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Pancreatic Neoplasms: HELP
Articles by Marco E. Bianchi
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Marco Bianchi wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article The IL-1/IL-1 receptor axis and tumor cell released inflammasome adaptor ASC are key regulators of TSLP secretion by cancer associated fibroblasts in pancreatic cancer. 2019

Brunetto, Emanuela / De Monte, Lucia / Balzano, Gianpaolo / Camisa, Barbara / Laino, Vincenzo / Riba, Michela / Heltai, Silvia / Bianchi, Marco / Bordignon, Claudio / Falconi, Massimo / Bondanza, Attilio / Doglioni, Claudio / Protti, Maria Pia. ·Tumor Immunology Unit, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Raffaele Scientific Institute, Via Olgettina 58, 20132, Milan, Italy. · Division of Immunology, Transplantation and Infectious Diseases, IRCCS San Raffaele Scientific Institute, Via Olgettina 58, 20132, Milan, Italy. · Vita-Salute San Raffaele University, Milan, Italy. · Pancreatic Surgery Unit and Pancreas Translational & Clinical Research Center, IRCCS San Raffaele Scientific Institute, Milan, Italy. · Division of Experimental Oncology, IRCCS San Raffaele Scientific Institute, Milan, Italy. · Innovative Immunotherapies Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. · Center for Translational Genomics and Bioinformatics, IRCCS San Raffaele Scientific Institute, Milan, Italy. · Chromatin Dynamics Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. · Division of Genetics and Cell Biology, IRCCS San Raffaele Scientific Institute, Milan, Italy. · MolMed SpA, Milan, Italy. · Pathology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. · Tumor Immunology Unit, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Raffaele Scientific Institute, Via Olgettina 58, 20132, Milan, Italy. protti.mariapia@hsr.it. · Division of Immunology, Transplantation and Infectious Diseases, IRCCS San Raffaele Scientific Institute, Via Olgettina 58, 20132, Milan, Italy. protti.mariapia@hsr.it. ·J Immunother Cancer · Pubmed #30760333.

ABSTRACT: BACKGROUND: The thymic stromal lymphopoietin (TSLP), a key cytokine for development of Th2 immunity, is produced by cancer associated fibroblasts (CAFs) in pancreatic cancer where predominant tumor infiltrating Th2 over Th1 cells correlates with reduced patients' survival. Which cells and molecules are mostly relevant in driving TSLP secretion by CAFs in pancreatic cancer is not defined. METHODS: We performed in vitro, in vivo and ex-vivo analyses. For in vitro studies we used pancreatic cancer cell lines, primary CAFs cultures, and THP1 cells. TSLP secretion by CAFs was used as a read-out system to identify in vitro relevant tumor-derived inflammatory cytokines and molecules. For in vivo studies human pancreatic cancer cells and CAFs were orthotopically injected in immunodeficient mice. For ex-vivo studies immunohistochemistry was performed to detect ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain) expression in surgical samples. Bioinformatics was applied to interrogate published data sets. RESULTS: We show in vitro that IL-1α and IL-1β released by pancreatic cancer cells and tumor cell-conditioned macrophages are crucial for TSLP secretion by CAFs. Treatment of immunodeficient mice orthotopically injected with human IL-1 positive pancreatic cancer cells plus CAFs using the IL-1R antagonist anakinra significantly reduced TSLP expression in the tumor. Importantly, we found that pancreatic cancer cells release alarmins, among which ASC, able to induce IL-1β secretion in macrophages. The relevance of ASC was confirmed ex-vivo by its expression in both tumor cells and tumor associated macrophages in pancreatic cancer surgical samples and survival data analyses showing statistically significant inverse correlation between ASC expression and survival in pancreatic cancer patients. CONCLUSIONS: Our findings indicate that tumor released IL-1α and IL-1β and ASC are key regulators of TSLP secretion by CAFs and their targeting should ultimately dampen Th2 inflammation and improve overall survival in pancreatic cancer.

