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1. The Italian SurveY on carDiac rEhabilitation 2008 (ISYDE 2008): study presentation

Author

Tramarin R., Ambrosetti M., De Feo S., Griffo R., Maslowsky F., Diaco T., Riccio C., Carlon R., Castello A., Ferratini M., Schweiger C., Chieffo C., Ciglia C., Lapolla A., Pietropaolo F., Furgi G., Martin G., Semprini P., Avallone A., Bertoli D., Belardinelli R., Soffiantino F., Scrutinio D., Maxia P., Coco R., Giustarini C., Anniboletti P., Favretto G., Vaghi P., Calisi P., Chiavetta C., Guarracini L., Marcellini G., Iannopollo M., Borello G., Matta M., Peccerillo N., Boncompagni . F, Amici A., Feraco E., Pulitanò G., Tripodi E., Capomolla S., Golino P., Parrilli G., Di Patria A., Di Gioia C., Micieli D., Perrotta S., Rubino A., Aulitto V., Riccio G., Codec L., Coruzzi P., Violi E., Nardini M., Urbinati S., Dcruz S., Piepoli M., Fucili A., Cerulli M., Roberto B., Balestra G., Tuniz D., Gori P., Marini R., Morgera T., Di Mario F., Volterrani M., Galati A., Salustri A., Jesi A.P., Lacch A., Loperfido F., Corsiglia L., Pantaleo P., Gigli G., Marchesi D., Febo O., Cobelli F., Malinverni C., Jones N., Anzà C., Frizelli R., Gei P., Acquistapace F., Pedretti R., Carugo S., Malfatto G., Meloni C., Giordano A., Schizzarotto A., Zanettini R., Bosco R., Occhi G., Aglieri S., Caprioli G., Cuocina N., Lazzaroni L., Laurenzi A., Savonelli C., Veniani M., Corda G., Meinecke C., Castiglioni G., Ravizza P., Giani P., Robustelli F., Gullace G., Passoni F., Barelli M.V., Richichi I., Rossi A., Politi A., Persico M., Giannuzzi P., Mazzucco G., Bosimini E., Riva G., Massobrio N., Gondoni L., Aina F., Ingignoli B., Cal M.V., Costante A., Villella M., La Rosa C., Sannia L., Barbanto P., Rametta R., Albanese D., Circo A., Raciti R., Scarnato L., Dispensa F., La Spina L., Stuto A., Vasco C., Gibiino S., Gabriele M., Dispensieri C., Carini V., Provvidenza M., Scalzini A., Macchi C., Fattirolli F., Vannucci M., Iacopetti L., Cordoni M., Gabriele F., Santoni R., Pitscheider W., Bettini R., Mandorla S., Anniboletti F., Patriarchi F., Baroni P.L., Bordin F., Biondi P., Bellotto F., Zanocco A., Ponchia A., Mantovani E., Li Greci E., Celegon L., Baracchi S., Pizzolato G., Peroni L., Apolloni E., Mosele G., Guarniero M., Roncon L., VIGORITO, CARLO, Tramarin, R., Ambrosetti, M., De Feo, S., Griffo, R., Maslowsky, F., Diaco, T., Riccio, C., Carlon, R., Castello, A., Ferratini, M., Schweiger, C., Chieffo, C., Vigorito, Carlo, Ciglia, C., Lapolla, A., Pietropaolo, F., Furgi, G., Martin, G., Semprini, P., Avallone, A., Bertoli, D., Belardinelli, R., Soffiantino, F., Scrutinio, D., Maxia, P., Coco, R., Giustarini, C., Anniboletti, P., Favretto, G., Vaghi, P., Calisi, P., Chiavetta, C., Guarracini, L., Marcellini, G., Iannopollo, M., Borello, G., Matta, M., Peccerillo, N., Boncompagni., F, Amici, A., Feraco, E., Pulitanò, G., Tripodi, E., Capomolla, S., Golino, P., Parrilli, G., Di Patria, A., Di Gioia, C., Micieli, D., Perrotta, S., Rubino, A., Aulitto, V., Riccio, G., Codec, L., Coruzzi, P., Violi, E., Nardini, M., Urbinati, S., Dcruz, S., Piepoli, M., Fucili, A., Cerulli, M., Roberto, B., Balestra, G., Tuniz, D., Gori, P., Marini, R., Morgera, T., Di Mario, F., Volterrani, M., Galati, A., Salustri, A., Jesi, A. P., Lacch, A., Loperfido, F., Corsiglia, L., Pantaleo, P., Gigli, G., Marchesi, D., Febo, O., Cobelli, F., Malinverni, C., Jones, N., Anzà, C., Frizelli, R., Gei, P., Acquistapace, F., Pedretti, R., Carugo, S., Malfatto, G., Meloni, C., Giordano, A., Schizzarotto, A., Zanettini, R., Bosco, R., Occhi, G., Aglieri, S., Caprioli, G., Cuocina, N., Lazzaroni, L., Laurenzi, A., Savonelli, C., Veniani, M., Corda, G., Meinecke, C., Castiglioni, G., Ravizza, P., Giani, P., Robustelli, F., Gullace, G., Passoni, F., Barelli, M. V., Richichi, I., Rossi, A., Politi, A., Persico, M., Giannuzzi, P., Mazzucco, G., Bosimini, E., Riva, G., Massobrio, N., Gondoni, L., Aina, F., Ingignoli, B., Cal, M. V., Costante, A., Villella, M., La Rosa, C., Sannia, L., Barbanto, P., Rametta, R., Albanese, D., Circo, A., Raciti, R., Scarnato, L., Dispensa, F., La Spina, L., Stuto, A., Vasco, C., Gibiino, S., Gabriele, M., Dispensieri, C., Carini, V., Provvidenza, M., Scalzini, A., Macchi, C., Fattirolli, F., Vannucci, M., Iacopetti, L., Cordoni, M., Gabriele, F., Santoni, R., Pitscheider, W., Bettini, R., Mandorla, S., Anniboletti, F., Patriarchi, F., Baroni, P. L., Bordin, F., Biondi, P., Bellotto, F., Zanocco, A., Ponchia, A., Mantovani, E., Li Greci, E., Celegon, L., Baracchi, S., Pizzolato, G., Peroni, L., Apolloni, E., Mosele, G., Guarniero, M., and Roncon, L.

