Supplementary Figures 1 - 8 from Dormant Cancer Cells Contribute to Residual Disease in a Model of Reversible Pancreatic Cancer

PDF file - 719K, Elevated c-MYC expression in human pancreatic cancer cell lines (S1); c-Myc is highly upregulated in a mouse model for pancreatic cancer (S2); Levels of c-Myc (exogenous and endogenous) in ductal and poorly differentiated pancreatic adenocarcinomas that were induced through upregulation of this oncogene in comparison to pancreatic tumors from Pdx1-Cre LSL-KrasG12D animals that carry two wildtype or one mutant allele of p53 (S3); Expression of Muc1, E-Cadherin, Pdx1, and Sox9 in the normal pancreas as well as ductal carcinomas and poorly differentiated carcinomas of transgenic mice expressing exogenous c-Myc (S4); Elevated levels of exogenous c-Myc induces expression of Bax and active Caspase-3 (S5); Ablation of c-Myc expression leads to reduced proliferation, increased expression of p53 as well as autophagy-related protein LC3 but a reduction in the levels of active Caspase-3 (S6); Downregulation of active Caspase-3 and upregulation of LC3 in pancreatic cancers that lack Cdkn2a (S7); Residual cancer cells do not express c-Myc, lack nuclear staining of Ki67 and are TUNEL negative (S8).