10 results on '"Parasole R."'
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2. Correspondence: Osteonecrosis in childhood acute lymphoblastic leukemia: a retrospective cohort study of the Italian Association of Pediatric Haemato-Oncology (AIEOP)
- Author
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Parasole, R., Valsecchi, M. G., Silvestri, D., Locatelli, Franco, Barisone, E., Petruzziello, F., Putti, M. C., Micalizzi, C., Colombini, A., Mura, R., Mina, T., Testi, A. M., Notarangelo, L. D., Santoro, N., Casini, T., Consarino, C., Nigro, L. L., Ziino, O., Giagnuolo, G., Rizzari, C., Conter, V., Locatelli F. (ORCID:0000-0002-7976-3654), Parasole, R., Valsecchi, M. G., Silvestri, D., Locatelli, Franco, Barisone, E., Petruzziello, F., Putti, M. C., Micalizzi, C., Colombini, A., Mura, R., Mina, T., Testi, A. M., Notarangelo, L. D., Santoro, N., Casini, T., Consarino, C., Nigro, L. L., Ziino, O., Giagnuolo, G., Rizzari, C., Conter, V., and Locatelli F. (ORCID:0000-0002-7976-3654)
- Abstract
NO ABSTRACT
- Published
- 2018
3. Long-term results of the Italian Association of Pediatric Hematology and Oncology (AIEOP) Studies 82, 87, 88, 91 and 95 for childhood acute lymphoblastic leukemia
- Author
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Conter V., Aricò M., Basso G., Biondi A., Barisone E., Messina C., Parasole R., De Rossi G., Locatelli F., Santoro N., Micalizzi C., Citterio M., Rizzari C., Silvestri D., Rondelli R., Lo Nigro L., Ziino O., Testi A.M., Masera G., Valsecchi M.G., Associazione Italiana di Ematologia ed Oncologia Pediatrica, PESSION, ANDREA, Conter V., Aricò M., Basso G., Biondi A., Barisone E., Messina C., Parasole R., De Rossi G., Locatelli F., Pession A., Santoro N., Micalizzi C., Citterio M., Rizzari C., Silvestri D., Rondelli R., Lo Nigro L., Ziino O., Testi AM., Masera G., Valsecchi MG., Associazione Italiana di Ematologia ed Oncologia Pediatrica., Conter, V, Aricò, M, Basso, G, Biondi, A, Barisone, E, Messina, C, Parasole, R, De Rossi, G, Locatelli, F, Pession, A, Santoro, N, Micalizzi, C, Citterio, M, Rizzari, C, Silvestri, D, Rondelli, R, Lo Nigro, L, Ziino, O, Testi, A, Masera, G, and Valsecchi, M
- Subjects
Male ,Oncology ,Cancer Research ,medicine.medical_specialty ,Pediatrics ,acute lymphoblastic leukemia ,childhood ,long-term results ,Time Factors ,Adolescent ,Time Factor ,Prognosi ,Medical Oncology ,Systemic therapy ,Follow-Up Studie ,Risk Factors ,Internal medicine ,Acute lymphocytic leukemia ,Antineoplastic Combined Chemotherapy Protocols ,medicine ,Humans ,Child ,Survival rate ,Childhood Acute Lymphoblastic Leukemia ,Antineoplastic Combined Chemotherapy Protocol ,Hematology ,business.industry ,Risk Factor ,Remission Induction ,Infant ,Cancer ,Precursor Cell Lymphoblastic Leukemia-Lymphoma ,Prognosis ,medicine.disease ,Minimal residual disease ,Survival Rate ,Treatment Outcome ,Italy ,El Niño ,Child, Preschool ,Female ,Cranial Irradiation ,business ,Follow-Up Studies ,Human - Abstract
We analyzed the long-term outcome of 4865 patients treated in Studies 82, 87, 88, 91 and 95 for childhood acute lymphoblastic leukemia (ALL) of the Italian Association of Pediatric Hematology and Oncology (AIEOP). Treatment was characterized by progressive intensification of systemic therapy and reduction of cranial radiotherapy. A progressive improvement of results with reduction of isolated central nervous system relapse rate was obtained. Ten-year event-free survival increased from 53% in Study 82 to 72% in Study 95, whereas survival improved from 64 to 82%. Since 1991, all patients were treated according to Berlin-Frankfurt-Muenster (BFM) ALL treatment strategy. In Study 91, reduced treatment intensity (25%) yielded inferior results, but intensification of maintenance with high-dose (HD)-L-asparaginase (randomized) allowed to compensate for this disadvantage; in high-risk patients (HR, 15%), substitution of intensive polychemotherapy blocks for conventional BFM backbone failed to improve results. A marked improvement of results was obtained in HR patients when conventional BFM therapy was intensified with three polychemotherapy blocks and double delayed intensification (Study 95). The introduction of minimal residual disease monitoring and evaluation of common randomized questions by AIEOP and BFM groups in the protocol AIEOP-BFM-ALL 2000 are expected to further ameliorate treatment of children with ALL.