Subjects
Heart Failure, Male, Internet, Time Factors, Heart Diseases, Cardiologia Riabilitativa, Data Collection, Myocardial Infarction, Rehabilitation Centers, Factor IX, Prevenzione secondaria, Italy, Risk Factors, Health Care Surveys, Practice Guidelines as Topic, Humans, Female, Longitudinal Studies, Public Health, ISYDE 2008, Coronary Artery Bypass, Follow-Up Studies
Abstract

In this paper, the Italian Society of Cardiac Rehabilitation and Prevention (GICR) presents the third survey on the status of cardiac rehabilitation (CR) in Italy. The Italian SurveY on carDiac rEhabilitation 2008 (ISYDE 2008) is a multicenter, observational study aimed at identifying the number and characteristics of Italian CR facilities, both in terms of health operators and interventions. Clinical records of all patients consecutively discharged within the whole network--composed of up to 200 CR units--from January 28 to February 10, 2008 will also be reviewed for diagnosis of admission, comorbidities, rehabilitation programs, and drug therapy, in order to obtain a snapshot of current implementation strategies in daily clinical practice. The survey will adopt a web-based methodology for data provision and transmission. Preliminary results of the survey are expected in the late summer 2008.

Published
2008

2. Global Secondary Prevention Strategies to Limit Event Recurrence After Myocardial Infarction

Author

Giannuzzi P., Temporelli P.L., Marchioli R., Maggioni A.P., Balestroni G., Ceci V., Chieffo C., Gattone M., Griffo R., Schweiger C., Tavazzi L., Urbinati S., Valagussa F., Vanuzzo D., Girardini D., Francesconi G., Vona M., Santoni R., Sarno C., Calisi P., Forzoni M., Boncompagni L., Tabouret G., Canci U., Rosato G., Stanco G., Gullace G., Carbone C., Gavazzi A., Mazzoleni D., Pinelli G., Frizzelli R., Tortelli O., Pantaleoni A., Mantovani E., Pettinati G., Storti G., Riccio C., Scrutinio D., Passantino A., Guiducci D., Zobbi G., Vanaria D., Barbanti P., Carini V., Coco R., Borrello G., Mazza M.L., Chiesa F., Sansoni C., Morbelli E., Rossi L., Ciglia C., Di Giovanni P., Cocchieri M., Dò V., Trudu A., Albonic D., Bendinelli S., Iori E., Balestra G., Giacometti N., Coppetti S., Priori S., Masotti G., Fattirolli F., Meniconi L., Paolucci P., Malinverni C., Quarenghi F., Fontanelli A., Marini R., Mandorla S., Provvidenza M., Giordano A., De Giuli F., Odoguardi L., Barsotti S., Moccetti T., Molteni A., Mauri F., Lecchi G., Bettini R., Bertoldi A., Zanettini R., Centeleghe P., Corallo S., Rainoldi M.L., Ferratini M., Tavanelli M., Leonetti G., Malfatto G., Pascotto P., Zanocco A., Buchberger R., Masaro G., Cobelli F., Sala L., Musca G., Cauteruccio M.A., Giallauria F., Mininni N., Morra P., Castello A., Sarullo F.M., Castelli D., Tramarin R., De Salvo