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Pancreatic Neoplasms: HELP
Articles by Giulia Mantini
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Giulia Mantini wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review New avenues in pancreatic cancer: exploiting microRNAs as predictive biomarkers and new approaches to target aberrant metabolism. 2019

Capula, Mjriam / Mantini, Giulia / Funel, Niccola / Giovannetti, Elisa. ·Cancer Pharmacology Lab, AIRC Start-Up Unit, Fondazione Pisa per la Scienza Pisa, Pisa, Italy. · Department of Medical Oncology, VU University Medical Center, Cancer Center Amsterdam, Amsterdam, Netherlands. ·Expert Rev Clin Pharmacol · Pubmed #31721608.

ABSTRACT:

2 Article Uridine Cytidine Kinase 2 as a Potential Biomarker for Treatment with RX-3117 in Pancreatic Cancer. 2019

El Hassouni, Btissame / Infante, Jessica / Mantini, Giulia / Ricci, Claudio / Funel, Niccola / Giovannetti, Elisa / Peters, Godefridus J. ·Department of Medical Oncology, Amsterdam UMC, VU University Medical Center, Amsterdam, the Netherlands. · Department of Civil and Industrial Engineering, University of Pisa, Pisa, Italy. · Cancer Pharmacology Lab, AIRC Start Up Unit, Pisa, Italy. · Fondazione Pisana per la Scienza, Pisa, Italy. · Department of Medical Oncology, Amsterdam UMC, VU University Medical Center, Amsterdam, the Netherlands gj.peters@amsterdamumc.nl. ·Anticancer Res · Pubmed #31262886.

ABSTRACT: BACKGROUND/AIM: The novel cytidine analog RX-3117, which is activated by uridine-cytidine kinase 2 (UCK2), shows encouraging activity in pancreatic and bladder cancer Phase IIa studies. In this study we highlight the potential role of UCK2 as a biomarker for selecting patients for RX-3117 treatment. PATIENTS AND METHODS: The online genomics analysis and visualization platform, R2, developed by the Oncogenomics department at the AMC (Amsterdam, The Netherlands) was used for in silico UCK2-mRNA correlation with overall survival of pancreatic cancer patients, while UCK2 protein expression was evaluated by immunohistochemistry on pancreatic tumor formalin-fixed-paraffin-embedded sections from independent pancreatic cancer patients. mRNA expression was also determined for SUIT-2, PANC-1 and PDAC-3. Lastly, the drug sensitivity to RX-3117 was investigated using the Sulforhodamine-B cytotoxicity assay. RESULTS: The in silico data showed that a high UCK2-mRNA expression was correlated with a shorter overall survival in pancreatic cancer patients. Moreover, UCK2 protein expression was high in 21/25 patients, showing a significantly shorter mean. Overall Survival (8.4 versus 34.3 months, p=0.045). Sensitivity to RX-3117 varied between 0.6 and 11 μM. CONCLUSION: Pancreatic cancer cells are sensitive to pharmacologically achievable RX-3117 concentrations and UCK2 might be exploited as a biomarker for patient treatment selection.

3 Article Role of c-MET Inhibitors in Overcoming Drug Resistance in Spheroid Models of Primary Human Pancreatic Cancer and Stellate Cells. 2019