- Published
- 2010
4. Pharmacogenetics and induction/consolidation therapy toxicities in acute lymphoblastic leukemia patients treated with AIEOP-BFM ALL 2000 protocol
- Author
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Franca, R., Rebora, P., Bertorello, N., Fagioli, F., Conter, V., Biondi, A., Colombini, A., Micalizzi, C., Zecca, M., Parasole, R., Petruzziello, F., Basso, G., Putti, M. C., Locatelli, Franco, D'Adamo, P., Valsecchi, M. G., Decorti, G., Rabusin, M., Locatelli F. (ORCID:0000-0002-7976-3654), Franca, R., Rebora, P., Bertorello, N., Fagioli, F., Conter, V., Biondi, A., Colombini, A., Micalizzi, C., Zecca, M., Parasole, R., Petruzziello, F., Basso, G., Putti, M. C., Locatelli, Franco, D'Adamo, P., Valsecchi, M. G., Decorti, G., Rabusin, M., and Locatelli F. (ORCID:0000-0002-7976-3654)
- Abstract
Drug-related toxicities represent an important clinical concern in chemotherapy, genetic variants could help tailoring treatment to patient. A pharmacogenetic multicentric study was performed on 508 pediatric acute lymphoblastic leukemia patients treated with AIEOP-BFM 2000 protocol: 28 variants were genotyped by VeraCode and Taqman technologies, deletions of GST-M1 and GST-T1 by multiplex PCR. Toxicities were derived from a central database: 251 patients (49.4%) experienced at least one gastrointestinal (GI) or hepatic (HEP) or neurological (NEU) grade III/IV episode during the remission induction phase: GI occurred in 63 patients (12.4%); HEP in 204 (40.2%) and NEU in 44 (8.7%). Logistic regression model adjusted for sex, risk and treatment phase revealed that ITPA rs1127354 homozygous mutated patients showed an increased risk of severe GI and NEU. ABCC1 rs246240 and ADORA2A rs2236624 homozygous mutated genotypes were associated to NEU and HEP, respectively. These three variants could be putative predictive markers for chemotherapy-related toxicities in AIEOP-BFM protocols.
- Published
- 2017
5. Pharmacogenetics and induction/consolidation therapy toxicities in acute lymphoblastic leukemia patients treated with AIEOP-BFM ALL 2000 protocol
- Author
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Franca, R, Rebora, P, Bertorello, N, Fagioli, F, Conter, V, Biondi, A, Colombini, A, Micalizzi, C, Zecca, M, Parasole, R, Petruzziello, F, Basso, G, Putti, M, Locatelli, F, D'Adamo, P, Valsecchi, M, Decorti, G, Rabusin, M, Rabusin, M., REBORA, PAOLA, BIONDI, ANDREA, VALSECCHI, MARIA GRAZIA, Franca, R, Rebora, P, Bertorello, N, Fagioli, F, Conter, V, Biondi, A, Colombini, A, Micalizzi, C, Zecca, M, Parasole, R, Petruzziello, F, Basso, G, Putti, M, Locatelli, F, D'Adamo, P, Valsecchi, M, Decorti, G, Rabusin, M, Rabusin, M., REBORA, PAOLA, BIONDI, ANDREA, and VALSECCHI, MARIA GRAZIA
- Abstract
Drug-related toxicities represent an important clinical concern in chemotherapy, genetic variants could help tailoring treatment to patient. A pharmacogenetic multicentric study was performed on 508 pediatric acute lymphoblastic leukemia patients treated with AIEOP-BFM 2000 protocol: 28 variants were genotyped by VeraCode and Taqman technologies, deletions of GST-M1 and GST-T1 by multiplex PCR. Toxicities were derived from a central database: 251 patients (49.4%) experienced at least one gastrointestinal (GI) or hepatic (HEP) or neurological (NEU) grade III/IV episode during the remission induction phase: GI occurred in 63 patients (12.4%); HEP in 204 (40.2%) and NEU in 44 (8.7%). Logistic regression model adjusted for sex, risk and treatment phase revealed that ITPA rs1127354 homozygous mutated patients showed an increased risk of severe GI and NEU. ABCC1 rs246240 and ADORA2A rs2236624 homozygous mutated genotypes were associated to NEU and HEP, respectively. These three variants could be putative predictive markers for chemotherapy-related toxicities in AIEOP-BFM protocols.