M., Porcellati C., Giovagnoni F., Anniboletti P.F., Calisti M.G., Vergoni W., Iacopetti L., Zelaschi F., D'Cruz S., Lopizzo A., Caiazza M., Gigli G., Pastine J., Pulitanò G., Ruggeri A., Piovaccari G., Semprini P., Zavatteri G., Diaco T., Lumia F., Tamiz A.M., Oliva G., Galati A., Picelli A., Picelli F., Bosco R., Marcellini G., Zanchè E., Martin G., Masutti S., Milani L., Pizzolato G.M., Occhi G., Partesana N., Baldi N., Polimeni G., Furgi G., Nicolino A., Bevilacqua R., Ingignoli B., Massobrio N., Avogliero G., Pedretti R., Vaninetti R., Donnangelo L., Chiatto M., Gori P., Garbin R., RICCARDI, GABRIELE, VIGORITO, CARLO, Giannuzzi, P., Temporelli, P. L., Marchioli, R., Maggioni, A. P., Balestroni, G., Ceci, V., Chieffo, C., Gattone, M., Griffo, R., Schweiger, C., Tavazzi, L., Urbinati, S., Valagussa, F., Vanuzzo, D., Girardini, D., Francesconi, G., Vona, M., Santoni, R., Sarno, C., Calisi, P., Forzoni, M., Boncompagni, L., Tabouret, G., Canci, U., Rosato, G., Stanco, G., Gullace, G., Carbone, C., Gavazzi, A., Mazzoleni, D., Pinelli, G., Frizzelli, R., Tortelli, O., Pantaleoni, A., Mantovani, E., Pettinati, G., Storti, G., Riccio, C., Scrutinio, D., Passantino, A., Guiducci, D., Zobbi, G., Vanaria, D., Barbanti, P., Carini, V., Coco, R., Borrello, G., Mazza, M. L., Chiesa, F., Sansoni, C., Morbelli, E., Rossi, L., Ciglia, C., Di Giovanni, P., Cocchieri, M., Dò, V., Trudu, A., Albonic, D., Bendinelli, S., Iori, E., Balestra, G., Giacometti, N., Coppetti, S., Priori, S., Masotti, G., Fattirolli, F., Meniconi, L., Paolucci, P., Malinverni, C., Quarenghi, F., Fontanelli, A., Marini, R., Mandorla, S., Provvidenza, M., Giordano, A., De Giuli, F., Odoguardi, L., Barsotti, S., Moccetti, T., Molteni, A., Mauri, F., Lecchi, G., Bettini, R., Bertoldi, A., Zanettini, R., Centeleghe, P., Corallo, S., Rainoldi, M. L., Ferratini, M., Tavanelli, M., Leonetti, G., Malfatto, G., Pascotto, P., Zanocco, A., Buchberger, R., Masaro, G., Cobelli, F., Riccardi, Gabriele, Sala, L., Musca, G., Cauteruccio, M. A., Vigorito, Carlo, Giallauria, F., Mininni, N., Morra, P., Castello, A., Sarullo, F. M., Castelli, D., Tramarin, R., De Salvo, M., Porcellati, C., Giovagnoni, F., Anniboletti, P. F., Calisti, M. G., Vergoni, W., Iacopetti, L., Zelaschi, F., D'Cruz, S., Lopizzo, A., Caiazza, M., Gigli, G., Pastine, J., Pulitanò, G., Ruggeri, A., Piovaccari, G., Semprini, P., Zavatteri, G., Diaco, T., Lumia, F., Tamiz, A. M., Oliva, G., Galati, A., Picelli, A., Picelli, F., Bosco, R., Marcellini, G., Zanchè, E., Martin, G., Masutti, S., Milani, L., Pizzolato, G. M., Occhi, G., Partesana, N., Baldi, N., Polimeni, G., Furgi, G., Nicolino, A., Bevilacqua, R., Ingignoli, B., Massobrio, N., Avogliero, G., Pedretti, R., Vaninetti, R., Donnangelo, L., Chiatto, M., Gori, P., and Garbin, R.

