8 results on '"Ciminale, Vincenzo"'
Search Results
2. Mitochondria as Functional Targets of Proteins Coded by Human Tumor Viruses
- Author
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D'Agostino, Donna M., primary, Bernardi, Paolo, additional, Chieco‐Bianchi, Luigi, additional, and Ciminale, Vincenzo, additional
- Published
- 2005
- Full Text
- View/download PDF
3. Reducing the global burden of HTLV-1 infection: An agenda for research and action
- Author
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Willems, Luc, Hasegawa, Hideki, Accolla, Roberto, Bangham, Charles, Bazarbachi, Ali, Bertazzoni, Umberto, Carneiro-Proietti, Anna Barbara de Freitas, Cheng, Hua, Chieco-Bianchi, Luigi, Ciminale, Vincenzo, Coelho-dos-Reis, Jordana, Esparza, José, Gallo, Robert C., Gessain, Antoine, Gotuzzo Herencia, José Eduardo, Hall, William, Harford, Joseph, Hermine, Olivier, Jacobson, Steven, Macchi, Beatrice, Macpherson, Calum, Mahieux, Renaud, Matsuoka, Masao, Murphy, Edward, Peloponese, Jean-Marie, Simon, Viviana, Tagaya, Yutaka, Taylor, Graham P., Watanabe, Toshiki, and Yamano, Yoshihisa
- Subjects
HTLV-1 infection ,Biomedical Research ,viruses ,Advisory Committees ,cost of illness ,global health ,HIV Infections ,Review ,medical research ,Spinal Cord Diseases ,Human immunodeficiency virus infection ,advisory committee ,Human immunodeficiency virus vaccine ,spinal cord disease ,Humans ,Leukemia-Lymphoma, Adult T-Cell ,purl.org/pe-repo/ocde/ford#1.06.02 [https] ,purl.org/pe-repo/ocde/ford#3.01.05 [https] ,human ,human T cell leukemia virus ,disease transmission ,tropical spastic paraparesis ,Human T-lymphotropic virus 1 ,isolation and purification ,disease course ,pathogenesis ,T cell leukemia ,transmission ,virus diseases ,prediction ,HTLV-I Infections ,Paraparesis, Tropical Spastic ,virology ,research priority ,priority journal - Abstract
Even though an estimated 10–20 million people worldwide are infected with the oncogenic retrovirus, human T-lymphotropic virus type 1 (HTLV-1), its epidemiology is poorly understood, and little effort has been made to reduce its prevalence. In response to this situation, the Global Virus Network launched a taskforce in 2014 to develop new methods of prevention and treatment of HTLV-1 infection and promote basic research. HTLV-1 is the etiological agent of two life-threatening diseases, adult T-cell leukemia and HTLV-associated myelopathy/tropical spastic paraparesis, for which no effective therapy is currently available. Although the modes of transmission of HTLV-1 resemble those of the more familiar HIV-1, routine diagnostic methods are generally unavailable to support the prevention of new infections. In the present article, the Taskforce proposes a series of actions to expand epidemiological studies; increase research on mechanisms of HTLV-1 persistence, replication and pathogenesis; discover effective treatments; and develop prophylactic and therapeutic vaccines.
- Published
- 2017
4. Reducing the global burden of HTLV-1 infection: An agenda for research and action.
- Author
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Willems L, Hasegawa H, Accolla R, Bangham C, Bazarbachi A, Bertazzoni U, Carneiro-Proietti AB, Cheng H, Chieco-Bianchi L, Ciminale V, Coelho-Dos-Reis J, Esparza J, Gallo RC, Gessain A, Gotuzzo E, Hall W, Harford J, Hermine O, Jacobson S, Macchi B, Macpherson C, Mahieux R, Matsuoka M, Murphy E, Peloponese JM, Simon V, Tagaya Y, Taylor GP, Watanabe T, and Yamano Y
- Subjects
- Advisory Committees, Cost of Illness, HIV Infections epidemiology, HIV Infections prevention & control, HIV Infections virology, Human T-lymphotropic virus 1 isolation & purification, Humans, Leukemia-Lymphoma, Adult T-Cell virology, Paraparesis, Tropical Spastic drug therapy, Paraparesis, Tropical Spastic prevention & control, Paraparesis, Tropical Spastic virology, Spinal Cord Diseases drug therapy, Spinal Cord Diseases prevention & control, Spinal Cord Diseases virology, Biomedical Research, Global Health, HTLV-I Infections drug therapy, HTLV-I Infections epidemiology, HTLV-I Infections prevention & control, HTLV-I Infections transmission
- Abstract
Even though an estimated 10-20 million people worldwide are infected with the oncogenic retrovirus, human T-lymphotropic virus type 1 (HTLV-1), its epidemiology is poorly understood, and little effort has been made to reduce its prevalence. In response to this situation, the Global Virus Network launched a taskforce in 2014 to develop new methods of prevention and treatment of HTLV-1 infection and promote basic research. HTLV-1 is the etiological agent of two life-threatening diseases, adult T-cell leukemia and HTLV-associated myelopathy/tropical spastic paraparesis, for which no effective therapy is currently available. Although the modes of transmission of HTLV-1 resemble those of the more familiar HIV-1, routine diagnostic methods are generally unavailable to support the prevention of new infections. In the present article, the Taskforce proposes a series of actions to expand epidemiological studies; increase research on mechanisms of HTLV-1 persistence, replication and pathogenesis; discover effective treatments; and develop prophylactic and therapeutic vaccines., (Copyright © 2016 Elsevier B.V. All rights reserved.)
