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Pancreatic Neoplasms: HELP
Articles by Jessica Brandi
Based on 4 articles published since 2009
(Why 4 articles?)
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Between 2009 and 2019, Jessica Brandi wrote the following 4 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Trichostatin A alters cytoskeleton and energy metabolism of pancreatic adenocarcinoma cells: An in depth proteomic study. 2018

Dalla Pozza, Elisa / Manfredi, Marcello / Brandi, Jessica / Buzzi, Arianna / Conte, Eleonora / Pacchiana, Raffaella / Cecconi, Daniela / Marengo, Emilio / Donadelli, Massimo. ·Department of Neuroscience, Biomedicine and Movement, University of Verona, Verona, Italy. · Department of Sciences and Technological Innovation, University of Piemonte Orientale, Alessandria, Italy. · ISALIT S.r.l., Spin-off of University of Piemonte Orientale, Novara, Italy. · Department of Biotechnology, Proteomics and Mass Spectrometry Laboratory, University of Verona, Verona, Italy. ·J Cell Biochem · Pubmed #29095525.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal of all human cancers with a high mortality rate. Resistance to conventional treatments and chemotherapeutics is a typical feature of PDAC. To investigate the causes of drug resistance it is essential to deeply investigate the mechanism of action of chemotherapeutics. In this study, we performed an in depth shotgun proteomic approach using the label-free proteomic SWATH-MS analysis to investigate novel insights of the mechanism of action of the histone deacetylase (HDAC) inhibitor trichostatin A (TSA) in PDAC cells. This proteomic analysis in PaCa44 cells and data elaboration of TSA-regulated proteins by bioinformatics showed an overall up-regulation of cytokeratins and other proteins related to the cytoskeleton organization, keratinization, and apoptotic cell death. On the contrary, a large amount of the down-regulated proteins by TSA treatment belongs to the cellular energetic metabolism and to the machinery of protein synthesis, such as ribosomal proteins, determining synergistic cell growth inhibition by the combined treatment of TSA and the glycolytic inhibitor 2-deoxy-d-glucose in a panel of PDAC cell lines. Data are available via ProteomeXchange with identifier PXD007801.

2 Article Proteomic analysis of pancreatic cancer stem cells: Functional role of fatty acid synthesis and mevalonate pathways. 2017

Brandi, Jessica / Dando, Ilaria / Pozza, Elisa Dalla / Biondani, Giulia / Jenkins, Rosalind / Elliott, Victoria / Park, Kevin / Fanelli, Giuseppina / Zolla, Lello / Costello, Eithne / Scarpa, Aldo / Cecconi, Daniela / Palmieri, Marta. ·University of Verona, Department of Biotechnology, Proteomics and Mass Spectrometry Laboratory, Verona 37134, Italy. · University of Verona, Department of Neuroscience, Biomedicine and Movement, Verona 37134, Italy. · University of Liverpool, MRC Centre for Drug Safety Science, Department of Molecular & Clinical Pharmacology, Liverpool L69 3GE, United Kingdom. · NIHR Liverpool Pancreas Biomedical Research Unit, Department of Molecular and Therapeutic Cancer Medicine, Royal Liverpool University Hospital, Liverpool L69 3GA, United Kingdom. · Department of Ecological and Biological Sciences, University of Tuscia, Viterbo, Italy. · University and Hospital Trust of Verona, Applied Research on Cancer Network (ARC-NET), Department of Pathology and Diagnostics, Verona 37134, Italy. · University of Verona, Department of Biotechnology, Proteomics and Mass Spectrometry Laboratory, Verona 37134, Italy. Electronic address: daniela.cecconi@univr.it. ·J Proteomics · Pubmed #27746256.