Subjects
Male, medicine.medical_specialty, Myocardial Infarction, GOSPEL, Angina Pectoris, law.invention, Angina, Randomized controlled trial, law, Internal medicine, Myocardial Revascularization, Secondary Prevention, Internal Medicine, medicine, Clinical endpoint, Humans, Myocardial infarction, Life Style, Stroke, Heart Failure, Cardiac Rehabilitation, business.industry, Surrogate endpoint, Hazard ratio, Middle Aged, medicine.disease, Heart failure, Physical therapy, Female, business, Stress, Psychological
Abstract

Background Secondary prevention is not adequately implemented after myocardial infarction (MI). We assessed the effect on quality of care and prognosis of a long-term, relatively intensive rehabilitation strategy after MI. Methods We conducted a multicenter, randomized controlled trial in patients following standard post-MI cardiac rehabilitation, comparing a long-term, reinforced, multifactorial educational and behavioral intervention with usual care. A total of 3241 patients with recent MI were randomized to a 3-year multifactorial continued educational and behavioral program (intervention group; n = 1620) or usual care (control group; n = 1621). The combination of cardiovascular (CV) mortality, nonfatal MI, nonfatal stroke, and hospitalization for angina pectoris, heart failure, or urgent revascularization procedure was the primary end point. Other end points were major CV events, major cardiac and cerebrovascular events, lifestyle habits, and drug prescriptions. Results End point events occurred in 556 patients (17.2%). Compared with usual care, the intensive intervention did not decrease the primary end point significantly (16.1% vs 18.2%; hazard ratio [HR], 0.88; 95% confidence interval [CI], 0.74-1.04). However, the intensive intervention decreased several secondary end points: CV mortality plus nonfatal MI and stroke (3.2% vs 4.8%; HR, 0.67; 95% CI, 0.47-0.95), cardiac death plus nonfatal myocardial infarction (2.5% vs 4.0%; HR, 0.64; 95% CI, 0.43-0.94), and nonfatal MI (1.4% vs 2.7%; HR, 0.52; 95% CI, 0.31-0.86). A marked improvement in lifestyle habits (ie, exercise, diet, psychosocial stress, less deterioration of body weight control) and in prescription of drugs for secondary prevention was seen in the intervention group. Conclusion The GOSPEL Study is the first trial to our knowledge to demonstrate that a multifactorial, continued reinforced intervention up to 3 years after rehabilitation following MI is effective in decreasing the risk of several important CV outcomes, particularly nonfatal MI, although the overall effect is small. Trial Registration ClinicalTrials.gov Identifier:NCT00421876

Published
2008

3. Human bone marrow mesenchymal stem cells display anti-cancer activity in SCID mice bearing disseminated non-Hodgkin's lymphoma xenografts

Author

Giorgio Zauli, Elisabetta Melloni, Lorenzo Caruso, Sabrina Ingrao, Sonia Zorzet, Raffaella Bosco, Paola Secchiero, Barbara Zavan, Federica Corallini, Claudio Tripodo, Secchiero, P, Zorzet, S, Tripodo, C, Corallini, F, Melloni, E, Caruso, L, Bosco, R, Ingrao, S, Zavan, B, Zauli G., Secchiero, P., Zorzet, Sonia, Tripodo, C., Corallini, F., Melloni, E., Caruso, L., Bosco, R., Ingrao, S., Zavan, B., and Zauli, G.

