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

Autor: Kay-Uwe Wagner, Hallgeir Rui, Jonathan R. Brody, Agnieszka K. Witkiewicz, Matthias Hebrok, John P. Morris, Michael A. Hollingsworth, Dominick J. DiMaio, Dean W. Felsher, Rene Opavsky, Surinder K. Batra, Aleata A. Triplett, Qian Zhang, Kazuhito Sakamoto, Chengbao Liu, Nirakar Rajbhandari, Wan-chi Lin
Rok vydání: 2023
DOI: 10.1158/0008-5472.22399502
Popis: 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).
Databáze: OpenAIRE