciolli S, Sambani C, Locasciulli A, Di Bona E, Lafage-Pochitaloff M, Martelli MF, Marynen P, and Mecucci C

Subjects
Acute Disease, Adult, Aged, Aged, 80 and over, Cytogenetic Analysis, Female, Humans, In Situ Hybridization, Fluorescence, Leukemia, Myeloid diagnosis, Male, Middle Aged, Myelodysplastic Syndromes diagnosis, Neoplasms, Second Primary diagnosis, Sensitivity and Specificity, Chromosomes, Human, Pair 6 genetics, Leukemia, Myeloid genetics, Myelodysplastic Syndromes genetics, Neoplasms, Second Primary genetics, Translocation, Genetic genetics
Abstract

Fluorescence in situ hybridization and comparative genomic hybridization characterized 6p rearrangements in eight primary and in 10 secondary myeloid disorders (including one patient with Fanconi anemia) and found different molecular lesions in each group. In primary disorders, 6p abnormalities, isolated in six patients, were highly heterogeneous with different breakpoints along the 6p arm. Reciprocal translocations were found in seven. In the 10 patients with secondary acute myeloid leukemia/myelodysplastic syndrome (AML/MDS), the short arm of chromosome 6 was involved in unbalanced translocations in 7. The other three patients showed full or partial trisomy of the 6p arm, that is, i(6)(p10) (one patient) and dup(6)(p) (two patients). In 5/7 patients with unbalanced translocations, DNA sequences were overrepresented at band 6p21 as either cryptic duplications (three patients) or cryptic low-copy gains (two patients). In the eight patients with cytogenetic or cryptic 6p gains, we identified a common overrepresented region extending for 5-6 megabases from the TNF gene to the ETV-7 gene. 6p abnormalities were isolated karyotype changes in four patients. Consequently, in secondary AML/MDS, we hypothesize that 6p gains are major pathogenetic events arising from acquired and/or congenital genomic instability.

Published
2006
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3. Treatment of aplastic anaemia with granulocyte-colony stimulating factor and risk of malignancy. Italian Aplastic Anaemia Study Group

Author

Locasciulli, A, Arcese, W, Locatelli, F, Di Bona, E, and Bacigalupo, A

Subjects
Adult, Male, Adolescent, Paroxysmal, Hemoglobinuria, Cyclosporine, Humans, Aged, Child, Mouth Neoplasms, Infant, Leukemia, Hemoglobinuria, Paroxysmal, Anemia, Aplastic, Treatment Outcome, Survival Analysis, Myelodysplastic Syndromes, Immunosuppressive Agents, Child, Preschool, Drug Therapy, Combination, Antilymphocyte Serum, Neoplasms, Granulocyte Colony-Stimulating Factor, Risk Factors, Follow-Up Studies, Middle Aged, Female, Drug Therapy, Preschool, Aplastic, Anemia, Combination, Settore MED/15 - Malattie del Sangue
Published
2001

4. Treatment of aplastic anaemia with granulocyte-colony stimulating factor and risk of malignancy. Italian Aplastic Anaemia Study Group.

Author

Locasciulli, Anna, Arcese, William, Locatelli, Franco, Di Bona, Eros, Bacigalupo, Andrea, Locasciulli, A, Arcese, W, Locatelli, F, Di Bona, E, Bacigalupo, A, and Italian Aplastic Anaemia Study Group

Subjects
*GRANULOCYTE-colony stimulating factor, *COLONY-stimulating factors (Physiology), *BLOOD diseases, *APLASTIC anemia treatment, *PHYSIOLOGY, *ANTILYMPHOCYTIC serum, *APLASTIC anemia, *COMBINATION drug therapy, *CLINICAL trials, *COMPARATIVE studies, *CYCLOSPORINE, *HEMOLYTIC anemia, *IMMUNOSUPPRESSIVE agents, *LEUKEMIA, *LONGITUDINAL method, *RESEARCH methodology, *MEDICAL cooperation, *MOUTH tumors, *MYELODYSPLASTIC syndromes, *RESEARCH, *SURVIVAL analysis (Biometry), *TUMORS, *EVALUATION research, *TREATMENT effectiveness, *THERAPEUTICS
Abstract

Granulocyte-colony stimulating factor (G-CSF) is being increasingly used in healthy volunteers to harvest haemopoietic stem cells. A possible role of G-CSF in the development of clonal disorders or leukaemia has been suggested. We analysed 144 patients with aplastic anaemia treated with immunosuppression protocols with or without G-CSF, with normal cytogenetics at diagnosis or immediately after immunosuppression. Our findings indicated that the risk of developing myelodysplasia or leukaemia was similar in patients with aplastic anaemia on immunosuppressive treatment with or without G-CSF. Therefore, it seems unlikely that G-CSF causes leukaemia in healthy volunteers. [ABSTRACT FROM AUTHOR]

Published
2001
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