Subjects
Pathology, medicine.medical_specialty, Stromal cell, Transplantation, Heterologous, Mice, Nude, lcsh:Medicine, mesenchimal stem cells, Mice, SCID, Mice, immune system diseases, hemic and lymphatic diseases, mesenchymal stem cells, non-Hodgkin's lymphoma, Animals, Humans, Medicine, human lymphoma xenograft, Oncology/Hematological Malignancies, lcsh:Science, SCID Mice, Multidisciplinary, Hematology/Bone Marrow and Stem Cell Transplantation, business.industry, Lymphoma, Non-Hodgkin, Lymphoblast, lcsh:R, Mesenchymal stem cell, Non-Hodgkin's Lymphoma, Mesenchymal Stem Cells, Hematopoietic Stem Cells, medicine.disease, Coculture Techniques, Lymphoma, Non-Hodgkin's lymphoma, Endothelial stem cell, Transplantation, Apoptosis, lcsh:Q, Hematology/Lymphomas and Chronic Lymphoblastic Leukemia, business, Research Article
Abstract

Background Although multimodality treatment can induce high rate of remission in many subtypes of non-Hodgkin's lymphoma (NHL), significant proportions of patients relapse with incurable disease. The effect of human bone marrow (BM) mesenchymal stem cells (MSC) on tumor cell growth is controversial, and no specific information is available on the effect of BM-MSC on NHL. Methodology/Principal Findings The effect of BM-MSC was analyzed in two in vivo models of disseminated non-Hodgkin's lymphomas with an indolent (EBV− Burkitt-type BJAB, median survival = 46 days) and an aggressive (EBV+ B lymphoblastoid SKW6.4, median survival = 27 days) behavior in nude-SCID mice. Intra-peritoneal (i.p.) injection of MSC (4 days after i.p. injection of lymphoma cells) significantly increased the overall survival at an optimal MSC∶lymphoma ratio of 1∶10 in both xenograft models (BJAB+MSC, median survival = 58.5 days; SKW6.4+MSC, median survival = 40 days). Upon MSC injection, i.p. tumor masses developed more slowly and, at the histopathological observation, exhibited a massive stromal infiltration coupled to extensive intra-tumor necrosis. In in vitro experiments, we found that: i) MSC/lymphoma co-cultures modestly affected lymphoma cell survival and were characterized by increased release of pro-angiogenic cytokines with respect to the MSC, or lymphoma, cultures; ii) MSC induce the migration of endothelial cells in transwell assays, but promoted endothelial cell apoptosis in direct MSC/endothelial cell co-cultures. Conclusions/Significance Our data demonstrate that BM-MSC exhibit anti-lymphoma activity in two distinct xenograft SCID mouse models of disseminated NHL.

Published
2010

4. Changes in T-Cell Responses Against Human Herpesvirus-8 Correlate with the Disease Course of Iatrogenic Kaposi's Sarcoma in a Patient with Undifferentiated Arthritis

Author

Francesco Volzone, Monica Morselli, Clodoveo Ferri, Leonardo Potenza, Fabio Ciceri, Fabio Forghieri, Patrizia Barozzi, Giovanni Riva, Mario Luppi, Chiara Bonini, Claudio Bordignon, Giulio Rossi, Denise Whitby, Raffaella Bosco, Thomas F. Schulz, Chiara Quadrelli, Daniela Vallerini, Giuseppe Torelli, Barozzi, P, Potenza, L, Riva, G, Vallerini, D, Quadrelli, C, Bosco, R, Morselli, M, Forghieri, F, Volzone, F, Rossi, G, Ferri, C, Bonini, MARIA CHIARA, Ciceri, Fabio, Bordignon, Claudio, Whitby, D, Schulz, Tf, Torelli, G, and Luppi, M.

