Domenico Ribatti

University of Catania, Catania, Sicily, Italy

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Publications (640)2349.97 Total impact

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    ABSTRACT: Bcl-6 translocation is a genetic alteration that is commonly detected in Primary Central Nervous System Lymphoma. The role of this protein in cerebral tumors is unclear. In this study we investigated Bcl-6 translocation and its transcriptional and translational levels in formalin-fixed, paraffin-embedded cerebral tissue sections from Glioblastoma (GBM), low-grade glioma (Astrocytoma grade II and III), and meningioma patients, and correlated them with apoptotic processes and p53 and caspase-3 expression. The results showed a frequency of 36.6% of Bcl-6 translocation in GBM patients and a decreased expression in low-grade glioma patients, correlated with the severity of the disease. Bcl-6 translocation induced an overexpression of both Bcl-6 protein and messenger in GBM, inhibiting apoptotic processes and caspases 3 expression. On the contrary, in low-grade gliomas and meningiomas Bcl-6 expression was reduced, resulting in an increase of apoptotic processes. Finally, p53 expression levels in brain tumors were comparable to Bcl-6 levels. Overall, these data demonstrate, for the first time, that the Bcl-6 gene translocates in GBM patients and that its translocation and expression are correlated with apoptosis inhibition, indicating a key role for this gene in the control of cellular proliferation. This study offers further insights into Glioblastoma biology, and supports Bcl-6 as a new diagnostic marker to evaluate the disease severity.
    Cancer Letters. 10/2014; 353(1):41.
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    ABSTRACT: Tumour pathogenesis in multiple myeloma (MM) correlates with a high vascular index. Therefore, targeting angiogenesis is an important therapeutic tool to reduce MM progression. This study aimed to investigate the role of invariant natural killer T (iNKT) cells in angiogenesis and the mechanisms behind the stimulation by α-Galactosylceramide (α-GalCer). We have previously found that α-GalCer could increase the survival of 5T33MM mice and here we demonstrate that α-GalCer reduces the microvessel density. We performed both in vivo and in vitro angiogenic assays to confirm this observation. We found that conditioned medium of α-GalCer stimulated iNKT cells reduced neovascularization in the chick chorioallantoic membrane and in matrigel plug assays. Moreover, we observed a reduction in proliferation, migration and network formation and an induction of apoptosis upon exposure of murine endothelial cell lines to this conditioned medium. We furthermore observed that the JAK-STAT signaling pathway was highly activated in endothelial cells in response to stimulated iNKT cells, indicating the possible role of IFN-γ in the anti-angiogenic process. In conclusion, these results highlight the possibility of recruiting iNKT cells to target MM and angiogenesis. This gives a rationale for combining immunotherapy with conventional anti-tumour treatments in view of increasing their therapeutic potential.
    British Journal of Haematology 08/2014; · 4.94 Impact Factor
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    ABSTRACT: Tryptase is a serine protease released from mast cells that plays a role in tumor angiogenesis. In this study we aimed to evaluate serum tryptase levels in 105 female early breast cancer patients before (STLBS) and after(STLAS) radical surgical resection, mast cell density positive to tryptase (MCDPT) and microvascular density (MVD).
    BMC Cancer 07/2014; 14(1):534. · 3.33 Impact Factor
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    ABSTRACT: Angiogenesis, the formation of new vessels, is found in Multiple Sclerosis (MS) demyelinating lesions following Vascular Endothelial Growth Factor (VEGF) release and the production of several other angiogenic molecules. The increased energy demand of inflammatory cuffs and damaged neural cells explains the strong angiogenic response in plaques and surrounding white matter. An angiogenic response has also been documented in an experimental model of MS, experimental allergic encephalomyelitis (EAE), where blood¿brain barrier disruption and vascular remodelling appeared in a pre-symptomatic disease phase. In both MS and EAE, VEGF acts as a pro-inflammatory factor in the early phase but its reduced responsivity in the late phase can disrupt neuroregenerative attempts, since VEGF naturally enhances neuron resistance to injury and regulates neural progenitor proliferation, migration, differentiation and oligodendrocyte precursor cell (OPC) survival and migration to demyelinated lesions. Angiogenesis, neurogenesis and oligodendroglia maturation are closely intertwined in the neurovascular niches of the subventricular zone, one of the preferential locations of inflammatory lesions in MS, and in all the other temporary vascular niches where the mutual fostering of angiogenesis and OPC maturation occurs. Angiogenesis, induced either by CNS inflammation or by hypoxic stimuli related to neurovascular uncoupling, appears to be ineffective in chronic MS due to a counterbalancing effect of vasoconstrictive mechanisms determined by the reduced axonal activity, astrocyte dysfunction, microglia secretion of free radical species and mitochondrial abnormalities. Thus, angiogenesis, that supplies several trophic factors, should be promoted in therapeutic neuroregeneration efforts to combat the progressive, degenerative phase of MS.