- Published
- 2017
- Full Text
- View/download PDF
5. Synergistic antitumor activity of recombinant human Apo2L/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in combination with carboplatin and pemetrexed in malignant pleural mesothelioma.
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Pasello G, Urso L, Silic-Benussi M, Schiavon M, Cavallari I, Marulli G, Nannini N, Rea F, Ciminale V, and Favaretto A
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- Animals, Apoptosis drug effects, Carboplatin administration & dosage, Cell Line, Tumor, Drug Synergism, Glutamates administration & dosage, Guanine administration & dosage, Guanine analogs & derivatives, Humans, Male, Mice, Mice, SCID, Pemetrexed, Receptors, TNF-Related Apoptosis-Inducing Ligand drug effects, Receptors, TNF-Related Apoptosis-Inducing Ligand metabolism, Recombinant Proteins, TNF-Related Apoptosis-Inducing Ligand administration & dosage, Tumor Suppressor Protein p53 drug effects, Antineoplastic Combined Chemotherapy Protocols pharmacology, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Mesothelioma drug therapy, Pleural Neoplasms drug therapy, Tumor Suppressor Protein p53 metabolism
- Abstract
Introduction: Malignant pleural mesothelioma (MPM) is an aggressive, currently incurable tumor with increasing incidence in industrialized countries. Tumor necrosis factor-related, apoptosis-inducing ligand (TRAIL) is a member of the TNF family, which induces cancer cell death through extrinsic apoptotic pathway, while sparing normal cells. The aim of this study was to investigate the antitumor activity of recombinant human Apo2L/TRAIL (dulanermin) in combination with chemotherapy in MPM in vitro and in vivo., Methods: In the present studies, we employed a panel of MPM cell lines to test the antitumor activity of recombinant human Apo2L/TRAIL (T) in combination with carboplatin and pemetrexed (CP) in vitro and SCID mice., Results: Results demonstrated a significant increase of apoptosis in cell lines treated with CPT compared with those receiving CP or T as single agents. This synergistic effect was dependent on the ability of CP to increase the expression of the TRAIL receptors DR4 and DR5 in a p53 manner. The CPT combination was also effective in blocking the growth of MPM cell lines in a SCID mice preclinical model., Conclusions: CPT increases MPM cell death in vitro and in vivo compared with CP. In vitro results suggest that chemotherapy sensitizes MPM to TRAIL-dependent apoptosis through p53 activation and subsequent upregulation of DRs.
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- 2014
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6. Kinetics and intracellular compartmentalization of HTLV-1 gene expression: nuclear retention of HBZ mRNAs.
- Author
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Rende F, Cavallari I, Corradin A, Silic-Benussi M, Toulza F, Toffolo GM, Tanaka Y, Jacobson S, Taylor GP, D'Agostino DM, Bangham CR, and Ciminale V
- Subjects
- Cell Compartmentation, Cell Nucleus genetics, Cell Nucleus virology, Gene Expression, Gene Products, rex genetics, Gene Products, rex metabolism, Gene Products, tax genetics, Gene Products, tax metabolism, Genes, Viral, Humans, Kinetics, RNA, Messenger genetics, RNA, Messenger metabolism, RNA, Viral genetics, RNA, Viral metabolism, Retroviridae Proteins, Basic-Leucine Zipper Transcription Factors genetics, HTLV-I Infections genetics, HTLV-I Infections virology, Human T-lymphotropic virus 1 genetics, Viral Proteins genetics
- Abstract
Human T-cell leukemia virus type 1 (HTLV-1) codes for 9 alternatively spliced transcripts and 2 major regulatory proteins named Tax and Rex that function at the transcriptional and posttranscriptional levels, respectively. We investigated the temporal sequence of HTLV-1 gene expression in primary cells from infected patients using splice site-specific quantitative RT-PCR. The results indicated a two-phase kinetics with the tax/rex mRNA preceding expression of other viral transcripts. Analysis of mRNA compartmentalization in cells transfected with HTLV-1 molecular clones demonstrated the strict Rex-dependency of the two-phase kinetics and revealed strong nuclear retention of HBZ mRNAs, supporting their function as noncoding transcripts. Mathematical modeling underscored the importance of a delay between the functions of Tax and Rex, which was supported by experimental evidence of the longer half-life of Rex. These data provide evidence for a temporal pattern of HTLV-1 expression and reveal major differences in the intracellular compartmentalization of HTLV-1 transcripts.