Subjects
medicine.medical_specialty, T-Lymphocytes, viruses, medicine.medical_treatment, Iatrogenic Disease, Arthritis, Opportunistic Infections, Antibodies, Viral, medicine.disease_cause, Herpesviridae, Immune system, Rheumatology, Internal medicine, medicine, Humans, Sarcoma, Kaposi, Kaposi's sarcoma, HHV-8, immunosuppression, business.industry, ELISPOT, Kaposi sarcoma, virus diseases, Immunosuppression, Middle Aged, Viral Load, medicine.disease, Anesthesiology and Pain Medicine, Herpesvirus 8, Human, Immunology, Disease Progression, undifferentiated arthritis, Female, business, Viral load, Immunosuppressive Agents, Follow-Up Studies
Abstract

Objectives: To describe the first in-depth analysis of both the T-cell responses against human herpesvirus-8 (HHV-8) and the HHV-8 viral load in 1 patient who developed iatrogenic HHV-8-associated-Kaposi's sarcoma (KS) following immunosuppressive treatment for undifferentiated arthritis and to review the literature on iatrogenic KS (IKS). Methods: T-cell responses against HHV-8 lytic and latent antigens were analyzed by ex vivo enzyme-linked immunospot (Elispot) and HHV-8 viral load was assessed by quantitative polymerase chain reaction, in sequential peripheral blood samples from a 55-year-old woman who developed skin/mucosal and visceral KS, while receiving treatment with cyclosporine, methotrexate, and methylprednisolone for undifferentiated arthritis. Results: KS may result from HHV-8 infection in patients undergoing immunosuppressive treatment for rheumatic diseases and this is the first case of IKS occurring in undifferentiated arthritis. A role for immune surveillance in the pathogenesis of IKS is supported by the observation of disease regression following discontinuation of immunosuppressive therapy. In a 4-year follow-up, we showed that variations of the virus-specific immune responses but not of the viral load correlated well with the disease course, characterized by 2 remission and subsequent relapse phases, following changes of immunosuppressive therapy. Conclusions: We have provided evidence of a clear-cut correlation between changes in immunologic markers of HHV-8 infection and the disease course of this viral associated tumor, concomitant with variations of immunosuppressive treatment. Thus, ex vivo enzyme-linked immunospot for HHV-8-specific T-cell responses represents a new tool for the clinical management of rheumatic patients with IKS. (C) 2009 Elsevier Inc. All rights reserved. Semin Arthritis Rheum 39:170-175 RI Rossi, Giulio/C-5576-2011

Published
2009

5. Fine tuning of protein kinase C (PKC) isoforms in cancer: shortening the distance from the laboratory to the bedside

Author

Elisabetta Melloni, Claudio Celeghini, Giorgio Zauli, E. Rimondi, Mauro Vaccarezza, Raffaella Bosco, Bosco, R., Melloni, E., Celeghini, Claudio, Rimondi, Erika, Vaccarezza, M., and Zauli, G.

Subjects
Gene isoform, Antineoplastic Agents, Biology, Isozyme, Serine, Neoplasms, Drug Discovery, Intracellular receptor, innovative drug compounds, Humans, Enzyme Inhibitors, PKC, Protein Kinase C, Protein kinase C, Pharmacology, Biological Products, PKCS, General Medicine, Oligonucleotides, Antisense, Small molecule, Cell biology, Isoenzymes, Biochemistry, Tumor progression, tumour cell biology, Peptides
Abstract

The serine/threonine protein kinase C (PKC) family was first identified as intracellular receptor(s) for the tumor promoting agents phorbol esters. Thirty years after the discovery of PKC, the role of specific PKC isoforms has been described in relationship with an altered pattern of expression in different types of cancer and a good number of small molecule inhibitors (inhibitory peptides, antisense oligonucleotides or natural compounds) targeting PKC are now available. Despite all these achievements and a huge amount of basic research studies on the biochemical regulation of PKC, there has been a delay in clinical trials with drugs targeting PKC function. This delay is easily explained taking into account the extreme biological complexity of the PKC family of isoforms and the incomplete understanding of the specific role of each PKC isozyme in different types of cancers. Some of the difficulties in developing pharmacological compounds selectively tuning the different PKCs have started to be overcome. In this review, the growing evidences of the role of the PKC isoforms α, βII, δ, ε, ζ and ι is in promoting or counteracting tumor progression will be discussed in relationship with promising therapeutic perspectives.