    Acta neuropathologica communications. 07/2014; 2(1):84.
  • Domenico Ribatti
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    ABSTRACT: Among the in vivo models, the chick embryo chorioallantoic membrane (CAM) has been used to implant several tumor types as well as malignant cell lines to study their growth rate, angiogenic potential and metastatic capability. This review article is focused on the major compelling literature data on the use of the CAM to investigate tumor growth and the metastatic process.
    Experimental cell research. 06/2014;
  • Domenico Ribatti, Michele Moschetta, Angelo Vacca
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    ABSTRACT: In patients with multiple myeloma (MM), the bone marrow (BM) contains hematopoietic stem cells (HSCs) and non-hematopoietic cells. HSCs are able to give rise to all types of mature blood cells, while the non hematopoietic component includes mesenchymal stem cells (MSCs), fibroblasts, osteoblasts, osteoclasts, chondroclasts, endothelial cells, endothelial progenitor cells (EPCs), B and T lymphocytes, NK cells, erythrocytes, megakaryocytes, platelets, macrophages and mast cells. All of these cells form specialized "niches" in the BM microenvironment which are close to the vasculature ("vascular niche") or to the endosteum ("osteoblast niche"). The "vascular niche" is rich in blood vessels where endothelial cells and mural cells (pericytes and smooth muscle cells) create a microenvironment that affects the behavior of several stem and progenitor cells. The vessel wall serves as an independent niche for the recruitment of endothelial progenitor cells, MSCs and HSCs. The activation by angiogenic factors and inflammatory cytokines switch the "vascular niche" to promote MM tumor growth and spread. This review will focus on the mechanisms involved in the generation of signals released by endothelial cells in the "vascular niche" that promote tumor growth and spread in MM. © 2014 Elsevier Ltd. All rights reserved.
    Thrombosis Research 05/2014; 133 Suppl 2:S102-6. · 3.13 Impact Factor
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    ABSTRACT: Calbindin-D28k (CB) is a calcium-binding protein largely distributed in the cerebellum of various species of vertebrates. As regards the human cerebellar cortex, precise data on the distribution of CB have not yet been reported. Aim of the present work was to analyze the distribution of CB in postmortem samples of human cerebellar cortex using light microscopy immunohistochemical techniques. Immunoreactivity to CB was detected within neuronal bodies and processes distributed in all cortex layers. In the molecular layer, the immunoreactivity was observed in subpopulations of stellate and basket neurons. In the Purkinje neuron layer, the immunoreactivity was observed in practically all the Purkinje neurons. In the granular layer, the immunoreactivity was observed in subpopulations of granules, of Golgi neurons, and also of other types of large neurons (candelabrum, Lugaro neurons, etc.). Immunoreactivity to CB was also observed in axon terminals distributed throughout the cortex according to layer-specific patterns of distribution. The qualitative and quantitative patterns of distribution of CB showed no difference among the different lobes of the cerebellar cortex. This study reports that CB is expressed by different neuron types, both inhibitory (GABAergic) and excitatory (glutamatergic), involved in both intrinsic and extrinsic circuits of the human cerebellar cortex. The study provides further insights on the functional role of CB and on the neuronal types of the cerebellar cortex in which it is expressed. Anat Rec, 2014. © 2014 Wiley Periodicals, Inc.
