Gene therapy in pancreatic cancer

Figure 1 Cell cycle checkpoints. Mitogenic signals activate cyclin D-dependent kinases, which phosphorylate RB and RB family proteins (p107 and p130) to facilitate entry into S phase. The p16INK4a protein inhibits cyclin D/Cdk4, 6 to activate RB and prevent entry into S phase. The p14ARF protein inhibits Mdm2 to induce p53, leading either to p53-dependent apoptosis or to induction of the Cdk2 inhibitor p21Cip1. The p21Cip1 protein inhibits cyclin E/Cdk2 and induces RB-dependent cell cycle arrest.

Figure 2 Schematic diagram of immunogene therapy. A: Immunogene therapy with altered cancer cells, which are harvested from patients (autologous cells) or from established cancer cell lines (allogeneic) and then cultured in vitro and inactivated to yield a vaccine; B: Immunogene therapy with in vivo gene transfer; C: Immunogene therapy using altered immune cells.

Figure 3 Clinical trials regarding administration routes of gene therapy in pancreatic cancer.