Tensegrity Model Hypothesis: May This Paradigm Be Useful to Explain Hepatic and Pancreatic Carcinogenesis in Patients with Persistent Hepatitis B or Hepatitis C Virus Infection?
Creators: name: Fiorino, Sirio
name: Bacchi-Reggiani, Letizia
name: Pontoriero, Laura
name: Gallo, Claudio
name: Chili, Elisabetta
name: Masetti, Michele
name: Zanini, Nicola
name: Grondona, Ana
name: Silvestri, Tania
name: Deleonardi, Gaia
name: Fornelli, Adele
name: Bondi, Arrigo
name: De Biase, Dario
name: Baccarini, Paola
name: Tallini, Giovanni
name: Tropeano, Antonio
name: Quartuccio, Valeria
name: Cuppini, Andrea
name: Castellani, Gastone
name: Jovine, Elio
Publisher: name: JOP. Journal of the Pancreas
Year: 2014
Subjects: Carcinoma, Hepatocellular; Hepacivirus; Hepatitis B virus; Mechanotransduction, Cellular; Pancreatic Carcinoma

description: <strong>Context</strong> Hepatitis B (HBV) and hepatitis C virus (HCV) possess well-known oncogenic properties and may promote carcinogenesis in liver. However antigens and replicative sequences of HBV/HCV have been also detected in different extra-hepatic tissues, including the pancreas. Although epidemiological studies and meta-analyses have recently suggested that HBV/HCV may be also risk factors for pancreatic cancer and several researches have investigated the possible mechanisms and intra-/extra-cellular paths involved in pancreatic and hepatic carcinogenesis, to date, these complex processes remain largely unexplained. <strong>Objectives</strong> In our paper, we aimed to propose a comprehensive and qualitative hypothetical model, describing how HBV/HCV may exert their oncogenic role. <strong>Methods</strong> We performed a systematic research of scientific literature, by searching MEDLINE, the Cochrane Library and EMBASE databases. The used keywords were: “chronic HBV/HCV”, “pancreatic cancer”, “liver carcinoma”, “carcinogenesis mechanisms”, “tensional integrity”, “cytoskeleton”, and “extracellular matrix”. <strong>Results</strong> Taking advantage from available studies, we suggest an unifying hypothesis based on results and data, obtained from different areas of research. In particular we considered the well-defined model of tensional integrity and correlated it to changes induced by HBV/HCV in viscoelastic properties/stiffness of cellular/extracellular microenvironments. These events perturb the tightly-regulated feedback loop, which usually couples the intracellular-generated forces to substrate rigidity of extracellular compartments. Therefore, such a change strongly affects intracellular functions and cellular fate, by promoting a substantial deregulation of critical intracellular biochemical activities and genome expression. <strong>Conclusions</strong> Our hypothesis might provide for the first time a reliable system, which correlates tensional integrity model with intra-/extra-cellular modifications, occurring in liver and pancreas during HBV/HCV-induced carcinogenesis. This approach might improve our understanding of pathogenetic mechanisms involved in the development of pancreatic and hepatic carcinogenesis , enhancing the possibility of their treatment. Furthermore, should the usefulness of this model be definitively confirmed, it might be also helpful to extend its field of application to other viruses-related cancers.<strong>Image:</strong> Signaling pathways (Figure 1)
description: JOP. Journal of the Pancreas, Vol 15, No 2 (2014): March - p. 84-218