    The Anatomical Record Advances in Integrative Anatomy and Evolutionary Biology 04/2014; · 1.34 Impact Factor
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    ABSTRACT: Angiogenesis is a common finding in chronic inflammatory diseases; however, its role in Sjögren's syndrome (SS) remains to be elucidated. Previous SS studies have demonstrated an increase in VEGF-A/VEGFR-2 system expression in minor salivary gland (MSG) biopsies from patients with SS, but differences in the new blood vessel formation between the different grades of disease severity have not been reported. Therefore, experiments were performed to demonstrate angiogenesis during different phases of primary SS (pSS) and to define the relationship between the microvessel density (MVD), macrophage infiltration and histiocyte distribution in SS MSG inflammatory lesions. In this series of experiments, immunohistochemistry was used to examine angiogenesis in serial sections of pSS MSG. Patients with pSS were classified accordingly with the grade of inflammatory lesions as I = low-grade (low focus score of 1 or 2), II = intermediate-grade (focus score of 3–6) and III = extensive inflammation in the MSG (high focus score of 12). Histological examination demonstrated that the MVD increased with the severity of the inflammatory lesions, and in addition, we found an increased infiltration of inflammatory and pro-angiogenic cells.These findings reveal that angiogenesis is intimately involved in the progression of pSS, may be central to the propagation of the chronic immune response observed in pSS and could represent a novel potential biomarker of pSS disease activity.
    International Journal of Experimental Pathology 04/2014; 95(2):131-7. · 2.04 Impact Factor
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    Domenico Ribatti
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    ABSTRACT: Angiogenesis is regulated, under both physiological and pathological conditions, by numerous "non-classic" pro-angiogenic factors, including fibroblast growth factor-2 (FGF-2), vascular endothelial growth factor (VEGF), and placental growth factor (PlGF), and "non-classic" pro-angiogenic factors, including granulocyte colony stimulating factor (G-CSF), granulocyte macrophage colony stimulating factor (GM-CSF), and erythropoietin (EPO). In the context of the most important discoveries in this field, this review article summarizes the important role played by the Italian scientists in the course of the last twenty years.
    Vascular cell. 04/2014; 6(1):8.
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    ABSTRACT: Primary Sjögren's syndrome (pSS) is a chronic autoimmune exocrine disease associated with variable lymphocytic infiltration of the affected organs (primarily salivary and lachrymal glands). To investigate the potential implication of nerve growth factor-β (NGF-β) and its high affinity receptor tyrosine kinase receptor A (TrkA) in the regulation of pSS inflammatory responses, we studied their expression in the human salivary gland epithelial cells (SGEC) cultures from pSS minor salivary glands (MSG) biopsies and their relationship with histopathological disease parameters. Here, we demonstrated an increased expression of the NGF-β/TrkA system in pSS SGEC, correlated with the MSG inflammation grade. The results demonstrate that the pro-inflammatory cytokines TNF-α and IL-6 enhance NGF-β production; on the contrary, NGF-β production was reduced in the presence of both Raf-1 kinase and MEK inhibitors. Furthermore, TNF-α/IL-6 treatment increased ERK1/2 phosphorylation. Inhibition of the EGF/EGFR system also decreased NGF-β release by pSS SGEC, indicating that the chronic inflammatory condition characteristic of pSS enhances NGF-β production via EGFR/Raf-1/MEK/ERK pathway activation. NGF-β and TrkA expression is elevated in salivary gland epithelial cells of primary Sjögren's syndrome (pSS). Overexpression of NGF-β/TrkA system in pSS occurs via EGFR/Raf-1/MEK/ERK pathway. In pSS, NGF-β overexpression was prevented by EGFR/Raf-1/MEK/ERK pathway inhibition.
    Journal of Molecular Medicine 02/2014; · 4.77 Impact Factor
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    ABSTRACT: The lysosomal hydrolase galactocerebrosidase (GALC) catalyzes the removal of galactose from galactosylceramide and from other sphingolipids. GALC deficiency is responsible for globoid cell leukodystrophy (GLD), or Krabbe's disease, an early lethal inherited neurodegenerative disorder characterized by the accumulation of the neurotoxic metabolite psychosine in the central nervous system (CNS). The poor outcome of current clinical treatments calls for novel model systems to investigate the biological impact of GALC down-regulation and for the search of novel therapeutic strategies in GLD. Zebrafish (Danio rerio) represents an attractive vertebrate model for human diseases. Here, lysosomal GALC activity was demonstrated in the brain of zebrafish adults and embryos. Accordingly, we identified two GALC co-orthologs (named galca and galcb) dynamically co-expressed in CNS during zebrafish development. Both genes encode for lysosomal enzymes endowed with GALC activity. Single down-regulation of galca or galcb by specific antisense morpholino oligonucleotides results in a partial decrease of GALC activity in zebrafish embryos that was abrogated in double galca/galcb morphants. However, no psychosine accumulation was observed in galca/galcb double morphants. Nevertheless, double galca/galcb knockdown caused reduction and partial disorganization of the expression of the early neuronal marker neuroD and an increase of apoptotic events during CNS development. These observations provide new insights into the pathogenesis of GLD, indicating that GALC loss-of-function may have pathological consequences in developing CNS independent of psychosine accumulation. Also, they underscore the potentiality of the zebrafish system in studying the pathogenesis of lysosomal neurodegenerative diseases, including GLD.