- Published
- 2017
6. Detection of PICALM-MLLT10 (CALM-AF10) and outcome in children with T-lineage acute lymphoblastic leukemia
- Author
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Lo Nigro, L, Mirabile, E, Tumino, M, Caserta, C, Cazzaniga, G, Rizzari, C, Silvestri, D, Buldini, B, Barisone, E, Casale, F, Luciani, Massimiliano, Locatelli, Franco, Messina, C, Micalizzi, C, Pession, A, Parasole, R, Santoro, N, Masera, G, Basso, G, Aricò, M, Valsecchi, M, Biondi, Alberto, Conter, V, Luciani, M, Locatelli, F (ORCID:0000-0002-7976-3654), Biondi, A (ORCID:0000-0002-2470-7858), Lo Nigro, L, Mirabile, E, Tumino, M, Caserta, C, Cazzaniga, G, Rizzari, C, Silvestri, D, Buldini, B, Barisone, E, Casale, F, Luciani, Massimiliano, Locatelli, Franco, Messina, C, Micalizzi, C, Pession, A, Parasole, R, Santoro, N, Masera, G, Basso, G, Aricò, M, Valsecchi, M, Biondi, Alberto, Conter, V, Luciani, M, Locatelli, F (ORCID:0000-0002-7976-3654), and Biondi, A (ORCID:0000-0002-2470-7858)
- Abstract
N/A
- Published
- 2013
7. Long-term results of the Italian Association of Pediatric Hematology and Oncology (AIEOP) Studies 82, 87, 88, 91 and 95 for childhood acute lymphoblastic leukemia
- Author
-
Conter, V, Aricò, M, Basso, G, Biondi, Alberto, Barisone, E, Messina, C, Parasole, R, De Rossi, G, Locatelli, Franco, Pession, A, Santoro, N, Micalizzi, C, Citterio, M, Rizzari, C, Silvestri, D, Rondelli, R, Lo Nigro, L, Ziino, O, Testi, A M, Masera, G, Valsecchi, M G, Biondi, A (ORCID:0000-0002-2470-7858), Locatelli, F (ORCID:0000-0002-7976-3654), Conter, V, Aricò, M, Basso, G, Biondi, Alberto, Barisone, E, Messina, C, Parasole, R, De Rossi, G, Locatelli, Franco, Pession, A, Santoro, N, Micalizzi, C, Citterio, M, Rizzari, C, Silvestri, D, Rondelli, R, Lo Nigro, L, Ziino, O, Testi, A M, Masera, G, Valsecchi, M G, Biondi, A (ORCID:0000-0002-2470-7858), and Locatelli, F (ORCID:0000-0002-7976-3654)
- Abstract
We analyzed the long-term outcome of 4865 patients treated in Studies 82, 87, 88, 91 and 95 for childhood acute lymphoblastic leukemia (ALL) of the Italian Association of Pediatric Hematology and Oncology (AIEOP). Treatment was characterized by progressive intensification of systemic therapy and reduction of cranial radiotherapy. A progressive improvement of results with reduction of isolated central nervous system relapse rate was obtained. Ten-year event-free survival increased from 53% in Study 82 to 72% in Study 95, whereas survival improved from 64 to 82%. Since 1991, all patients were treated according to Berlin-Frankfurt-Muenster (BFM) ALL treatment strategy. In Study 91, reduced treatment intensity (25%) yielded inferior results, but intensification of maintenance with high-dose (HD)-L-asparaginase (randomized) allowed to compensate for this disadvantage; in high-risk patients (HR, 15%), substitution of intensive polychemotherapy blocks for conventional BFM backbone failed to improve results. A marked improvement of results was obtained in HR patients when conventional BFM therapy was intensified with three polychemotherapy blocks and double delayed intensification (Study 95). The introduction of minimal residual disease monitoring and evaluation of common randomized questions by AIEOP and BFM groups in the protocol AIEOP-BFM-ALL 2000 are expected to further ameliorate treatment of children with ALL. Leukemia (2010) 24, 255-264; doi: 10.1038/leu.2009.250; published online 17 December 2009
- Published
- 2010
8. KCTD15 deregulation is associated with alterations of the NF-κB signaling in both pathological and physiological model systems.