2 Article Interobserver agreement in contrast harmonic endoscopic ultrasound. 2012

Fusaroli, Pietro / Kypraios, Dimitrios / Mancino, Maria Grazia / Spada, Alessia / Benini, Maria Chiara / Bianchi, Marco / Bocus, Paolo / De Angelis, Claudio / De Luca, Leonardo / Fabbri, Carlo / Grillo, Antonino / Marzioni, Marco / Reggio, Dario / Togliani, Thomas / Zanarini, Stefano / Caletti, Giancarlo. ·Department of Clinical Medicine, GI Unit, University of Bologna/Imola Hospital, Italy Gastroenterology Unit, Bellaria Hospital, Bologna, Italy. pietro.fusaroli@unibo.it ·J Gastroenterol Hepatol · Pubmed #22414180.

ABSTRACT: BACKGROUND AND AIM: Contrast harmonic endoscopic ultrasound (CH-EUS) was recently introduced to clinical practice; its reproducibility among endosonographers is unknown. Our aim was to assess the interobserver agreement (IA) in CH-EUS. METHODS: Fifteen endosonographers (eight experienced and seven non-experienced) from 11 Italian EUS centers evaluated 80 video-cases (40 solid pancreatic lesions, 20 pancreatic cystic lesions and 20 submucosal lesions) of CH-EUS, according to the degree of enhancement, the pattern of distribution and the washout of the contrast agent. IA within each group and between the two groups of observers was assessed with the Fleiss kappa statistic. RESULTS: Overall IA was moderate for the uptake and fair for the pattern of distribution and the washout. In solid pancreatic lesions, IA was moderate for the uptake and fair for the pattern and the washout. In cystic pancreatic lesions, IA was uniformly moderate for the assessment of uptake, slight for the pattern and fair for the washout. In submucosal tumors, IA was substantial for the uptake, slight for the pattern and fair for the washout. Non-experienced endosonographers demonstrated, in most cases, comparable IA with the experienced ones. CONCLUSIONS: Interobserver agreement among endosonographers for CH EUS was satisfactory. In particular, overall IA varied from slight to substantial, being fair in the majority of cases. Inherent structural features of the lesions, as well as technical differences between the variables assessed, could have accounted for the fluctuation of the results. Outcomes of IA were reproducible between experienced and non-experienced endosonographers.

3 Article Endogenous HMGB1 regulates autophagy. 2010

Tang, Daolin / Kang, Rui / Livesey, Kristen M / Cheh, Chun-Wei / Farkas, Adam / Loughran, Patricia / Hoppe, George / Bianchi, Marco E / Tracey, Kevin J / Zeh, Herbert J / Lotze, Michael T. ·Damage Associated Molecular Pattern Molecule Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA 15219, USA. tangd2@upmc.edu ·J Cell Biol · Pubmed #20819940.

ABSTRACT: Autophagy clears long-lived proteins and dysfunctional organelles and generates substrates for adenosine triphosphate production during periods of starvation and other types of cellular stress. Here we show that high mobility group box 1 (HMGB1), a chromatin-associated nuclear protein and extracellular damage-associated molecular pattern molecule, is a critical regulator of autophagy. Stimuli that enhance reactive oxygen species promote cytosolic translocation of HMGB1 and thereby enhance autophagic flux. HMGB1 directly interacts with the autophagy protein Beclin1 displacing Bcl-2. Mutation of cysteine 106 (C106), but not the vicinal C23 and C45, of HMGB1 promotes cytosolic localization and sustained autophagy. Pharmacological inhibition of HMGB1 cytoplasmic translocation by agents such as ethyl pyruvate limits starvation-induced autophagy. Moreover, the intramolecular disulfide bridge (C23/45) of HMGB1 is required for binding to Beclin1 and sustaining autophagy. Thus, endogenous HMGB1 is a critical pro-autophagic protein that enhances cell survival and limits programmed apoptotic cell death.