    Biochimica et Biophysica Acta 01/2014; · 4.66 Impact Factor
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    ABSTRACT: TRAIL, a cytokine of the Tumor Necrosis Factor (TNF) superfamily, is a potent cell-apoptosis inducer, although its effects vary as a function of concentration. In fact, low concentrations of TRAIL are associated with non-apoptotic effects, such as cell proliferation. Here, the effects of TRAIL at different concentrations have been evaluated on mitogenesis and migration on human umbilical vein endothelial cells (HUVEC) in vitro, as well as in the chick embryo chorioallantoic membrane (CAM) angiogenesis model in vivo. TRAIL at low concentrations promoted either mitogenesis or migration of HUVEC cells, evaluated with the wound healing method. Cleavage of caspase-8 was evaluated along with the expression of the caspase-8-like molecule c-FLIPL . Low concentrations of TRAIL failed to induce caspase-8 processing whereas high concentrations induced apoptosis of HUVEC and activation of caspase-8. Moreover, TRAIL induced a significant angiogenic response in the CAM assay in vivo, comparable to that of vascular endothelial growth factor. These data suggest that non-apoptotic effects of TRAIL include mitogenesis and increased mobility of endothelial cells, as well as eventually angiogenesis. In addition, results demonstrate that c-FLIPL level is also modulated by different TRAIL concentration suggesting its involvement in the divergent effects of TRAIL. In conclusion, this study envisions a pro-angiogenic role of TRAIL, suggesting that the TRAIL may represent a target for pharmacological manipulation. This article is protected by copyright. All rights reserved.
    FEBS Journal 01/2014; · 4.25 Impact Factor
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    ABSTRACT: Hepatocellular carcinoma (HCC) is the fifth most common cause of cancer in the world. According to Barcelona Clinic Liver Cancer modified criteria, patients with early stage disease are candidate to radiofrequency ablation (RFA), while patients with intermediate stage HCC are usually treated by transarterial chemoembolization (TACE). TACE and RFA induce a transient devascularisation effect followed by strong neo-angiogenic stimulus. In fact, after these procedures, it has been demonstrated an up-regulation of pro-angiogenic and growth factors such as vascular endothelial growth factor-A, which might contribute to accelerated progression in patients with incomplete response. Several studies have demonstrated that MAP-kinase and AKT pathways, in addition to neo-angiogenesis, have an important role in the development of HCC. In advanced HCC, anti-angiogenic therapy and tyrosine kinases inhibitors showed potential clinical benefit. Actually, a number of clinical studies are ongoing testing these agents in combination with TACE or RFA. In this paper, we have reviewed the most recent preclinical and clinical results of such trials.
    World Journal of Gastroenterology 01/2014; 20(2):486-497. · 2.55 Impact Factor
  • Domenico Ribatti, Enrico Crivellato
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    ABSTRACT: Mast cells were first identified by Paul Ehrlich in 1878, when he was still a medical student. Many fundamental aspects of mast cell ontogeny have been elucidated since Ehrlich's first identification. Demonstration of mast cell derivation from bone marrow precursors could be established in 1977 when Kitamura's group first showed reconstitution of mast cells in mast cell-deficient mice by the adaptive transfer of wild type bone marrow and indicated that these cells were of hematopoietic origin. It is now definitively established that development of mast cells in bone marrow occurs along the myeloid pathway. However, several aspects need further clarification. In particular, identification and chemical characterization of growth factors expressing mast cell differentiating properties and the relationship between mast cell and basophils developmental pathways.
