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Cerqui E.,A.O. Spedali Civili | Pelizzari A.,A.O. Spedali Civili | Schieppati F.,A.O. Spedali Civili | Borlenghi E.,A.O. Spedali Civili | And 7 more authors.
Leukemia and Lymphoma

"Real life" data are needed to complement published trials on the efficacy of lenalidomide in patients with myelodysplastic syndrome (MDS) and del(5q) and on the risk of inducing acute myeloid leukemia (AML) progression. Here, we present results of lenalidomide treatment in a consecutive, population-based series of 21 red blood cell (RBC) transfusion-dependent elderly patients with multiple comorbidities. Of 18 evaluable patients (median follow-up: 22 months), 17 achieved an erythroid hematologic response (HI-E) and 16 an RBC transfusion independence. Cytogenetic response (CyR) rate was 80%, median overall survival was 48 months (range 3-164), and 5-year leukemia-free survival was 84%. Three patients progressed to AML; one, with baseline TP53 mutation, achieved HI-E, partial CyR, and did not progress to AML. Eighteen patients experienced hematological adverse events. Overall, lenalidomide was very effective and well tolerated even in unselected elderly patients with multiple comorbidities and did not appear to increase the risk of AML. © 2015 Informa UK, Ltd. Source

Baffelli R.,Stem Cell Laboratory | Notarangelo L.D.,Pediatric Onco Haematology and BMT Unit | Imberti L.,Centro Ricerca Emato oncologica AIL CREA | Hershfield M.S.,Duke University | And 5 more authors.
Journal of Clinical Immunology

Purpose: We carried out a retrospective analysis of 27 patients with Adenosine Deaminase (ADA) deficiency diagnosed in a single center from 1997 to the 2013, for evaluating whether data regarding types of disease-inducing mutations, biochemical and immunological features as well as clinical outcomes of patients treated with enzyme replacement or transplantation, were comparable to those obtained in multicenter studies. Methods: The ADA deficiency diagnosis was performed with biochemical, immunological and molecular techniques. Ten patients treated with hematopoietic stem cell transplantation and three in treatment with enzyme replacement were followed up in our center. Results: Twenty-four different mutations were identified and five were not previously reported. Identical mutations were found among patients from the same Romani ethnic group or from the same geographical region. A more rapid recovery was observed in enzyme replacement treated patients in comparison with those transplanted that, however, showed a continuous and long-lasting improvement both in terms of immune and metabolic recovery. Conclusion: The data obtained in our single center are comparable with those that have been reported in multicenter surveys. © 2015, Springer Science+Business Media New York. Source

Imberti L.,Centro Ricerca Emato oncologica AIL CREA | Scarsi M.,Spedali Civili of Brescia | Zanotti C.,Centro Ricerca Emato oncologica AIL CREA | Chiarini M.,Centro Ricerca Emato oncologica AIL CREA | And 3 more authors.
Journal of Translational Medicine

Background: CD28neg T cells, which display functional characteristic of oligoclonally expanded cytotoxic memory T lymphocytes, are believed to be pathologically relevant in rheumatoid arthritis manifestation. The CD28 co-stimulation blockade by abatacept can prevent the generation of CD28neg T-cell populations in these patients. Methods: Samples were obtained before and after 12months of abatacept therapy. T-cell phenotype and T-cell receptor diversity were evaluated by flow cytometry and complementarity-determining region-3 spectratyping, respectively, while telomerase reverse-transcriptase gene level was measured by real-time PCR. Results: Abatacept induces a decrease of the percentage and number of CD4+CD28neg T cells and a reduction of T-cell repertoire restrictions; these features are directly correlated. Thymic output and telomerase activity are not modified by the therapy. Conclusions: Abatacept-induced decrease of peripheral T-cell repertoire restrictions can due to a reduced generation of senescent, chronically stimulated CD4+CD28neg T cells. © 2015 Imberti et al. Source

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