Firuzi, Omidreza / Che, Pei Pei / El Hassouni, Btissame / Buijs, Mark / Coppola, Stefano / Löhr, Matthias / Funel, Niccola / Heuchel, Rainer / Carnevale, Ilaria / Schmidt, Thomas / Mantini, Giulia / Avan, Amir / Saso, Luciano / Peters, Godefridus J / Giovannetti, Elisa. ·Medicinal and Natural Products Chemistry Research Center, Shiraz University of Medical Sciences, 71348-14336 Shiraz, Iran. firuzio@sums.ac.ir. · Department of Medical Oncology, Cancer Center Amsterdam, Amsterdam UMC, VU University Medical Center (VUmc), 1081 HV, Amsterdam, The Netherlands. firuzio@sums.ac.ir. · Department of Medical Oncology, Cancer Center Amsterdam, Amsterdam UMC, VU University Medical Center (VUmc), 1081 HV, Amsterdam, The Netherlands. p.che@vumc.nl. · Department of Medical Oncology, Cancer Center Amsterdam, Amsterdam UMC, VU University Medical Center (VUmc), 1081 HV, Amsterdam, The Netherlands. b.elhassouni@vumc.nl. · Department of Medical Oncology, Cancer Center Amsterdam, Amsterdam UMC, VU University Medical Center (VUmc), 1081 HV, Amsterdam, The Netherlands. m.j.n2.buijs@student.vu.nl. · Physics of Life Processes, Huygens-Kamerlingh Onnes Laboratory, Leiden University, 2333 CA, Leiden, The Netherlands. coppola@physics.leidenuniv.nl. · Division of Surgery, CLINTEC, Karolinska Institutet, SE-171, Stockholm, Sweden. matthias.lohr@ki.se. · Cancer Pharmacology Lab, AIRC Start Up Unit, University of Pisa, 56124 Pisa, Italy. niccola.funel@gmail.com. · Division of Surgery, CLINTEC, Karolinska Institutet, SE-171, Stockholm, Sweden. rainer.heuchel@ki.se. · Department of Medical Oncology, Cancer Center Amsterdam, Amsterdam UMC, VU University Medical Center (VUmc), 1081 HV, Amsterdam, The Netherlands. ilaria187@gmail.com. · Cancer Pharmacology Lab, AIRC Start Up Unit, University of Pisa, 56124 Pisa, Italy. ilaria187@gmail.com. · Physics of Life Processes, Huygens-Kamerlingh Onnes Laboratory, Leiden University, 2333 CA, Leiden, The Netherlands. Schmidt@physics.leidenuniv.nl. · Department of Medical Oncology, Cancer Center Amsterdam, Amsterdam UMC, VU University Medical Center (VUmc), 1081 HV, Amsterdam, The Netherlands. g.mantini@vumc.nl. · Metabolic syndrome Research center, Mashhad University of Medical Sciences, 91778-99191 Mashhad, Iran. AvanA@mums.ac.ir. · Department of Physiology and Pharmacology "Vittorio Erspamer", Sapienza University, 00185, Rome, Italy. luciano.saso@uniroma1.it. · Department of Medical Oncology, Cancer Center Amsterdam, Amsterdam UMC, VU University Medical Center (VUmc), 1081 HV, Amsterdam, The Netherlands. g.j.peters@vumc.nl. · Department of Medical Oncology, Cancer Center Amsterdam, Amsterdam UMC, VU University Medical Center (VUmc), 1081 HV, Amsterdam, The Netherlands. e.giovannetti@vumc.nl. · Cancer Pharmacology Lab, AIRC Start Up Unit, University of Pisa, 56124 Pisa, Italy. e.giovannetti@vumc.nl. · Fondazione Pisana per la Scienza, 56017, Pisa, Italy. e.giovannetti@vumc.nl. ·Cancers (Basel) · Pubmed #31072019.

ABSTRACT: Pancreatic stellate cells (PSCs) are a key component of tumor microenvironment in pancreatic ductal adenocarcinoma (PDAC) and contribute to drug resistance. c-MET receptor tyrosine kinase activation plays an important role in tumorigenesis in different cancers including PDAC. In this study, effects of PSC conditioned medium (PCM) on c-MET phosphorylation (by immunocytochemistry enzyme-linked immunosorbent assay (ELISA)) and drug response (by sulforhodamine B assay) were investigated in five primary PDAC cells. In novel 3D-spheroid co-cultures of cyan fluorescence protein (CFP)-firefly luciferase (Fluc)-expressing primary human PDAC cells and green fluorescence protein (GFP)-expressing immortalized PSCs, PDAC cell growth and chemosensitivity were examined by luciferase assay, while spheroids' architecture was evaluated by confocal microscopy. The highest phospho-c-MET expression was detected in PDAC5 and its subclone sorted for "stage specific embryonic antigen-4" (PDAC5 (SSEA4)). PCM of cells pre-incubated with PDAC conditioned medium, containing increased hepatocyte growth factor (HGF) levels, made PDAC cells significantly more resistant to gemcitabine, but not to c-MET inhibitors. Hetero-spheroids containing both PSCs and PDAC5 (SSEA4) cells were more resistant to gemcitabine compared to PDAC5 (SSEA4) homo-spheroids. However, c-MET inhibitors (tivantinib, PHA-665752 and crizotinib) were equally effective in both spheroid models. Experiments with primary human PSCs confirmed the main findings. In conclusion, we developed spheroid models to evaluate PSC-PDAC reciprocal interaction, unraveling c-MET inhibition as an important therapeutic option against drug resistant PDAC.