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Pancreatic Neoplasms: HELP
Articles by Gianpietro Semenzato
Based on 3 articles published since 2009
(Why 3 articles?)

Between 2009 and 2019, Gianpietro Semenzato wrote the following 3 articles about Pancreatic Neoplasms.
+ Citations + Abstracts
1 Article Direct Pharmacological Targeting of a Mitochondrial Ion Channel Selectively Kills Tumor Cells In Vivo. 2017

Leanza, Luigi / Romio, Matteo / Becker, Katrin Anne / Azzolini, Michele / Trentin, Livio / Managò, Antonella / Venturini, Elisa / Zaccagnino, Angela / Mattarei, Andrea / Carraretto, Luca / Urbani, Andrea / Kadow, Stephanie / Biasutto, Lucia / Martini, Veronica / Severin, Filippo / Peruzzo, Roberta / Trimarco, Valentina / Egberts, Jan-Hendrik / Hauser, Charlotte / Visentin, Andrea / Semenzato, Gianpietro / Kalthoff, Holger / Zoratti, Mario / Gulbins, Erich / Paradisi, Cristina / Szabo, Ildiko. ·Department of Biology, University of Padova, viale G. Colombo 3, 35121 Padova, Italy. · Department of Chemical Sciences, University of Padova, via F. Marzolo 1, 35121 Padova, Italy. · Department of Molecular Biology, University of Duisburg-Essen, Hufelandstrasse 55, 45122 Essen, Germany. · Department of Biomedical Sciences, University of Padova, viale G. Colombo 3, 35121 Padova, Italy; CNR Institute of Neuroscience, viale G. Colombo 3, 35121 Padova, Italy. · Department of Medicine, Hematology and Immunological Branch, University of Padova, and Venetian Institute for Molecular Medicine (VIMM), via G. Orus 2, 35129 Padova, Italy. · Institute for Experimental Cancer Research, Medical Faculty, CAU, Kiel, and Department of Surgery, UKSH, Campus Kiel, Arnold-Heller-Strasse 3 (Haus 17), 24105 Kiel, Germany. · Department of Molecular Biology, University of Duisburg-Essen, Hufelandstrasse 55, 45122 Essen, Germany; Department of Surgery, University of Cincinnati, 231 Albert Sabin Way, Cincinnati, OH 45267-0558, USA. Electronic address: erich.gulbins@uni-due.de. · Department of Chemical Sciences, University of Padova, via F. Marzolo 1, 35121 Padova, Italy. Electronic address: cristina.paradisi@unipd.it. · Department of Biology, University of Padova, viale G. Colombo 3, 35121 Padova, Italy; CNR Institute of Neuroscience, viale G. Colombo 3, 35121 Padova, Italy. Electronic address: ildi@civ.bio.unipd.it. ·Cancer Cell · Pubmed #28399409.

ABSTRACT: The potassium channel Kv1.3 is highly expressed in the mitochondria of various cancerous cells. Here we show that direct inhibition of Kv1.3 using two mitochondria-targeted inhibitors alters mitochondrial function and leads to reactive oxygen species (ROS)-mediated death of even chemoresistant cells independently of p53 status. These inhibitors killed 98% of ex vivo primary chronic B-lymphocytic leukemia tumor cells while sparing healthy B cells. In orthotopic mouse models of melanoma and pancreatic ductal adenocarcinoma, the compounds reduced tumor size by more than 90% and 60%, respectively, while sparing immune and cardiac functions. Our work provides direct evidence that specific pharmacological targeting of a mitochondrial potassium channel can lead to ROS-mediated selective apoptosis of cancer cells in vivo, without causing significant side effects.

2 Article Pancreatic tumors and immature immunosuppressive myeloid cells in blood and spleen: role of inhibitory co-stimulatory molecules PDL1 and CTLA4. An in vivo and in vitro study. 2013

Basso, Daniela / Fogar, Paola / Falconi, Massimo / Fadi, Elisa / Sperti, Cosimo / Frasson, Chiara / Greco, Eliana / Tamburrino, Domenico / Teolato, Sara / Moz, Stefania / Bozzato, Dania / Pelloso, Michela / Padoan, Andrea / De Franchis, Giuseppe / Gnatta, Elisa / Facco, Monica / Zambon, Carlo-Federico / Navaglia, Filippo / Pasquali, Claudio / Basso, Giuseppe / Semenzato, Gianpietro / Pedrazzoli, Sergio / Pederzoli, Paolo / Plebani, Mario. ·Department of Medicine, University of Padova, Padova, Italy. daniela.basso@sanita.padova.it ·PLoS One · Pubmed #23359812.