Published
2011

6. Anti-leukemic activity of dasatinib in both p53(wild-type) and p53(mutated) B malignant cells

Author

Silvano Capitani, Claudio Celeghini, Rebecca Voltan, Marco Rabusin, Federica Corallini, Raffaella Bosco, Paola Secchiero, Bosco, R., Rabusin, M., Voltan, R., Celeghini, Claudio, Corallini, F., Capitani, S., and Secchiero, P.

Subjects
MAPK/ERK pathway, p53, STAT3 Transcription Factor, Time Factors, Cell Survival, p38 mitogen-activated protein kinases, Dasatinib, Antineoplastic Agents, Apoptosis, Leukemic cells, p38 Mitogen-Activated Protein Kinases, hemic and lymphatic diseases, Cell Line, Tumor, medicine, Humans, Pharmacology (medical), Granulocyte Precursor Cells, Phosphorylation, STAT3, Protein Kinase Inhibitors, Pharmacology, Mitogen-Activated Protein Kinase 1, B-Lymphocytes, Mitogen-Activated Protein Kinase 3, biology, Leukemia, Prolymphocytic, B-Cell, Kinase, Chemistry, Wild type, leukemic cell, Cell cycle, G1 Phase Cell Cycle Checkpoints, Thiazoles, Pyrimidines, Oncology, Mutation, biology.protein, Cancer research, Tumor Suppressor Protein p53, medicine.drug
Abstract

The multi-kinase inhibitor Dasatinib induced a variable but significant decrease of viability in both p53(wild-type) (EHEB, JVM-2, JVM-3) and p53(mutated) (MEC-1, MEC-2, BJAB) prolymphocytic B leukemic cells, due to a combination of cell cycle block in G1 and apoptosis. Antibody phospho-kinase array analysis revealed that Dasatinib inhibited the phosphorylation of various kinases, including ERK1/2 and p38/MAPK as well as of STAT3 transcription factors, in both p53(wild-type) and p53(mutated) cells. Therefore, Dasatinib might offer a novel therapeutic strategy not only for p53(wild-type), but also for p53(mutated) B malignancies that have the worst prognosis and urgently need innovative therapeutic approaches.

Published
2010

7. Recent advances in the therapeutic perspectives of nutlin-3

Author

Paola Secchiero, Giorgio Zauli, Claudio Celeghini, Raffaella Bosco, Secchiero, P., Bosco, R., Celeghini, Claudio, and Zauli, G.

Subjects
Cell cycle checkpoint, senescence, synergistic, pediatric malignancies, Pharmacology, chemotherapy, Piperazines, chemistry.chemical_compound, Neoplasms, Antineoplastic Combined Chemotherapy Protocols, Drug Discovery, Cytotoxic T cell, Pediatric malignancies, hematological malignancies, p53 pathway, apoptosis, therapeutic combinations, Nutlin-3, MDM2, HDM2, PEDIATRIC TUMORS, malignancies, P-gp, p53-independent, leukemia, endothelial, autophagic, pharmacokinetics, biology, Retinoblastoma, Imidazoles, Drug Synergism, Proto-Oncogene Proteins c-mdm2, Nutlin, Small molecule, Mdm2, Cell type, Antineoplastic Agents, medicine, Humans, business.industry, Genes, p53, medicine.disease, chemistry, Apoptosis, biology.protein, Cancer research, Tumor Suppressor Protein p53, business, pediatric malignancies, hematological malignancies, p53 pathway, apoptosis, senescence, therapeutic combinations
Abstract

Nutlin-3 is a small molecule inhibitor of the MDM2/p53 interaction, which leads to the non-genotoxic p53 stabilization, activation of cell cycle arrest and apoptosis pathways. A series of recent studies have strengthened the concept that selective, non-genotoxic p53 activation by Nutlin-3 might represent an alternative to the current cytotoxic chemotherapy, in particular for pediatric tumors and for hematological malignancies, which retain a high percentage of p53(wild-type) status at diagnosis. Like most other drugs employed in cancer therapy, it will be unlikely that Nutlin-3 will be used as a monotherapy. In this respect, Nutlin-3 shows a synergistic cytotoxic effect when used in combination with innovative drugs, such as TRAIL or bortozemib. Although Nutlin-3 is currently in phase I clinical trial for the treatment of retinoblastoma, its effects on normal tissues and cell types remain largely to be determined and will require further investigation in the future years.

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