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. 2013 Feb 26;41(8):e92. doi: 10.1093/nar/gkt115

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© The Author(s) 2013. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 5. — Hydrodynamic injection of PB multigene vectors induce liver cancer in the Fah-deficient mouse model. (a) Multigene PB transposon vector used for hydrodynamic tail vein injection. PB-Quad-EXP-shTrp53/NRAS^G12V/Fah/Luc, short hairpin to Trp53, constitutively active NRAS^G12V cDNA, fumarylacetoacetate hydrolase (Fah) cDNA and Luciferase cDNA all under the control of independent human elongation factor 1 alpha (EF1A) promoters. (b) Representative luciferase imaging of a mouse two weeks post-hydrodynamic injection. (c) Gross examination of the liver on necropsy identified numerous tumour nodules that were formalin fixed for H&E and immunohistochemical analysis. (d) Immunohistochemical staining results for NRAS, Fah and Ki-67 with appropriate no primary controls. T, tumour; P, parenchyma; higher magnification shown as insert box.