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Pancreatic Neoplasms: HELP
Articles by Giulia Biondani
Based on 3 articles published since 2009
(Why 3 articles?)
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Between 2009 and 2019, Giulia Biondani wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Extracellular matrix composition modulates PDAC parenchymal and stem cell plasticity and behavior through the secretome. 2018

Biondani, Giulia / Zeeberg, Katrine / Greco, Maria Raffaella / Cannone, Stefania / Dando, Ilaria / Dalla Pozza, Elisa / Mastrodonato, Maria / Forciniti, Stefania / Casavola, Valeria / Palmieri, Marta / Reshkin, Stephan Joel / Cardone, Rosa Angela. ·Department of Neuroscience, Biomedicine and Movement, Biochemistry Section, University of Verona, Italy. · Department of Biosciences, Biotechnology and Biopharmaceutics, University of Bari, Italy. · Department of Biology, University of Bari, Italy. ·FEBS J · Pubmed #29660229.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers. Its aggressiveness is driven by an intense fibrotic desmoplastic reaction in which the increasingly collagen I-rich extracellular matrix (ECM) and several cell types, including cancer stem cells (CSCs), create a tumor-supportive environment. However, how ECM composition regulates CSC dynamics and their relationship with the principle parenchymal tumor population to promote early invasive growth is not yet characterized. For this, we utilized a platform of 3D organotypic cultures composed of laminin-rich Matrigel, representative of an early tumor, plus increasing concentrations of collagen I to simulate malignant stroma progression. As ECM collagen I increases, CSCs progress from a rapidly growing, vascular phenotype to a slower growing, avascular phase, while maintaining their endothelial-like gene signatures. This transition is supported autocrinically by the CSCs and paracrinically by the parenchymal cells via their ECM-dependent secretomes. Indeed, when growing on an early tumor ECM, the CSCs are dedicated toward the preparation of a vascular niche by (a) activating their growth program, (b) secreting high levels of proangiogenic factors which stimulate both angiogenesis and vasculogenic mimicry, and (c) overexpressing VEGFR-2, which is activated by VEGF secreted by both the CSC and parenchymal cells. On Matrigel, the more differentiated parenchymal tumor cell population had reduced growth but a high invasive capacity. This concerted high local invasion of parenchymal cells into the CSC-derived vascular network suggests that a symbiotic relationship between the parenchymal cells and the CSCs underlies the initiation and maintenance of early PDAC infiltration and metastasis.

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.