    Immunology letters 01/2014; · 2.91 Impact Factor
  • Domenico Ribatti, Angelo Vacca
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    ABSTRACT: Both innate and adaptive immune cells are involved in the mechanisms of endothelial cell proliferation, migration and activation, via production and release of a large spectrum of pro-angiogenic mediators, thus creating the specific microenvironment that favors increased rate of tissue vascularization. In this article, we focus on the immune cell component of the angiogenic process occurring during multiple myeloma progression. We also provide information on some anti-angiogenic properties of immune cells that may be applied for a potential pharmacological use as anti-angiogenic agents in the disease treatment.
    Advances in experimental medicine and biology 01/2014; 816:361-76. · 1.83 Impact Factor
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    ABSTRACT: Angiogenesis is an hallmark of tumor growth and progression in solid and hematological malignancies. Different cellular components of the tumor microenvironment such as macrophages, mast cells, circulating endothelial cells and angiogenic factors, including vascular endothelial growth factor and its receptors are involved in the maintenance of Hodgkin lymphoma. In this review article, we highlight relevant literature focusing on the relationships between angiogenesis and Hodgkin Lymphoma as well as discussing anti-angiogenic treatments in this malignancy.
    Leukemia Research. 01/2014;
  • Angelo Vacca, Roberto Ria, Antonia Reale, Domenico Ribatti
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    ABSTRACT: Angiogenesis is a constant hallmark of multiple myeloma progression and has prognostic potential. Multiple myeloma cells interact with surrounding host cells and extracellular matrix, this crosstalk affecting the most important aspects of the malignant phenotype, both at primary and secondary tumor sites. The pathophysiology of multiple myeloma-induced angiogenesis involves both direct production of angiogenic cytokines by plasma cells and their induction within the bone marrow microenvironment cells. A direct involvement of bone marrow macrophages and mast cells in vasculogenic mimicry has been demonstrated, thus contributing together with circulating endothelial cells and endothelial precursor cells to the multiple myeloma neovascularization. The role of host cells or the niche microenvironment and extracellular matrix represents an intense area of research, finalized at a better understanding of the pathophysiological modifications of the complete tumor entity, i.e. malignant cells and microenvironment.
    Progress in allergy 01/2014; 99:180-96.
  • Domenico Ribatti
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    ABSTRACT: Vertebrate make billions of different antibodies, each with a bonding site that recognizes a specific region of a macromolecule. The hybridoma technique allows monoclonal antibodies, highly specific antibodies produced in the laboratory by a variety of methods. In the last 35 years since the first process for creating monoclonal antibodies was introduced, their application have improved the growing biotechnology industry, but the most important application concerns the therapy of human malignancies.
    Immunology Letters. 01/2014;
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    ABSTRACT: Bone marrow contains hematopoietic stem cells (HSCs) and non hematopoietic cells. HSCs are able to give rise to all types of mature blood cells, while the non hematopoietic component includes osteoblasts/osteoclasts, endothelial cells, endothelial progenitor cells and mesenchymal stem cells. All of these cells form specialized "niches" which are close to the vasculature ("vascular niche") or to the endosteum ("osteoblast niche"). The "vascular niche" is rich in blood vessels where endothelial cells and mural cells (pericytes and smooth muscle cells) create a microenvironment that affects the behavior of several stem and progenitor cells. The vessel wall serves as an independent niche for the recruitment of endothelial progenitor cells, mesenchymal stem cells and HSCs. The activation by angiogenic factors and inflammatory cytokines switch of the "vascular niche" promote tumor growth. This review article will focus on the description of the mechanisms involved in the generation of signals released by endothelial cells in the "vascular niche" that promote tumor growth in multiple myeloma.
    Frontiers in Bioscience 01/2014; 19:304-11. · 3.29 Impact Factor
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    ABSTRACT: A tissue-engineered oesophageal scaffold could be very useful for the treatment of pediatric and adult patients with benign or malignant diseases such as carcinomas, trauma or congenital malformations. Here we decellularize rat oesophagi inside a perfusion bioreactor to create biocompatible biological rat scaffolds that mimic native architecture, resist mechanical stress and induce angiogenesis. Seeded allogeneic mesenchymal stromal cells spontaneously differentiate (proven by gene-, protein and functional evaluations) into epithelial- and muscle-like cells. The reseeded scaffolds are used to orthotopically replace the entire cervical oesophagus in immunocompetent rats. All animals survive the 14-day study period, with patent and functional grafts, and gain significantly more weight than sham-operated animals. Explanted grafts show regeneration of all the major cell and tissue components of the oesophagus including functional epithelium, muscle fibres, nerves and vasculature. We consider the presented tissue-engineered oesophageal scaffolds a significant step towards the clinical application of bioengineered oesophagi.