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- 2011
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7. Redox regulation of T-cell turnover by the p13 protein of human T-cell leukemia virus type 1: distinct effects in primary versus transformed cells.
- Author
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Silic-Benussi M, Cavallari I, Vajente N, Vidali S, Chieco-Bianchi L, Di Lisa F, Saggioro D, D'Agostino DM, and Ciminale V
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- Cell Line, Cells, Cultured, Gene Expression Regulation, Viral, Genetic Vectors genetics, Green Fluorescent Proteins genetics, Green Fluorescent Proteins metabolism, HeLa Cells, Host-Pathogen Interactions, Human T-lymphotropic virus 1 physiology, Humans, Jurkat Cells, Lentivirus genetics, Microscopy, Confocal, Mitochondria metabolism, Oxidation-Reduction, RNA Interference, Retroviridae Proteins genetics, Reverse Transcriptase Polymerase Chain Reaction, T-Lymphocytes cytology, T-Lymphocytes virology, Transduction, Genetic, Human T-lymphotropic virus 1 metabolism, Reactive Oxygen Species metabolism, Retroviridae Proteins metabolism, T-Lymphocytes metabolism
- Abstract
The present study investigated the function of p13, a mitochondrial protein of human T-cell leukemia virus type 1 (HTLV-1). Although necessary for viral propagation in vivo, the mechanism of function of p13 is incompletely understood. Drawing from studies in isolated mitochondria, we analyzed the effects of p13 on mitochondrial reactive oxygen species (ROS) in transformed and primary T cells. In transformed cells (Jurkat, HeLa), p13 did not affect ROS unless the cells were subjected to glucose deprivation, which led to a p13-dependent increase in ROS and cell death. Using RNA interference we confirmed that expression of p13 also influences glucose starvation-induced cell death in the context of HTLV-1-infected cells. ROS measurements showed an increasing gradient from resting to mitogen-activated primary T cells to transformed T cells (Jurkat). Expression of p13 in primary T cells resulted in their activation, an effect that was abrogated by ROS scavengers. These findings suggest that p13 may have a distinct impact on cell turnover depending on the inherent ROS levels; in the context of the HTLV-1 propagation strategy, p13 could increase the pool of "normal" infected cells while culling cells acquiring a transformed phenotype, thus favoring lifelong persistence of the virus in the host.
- Published
- 2010
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8. Hypoxia inducible factor-1alpha inactivation unveils a link between tumor cell metabolism and hypoxia-induced cell death.
- Author
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Favaro E, Nardo G, Persano L, Masiero M, Moserle L, Zamarchi R, Rossi E, Esposito G, Plebani M, Sattler U, Mann T, Mueller-Klieser W, Ciminale V, Amadori A, and Indraccolo S
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- Animals, Cell Death, Cell Hypoxia, Cell Line, Tumor, Cell Proliferation, Female, Gene Silencing, Humans, Lentivirus, Mice, Mice, SCID, Phenotype, RNA, Small Interfering metabolism, Hypoxia-Inducible Factor 1, alpha Subunit metabolism, Ovarian Neoplasms metabolism, Ovarian Neoplasms pathology
- Abstract
Hypoxia and the acquisition of a glycolytic phenotype are intrinsic features of the tumor microenvironment. The hypoxia inducible factor-1alpha (HIF-1alpha) pathway is activated under hypoxic conditions and orchestrates a complex transcriptional program that enhances cell survival. Although the consequences of HIF-1alpha inactivation in cancer cells have been widely investigated, only a few studies have addressed the role of HIF-1alpha in the survival of cancer cells endowed with different glycolytic capacities. In this study, we investigated this aspect in ovarian cancer cells. Hypoxia-induced toxicity was increased in highly glycolytic cells compared with poorly glycolytic cells; it was also associated with a sharp decrease in intracellular ATP levels and was prevented by glucose supplementation. Stable HIF-1alpha silencing enhanced hypoxia-induced cell death in vitro due to a lack of cell cycle arrest. Tumors bearing attenuated HIF-1alpha levels had similar growth rates and vascularization as did controls, but tumors showed higher proliferation levels and increased necrosis. Moreover, tumors formed by HIF-1alpha deficient cells had higher levels of lactate and lower ATP concentrations than controls as shown by metabolic imaging. The findings that such metabolic properties can affect the survival of cancer cells under hypoxic conditions and that these properties contribute to the determination of the consequences of HIF-1alpha inactivation could have important implications on the understanding of the effects of anti-angiogenic and HIF-1alpha-targeting drugs in cancer.
- Published
- 2008
- Full Text
- View/download PDF
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