- Author
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Smaldone G, Coppola L, Pane K, Franzese M, Beneduce G, Parasole R, Menna G, Vitagliano L, Salvatore M, and Mirabelli P
- Subjects
- HEK293 Cells, HeLa Cells, Hematopoietic Stem Cells metabolism, Humans, I-kappa B Kinase metabolism, NF-kappa B metabolism, Potassium Channels metabolism, Precursor Cell Lymphoblastic Leukemia-Lymphoma metabolism, Precursor Cell Lymphoblastic Leukemia-Lymphoma pathology, T-Lymphocytes metabolism, Tumor Cells, Cultured, Up-Regulation, Potassium Channels genetics, Precursor Cell Lymphoblastic Leukemia-Lymphoma genetics, Signal Transduction
- Abstract
Like other KCTD proteins, KCTD15 is involved in important albeit distinct biological processes as cancer, neural crest formation, and obesity. Here, we characterized the role of KCTD15 in different physiological/pathological states to gain insights into its diversified function(s). The silencing of KCTD15 in MLL-rearranged leukemia models induced attenuation of the NF-κB pathway associated with a downregulation of pIKK-β and pIKB-α. Conversely, the activation of peripheral blood T cells upon PMA/ionomycin stimulation remarkably upregulated KCTD15 and, simultaneously, pIKK-β and pIKB-α. Moreover, a significant upregulation of KCTD15 was also observed in CD34 hematopoietic stem/progenitor cells where the NF-κB pathway is physiologically activated. The association between KCTD15 upregulation and increased NF-κB signaling was confirmed by luciferase assay as well as KCTD15 and IKK-β proximity ligation and immunoprecipitation experiments. The observed upregulation of IKK-β by KCTD15 provides a novel and intriguing interpretative key for understanding the protein function in a wide class of physiological/pathological conditions ranging from neuronal development to cancer and obesity/diabetes., (© 2021. The Author(s).)
- Published
- 2021
- Full Text
- View/download PDF
9. KCTD15 is overexpressed in human childhood B-cell acute lymphoid leukemia.
- Author
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Smaldone G, Beneduce G, Incoronato M, Pane K, Franzese M, Coppola L, Cordella A, Parasole R, Ripaldi M, Nassa G, Soricelli A, Vitagliano L, Mirabelli P, and Salvatore M
- Subjects
- Antineoplastic Combined Chemotherapy Protocols adverse effects, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Apoptosis genetics, Biomarkers, Tumor, Child, Preschool, Female, Gene Rearrangement, Histone-Lysine N-Methyltransferase genetics, Humans, Induction Chemotherapy, Male, Myeloid-Lymphoid Leukemia Protein genetics, Precursor Cell Lymphoblastic Leukemia-Lymphoma diagnosis, Precursor Cell Lymphoblastic Leukemia-Lymphoma drug therapy, Prognosis, Gene Expression Regulation, Leukemic, Potassium Channels genetics, Precursor Cell Lymphoblastic Leukemia-Lymphoma genetics
- Abstract
Leukemic cells originate from the malignant transformation of undifferentiated myeloid/lymphoid hematopoietic progenitors normally residing in bone marrow. As the precise molecular mechanisms underlying this heterogeneous disease are yet to be disclosed, the identification and the validation of novel actors in leukemia is of extreme importance. Here, we show that KCTD15, a member of the emerging class of KCTD ((K)potassium Channel Tetramerization Domain containing) proteins, is strongly upregulated in patients affected by B-cell type acute lymphoblastic leukemia (B-ALL) and in continuous cell lines (RS4;11, REH, TOM-1, SEM) derived from this form of childhood leukemia. Interestingly, KCTD15 downregulation induces apoptosis and cell death suggesting that it has a role in cellular homeostasis and proliferation. In addition, stimulation of normal lymphocytes with the pokeweed mitogen leads to increased KCTD15 levels in a fashion comparable to those observed in proliferating leukemic cells. In this way, the role of KCTD15 is likely not confined to the B-ALL pathological state and extends to activation and proliferation of normal lymphocytes. Collectively, data here presented indicate that KCTD15 is an important and hitherto unidentified player in childhood lymphoid leukemia, and its study could open a new scenario for the identification of altered and still unknown molecular pathways in leukemia.
- Published
- 2019
- Full Text
- View/download PDF
10. Palonosetron to prevent nausea and vomiting in children undergoing BMT: efficacy and safety.
- Author
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Ripaldi M, Parasole R, De Simone G, D'Amico MR, Migliorati R, Zanotta G, Loffredo G, Petruzziello F, and Poggi V
- Subjects
- Adolescent, Child, Child, Preschool, Female, Humans, Infant, Male, Nausea etiology, Neoplasms surgery, Palonosetron, Retrospective Studies, Serotonin Antagonists therapeutic use, Vomiting etiology, Antiemetics therapeutic use, Bone Marrow Transplantation adverse effects, Isoquinolines therapeutic use, Nausea prevention & control, Quinuclidines therapeutic use, Vomiting prevention & control
- Published
- 2010
- Full Text
- View/download PDF
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