    Nature Communications 01/2014; 5:3562. · 10.02 Impact Factor

Publication Stats

12k Citations
2,349.97 Total Impact Points

Institutions

  • 2014
    • University of Catania
      Catania, Sicily, Italy
    • Brazilian National Cancer Institute
      Rio de Janeiro, Rio de Janeiro, Brazil
  • 1985–2014
    • Università degli Studi di Bari Aldo Moro
      • Dipartimento di Scienze Biomediche ed Oncologia Umana (DIMO)
      Bari, Apulia, Italy
  • 2013
    • University of Rome Tor Vergata
      • Department of Industrial Engineering
      Roma, Latium, Italy
  • 2009–2013
    • Ospedale Oncologico "Giovanni Paolo II" di Bari
      Bari, Apulia, Italy
    • Centro Cardiologico Monzino
      Milano, Lombardy, Italy
    • Hebrew University of Jerusalem
      • School of Pharmacy
      Jerusalem, Jerusalem District, Israel
  • 2005–2013
    • Università degli studi di Foggia
      • Department of Medical and Surgical Sciences
      Foggia, Apulia, Italy
    • Ospedali Vito Fazzi
      Lecce, Apulia, Italy
  • 2003–2013
    • Policlinico di Bari
      • Department of Surgery
      Bari, Apulia, Italy
  • 2007–2012
    • IRCCS Istituto G. Gaslini
      • Department of Experimental and Laboratory Medicine
      Genova, Liguria, Italy
    • Vascular and Interventional Radiology
      Chicago, Illinois, United States
  • 2001–2012
    • University of Leuven
      • Department of Biomedical Kinesiology
      Louvain, Flanders, Belgium
  • 2008–2011
    • University-Hospital of Padova
      Padua, Veneto, Italy
    • Victor Babes University of Medicine and Pharmacy of Timisoara
      Freidorf, Timiş, Romania
    • Mario Negri Institute for Pharmacological Research
      • Department of Oncology
      Milano, Lombardy, Italy
  • 2007–2011
    • University of Padova
      • • Department of Biomedical Sciences - DSB
      • • Department of Biology
      Padova, Veneto, Italy
  • 2003–2011
    • University of Udine
      • • Department of Experimental and Clinical Medical Sciences
      • • Department of Medical and Biological Sciences
      Udine, Friuli Venezia Giulia, Italy
  • 2010
    • Università degli studi di Parma
      • Department of Clinical and Experimental Medicine
      Parma, Emilia-Romagna, Italy
    • National Research Council
      Roma, Latium, Italy
  • 2009–2010
    • Università degli studi di Cagliari
      • Department of Environmental and Life Science
      Cagliari, Sardinia, Italy
    • Universitatea de Medicina si Farmacie Craiova
      • Faculty of Dentistry
      Croiova, Dolj, Romania
  • 2005–2010
    • CRO Centro di Riferimento Oncologico di Aviano
      • Division of Experimental and Clinical Pharmacology
      Aviano, Friuli Venezia Giulia, Italy
  • 2002–2010
    • Istituto Dermopatico dell'Immacolata
      Roma, Latium, Italy
  • 2002–2009
    • Azienda Ospedaliera Pugliese Ciaccio
      • Department of Oncology and Hematology
      Catanzaro, Calabria, Italy
  • 1996–2009
    • Università degli Studi di Brescia
      • Department of Clinical and Experimental Sciences
      Brescia, Lombardy, Italy
  • 2004–2008
    • The Human Anatomy and Physiology Society
      Italy, Texas, United States
  • 2006
    • Università degli Studi di Siena
      Siena, Tuscany, Italy
    • Istituto Superiore di Sanità
      • Department of Haematology, Oncology and Molecular Medicine
      Roma, Latium, Italy
  • 2002–2004
    • Istituto di Ricerche Chimiche e Biochimiche G. Ronzoni
      Milano, Lombardy, Italy
  • 2000
    • Istituto Ortopedico Rizzoli
      • Laboratory of Experimental Oncology
      Bolonia, Emilia-Romagna, Italy