Generation and characterization of islet cell tumor in pTet-on/pTRE-SV40Tag double-transgenic mice model

SV40 T antigen disrupted the cell metabolism and the balance between proliferation and apoptosis in lens tumors of transgenic mice

“…High rates of recovery of SV40 DNA sequences from cancer tissues have indicated that SV40 infection might play some role in the development of mesothelioma, brain tumors, bone tumors, osteosarcoma, non-Hodgkin lymphoma, choroid plexus tumors and ependymomas (Poulin and DeCaprio 2006;Shah 2007;Galateau-Salle et al 1998;Bersagel et al 1992;Carbone et al 1994Carbone et al , 1996Woloschak et al 1995;Martini et al 1996). Additionally, transgenic mice expressing the SV40 T-antigen could develop colon carcinoma (Gum et al 2004), thymic carcinoma (Park et al 1996), pancreatic islet tumor (Casanovas et al 2005;Shen et al 2007), hepatocellular and biliary cell tumor (Enomoto et al 1998), mammary tumor (Shibata et al 1999), and brain tumor (Chiu et al 2000). The process of cellular transformation induced by SV40 typically depends on the integration of the viral DNA into the host genome in a manner that allows a high level of expression of the major viral oncogenic proteins, large T antigen, and small t antigen.…”

Molecular Profiling of Pancreatic Neuroendocrine Tumors in Sporadic and Von Hippel-Lindau Patients

“…Our study reveals that both PDGFRB and the EGFR (ERBB1) are expressed at higher levels in VHL tumors, which supports further investigation of specific targeted anti-PDGFR and EGFR treatment in patients with VHL presenting with a PanNET. Insulin receptor substrate 1 (IRS1), an important mediator in insulin-like growth factor1/insulin signaling, is an adaptor molecule in signal transduction that play a role in development of PanNET (48)(49)(50)(51). Interestingly, IRS1 was expressed at higher levels in VHL tumors.…”

The Genomic Revolution and Endocrine Pathology

“…This model was specifically designed to clarify neuroendocrine cell biology and tumorigenesis. Other examples of expected neuroendocrine tumor models are the RIP-Tag2 and the pTet-on/pTRE-SV40 mice, both modeling islet cell tumors, and the c-kit -SV40 mice that develop multiple neuroendocrine tumors [30,31]. The difficulty here lies in separating what molecular events are truly expected of neuroendocrine differentiation in a certain organ from the fortuitous effects of SV40 alone, regardless of the promoter used.…”