ABSTRACT: BACKGROUND: Blood and spleen expansion of immature myeloid cells (IMCs) might compromise the immune response to cancer. We studied in vivo circulating and splenic T lymphocyte and IMC subsets in patients with benign and malignant pancreatic diseases. We ascertained in vitro whether pancreatic adenocarcinoma (PDAC)-associated IMC subsets are induced by tumor-derived soluble factors and whether they are immunosuppressive focusing on the inhibitory co-stimulatory molecules PDL1 and CTLA4. METHODOLOGY AND PRINCIPAL FINDINGS: 103 pancreatic and/or splenic surgical patients were enrolled including 52 PDAC, 10 borderline and 10 neuroendocrine tumors (NETs). Lymphocytes and IMCs were analysed by flow cytometry in blood, in spleen and in three PDAC cell conditioned (CM) or non conditioned PBMC. PDL1 and CTLA4 were studied in 30 splenic samples, in control and conditioned PBMC. IMCs were FACS sorted and co-coltured with allogenic T lymphocytes. In PDAC a reduction was found in circulating CD8(+) lymphocytes (p = 0.004) and dendritic cells (p = 0.01), which were reduced in vitro by one PDAC CM (Capan1; p = 0.03). Blood myeloid derived suppressive cells (MDSCs) CD33(+)CD14(-)HLA-DR(-) were increased in PDAC (p = 0.022) and were induced in vitro by BxPC3 CM. Splenic dendritic cells had a higher PDL1 expression (p = 0.007), while CD33(+)CD14(+)HLA-DR(-) IMCs had a lower CTLA4 expression (p = 0.029) in PDAC patients. In vitro S100A8/A9 complex, one of the possible inflammatory mediators of immune suppression in PDAC, induced PDL1 (p = 0.018) and reduced CTLA4 expression (p = 0.028) among IMCs. IMCs not expressing CTLA4 were demonstrated to be immune suppressive. CONCLUSION: In PDAC circulating dendritic and cytotoxic T cells are reduced, while MDSCs are increased and this might favour tumoral growth and progression. The reduced CTLA4 expression found among splenic IMCs of PDAC patients was demonstrated to characterize an immune suppressive phenotype and to be consequent to the direct exposure of myeloid cells to pancreatic cancer derived products, S100A8/A9 complex in particular.

3 Article Pancreatic cancer alters human CD4+ T lymphocyte function: a piece in the immune evasion puzzle. 2011

Fogar, Paola / Basso, Daniela / Fadi, Elisa / Greco, Eliana / Pantano, Giorgia / Padoan, Andrea / Bozzato, Dania / Facco, Monica / Sanzari, Maria Colomba / Teolato, Sara / Zambon, Carlo-Federico / Navaglia, Filippo / Semenzato, Gianpietro / Pedrazzoli, Sergio / Plebani, Mario. ·Department of Laboratory Medicine, University of Padova, Padova, Italy. ·Pancreas · Pubmed #21792088.

ABSTRACT: OBJECTIVES: To verify whether the dysregulation of CD4 T cells concurs in worsening the outcome of pancreatic cancer, we compared the effects of pancreatic cancer and other gastrointestinal cancer cell-conditioned media on the (1) proliferation, migration, and differentiation of CD4 T cells and (2) expansion of CD4 memory (CD45RO), naive (CD45RA), activated (CD69), and regulatory (CD25) subsets. METHODS: After culture of CD4 T cells in control, pancreatic (BxPC3, Capan1, MiaPaCa2), or gastrointestinal cancer (AGS, HepG2, HT29) cell-conditioned media, we evaluated proliferation, migration, interferon γ (IFNγ) production, and CD45RA, CD45RO, CD69, and CD25 membrane expression in control and conditioned CD4 T cells. RESULTS: Only pancreatic cancer-conditioned media (1) inhibited CD4 T-cell proliferation (P < 0.001) and migration under human stromal cell-derived factor-α chemotaxis (P < 0.001) and (2) induced CD4 T-cell IFNγ production (P < 0.05) and the expansion of the CD69-positive subset (P < 0.001) with respect to the control, with no changes being found in the CD45RA, CD45RO, and CD25 subsets. CONCLUSIONS: The in vitro findings achieved in the present study demonstrate that pancreatic cancer cells inhibit CD4 T-cell proliferation and migration, induce IFNγ production, and favor a CD69 subset expansion, suggesting that CD4 T cells play an important role in pancreatic cancer immune evasion.