ABSTRACT: Recently, we have shown that the secretome of pancreatic cancer stem cells (CSCs) is characterized by proteins that participate in cancer differentiation, invasion, and metastasis. However, the differentially expressed intracellular proteins that lead to the specific characteristics of pancreatic CSCs have not yet been identified, and as a consequence the deranged metabolic pathways are yet to be elucidated. To identify the modulated proteins of pancreatic CSCs, iTRAQ-based proteomic analysis was performed to compare the proteome of Panc1 CSCs and Panc1 parental cells, identifying 230 modulated proteins. Pathway analysis revealed activation of glycolysis, the pentose phosphate pathway, the pyruvate-malate cycle, and lipid metabolism as well as downregulation of the Krebs cycle, the splicesome and non-homologous end joining. These findings were supported by metabolomics and immunoblotting analysis. It was also found that inhibition of fatty acid synthase by cerulenin and of mevalonate pathways by atorvastatin have a greater anti-proliferative effect on cancer stem cells than parental cells. Taken together, these results clarify some important aspects of the metabolic network signature of pancreatic cancer stem cells, shedding light on key and novel therapeutic targets and suggesting that fatty acid synthesis and mevalonate pathways play a key role in ensuring their viability. BIOLOGICAL SIGNIFICANCE: To better understand the altered metabolic pathways of pancreatic cancer stem cells (CSCs), a comprehensive proteomic analysis and metabolite profiling investigation of Panc1 and Panc1 CSCs were carried out. The findings obtained indicate that Panc1 CSCs are characterized by upregulation of glycolysis, pentose phosphate pathway, pyruvate-malate cycle, and lipid metabolism and by downregulation of Krebs cycle, spliceosome and non-homologous end joining. Moreover, fatty acid synthesis and mevalonate pathways are shown to play a critical contribution to the survival of pancreatic cancer stem cells. This study is helpful for broadening the knowledge of pancreatic cancer stem cells and could accelerate the development of novel therapeutic strategies.

3 Article Pancreatic ductal adenocarcinoma cell lines display a plastic ability to bi‑directionally convert into cancer stem cells. 2015

Dalla Pozza, Elisa / Dando, Ilaria / Biondani, Giulia / Brandi, Jessica / Costanzo, Chiara / Zoratti, Elisa / Fassan, Matteo / Boschi, Federico / Melisi, Davide / Cecconi, Daniela / Scupoli, Maria Teresa / Scarpa, Aldo / Palmieri, Marta. ·Department of Life and Reproduction Sciences, Section of Biochemistry, University of Verona, Verona, Italy. · Department of Biotechnology, University of Verona, Verona, Italy. · Applied Research on Cancer Network (ARC‑NET) and Department of Pathology and Diagnostics, University and Hospital Trust of Verona, Verona, Italy. · Department of Computer Science, University of Verona, Verona, Italy. · Department of Medicine, Oncology Unit, University and Hospital Trust of Verona, Verona, Italy. ·Int J Oncol · Pubmed #25502497.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is often diagnosed when metastatic events have occurred. Cancer stem cells (CSCs) play an important role in tumor initiation, metastasis, chemoresistance and relapse. A growing number of studies have suggested that CSCs exist in a dynamic equilibrium with more differentiated cancer cells via a bi‑directional regeneration that is dependent on the environmental stimuli. In this investigation, we obtain, by using a selective medium, PDAC CSCs from five out of nine PDAC cell lines, endowed with different tumorsphere‑forming ability. PDAC CSCs were generally more resistant to the action of five anticancer drugs than parental cell lines and were characterized by an increased expression of EpCAM and CD44v6, typical stem cell surface markers, and a decreased expression of E‑cadherin, the main marker of the epithelial state. PDAC CSCs were able to re‑differentiate into parental cells once cultured in parental growth condition, as demonstrated by re‑acquisition of the epithelial morphology, the decreased expression levels of EpCAM and CD44v6 and the increased sensitivity to anticancer drugs. Finally, PDAC CSCs injected into nude mice developed a larger subcutaneous tumor mass and showed a higher metastatic activity compared to parental cells. The present study demonstrates the ability to obtain CSCs from several PDAC cell lines and that these cells are differentially resistant to various anticancer agents. This variability renders them a model of great importance to deeply understand pancreatic adenocarcinoma biology, to discover new biomarkers and to screen new therapeutic compounds.

4 Article Comparative proteomic and phosphoproteomic profiling of pancreatic adenocarcinoma cells treated with CB1 or CB2 agonists. 2013

Brandi, Jessica / Dando, Ilaria / Palmieri, Marta / Donadelli, Massimo / Cecconi, Daniela. ·Proteomics and Mass Spectrometry Laboratory, Department of Biotechnology, University of Verona, Verona, Italy. ·Electrophoresis · Pubmed #23463621.

ABSTRACT: The pancreatic adenocarcinoma cell line Panc1 was treated with cannabinoid receptor ligands (arachidonylcyclopropylamide or GW405833) in order to elucidate the molecular mechanism of their anticancer effect. A proteomic approach was used to analyze the protein and phosphoprotein profiles. Western blot and functional data mining were also employed in order to validate results, classify proteins, and explore their potential relationships. We demonstrated that the two cannabinoids act through a widely common mechanism involving up- and down-regulation of proteins related to energetic metabolism and cell growth regulation. Overall, the results reported might contribute to the development of a therapy based on cannabinoids for pancreatic adenocarcinoma.