Mouse lung adenocarcinomas induced by Kras-G12D in Tp53 null background with and without Rad18 knockout
The DNA repair protein Rad18 activates Trans-Lesion Synthesis DNA polymerases that are DNA damage-tolerant and potentially error-prone. Rad18 is also frequently overexpressed and pathologically activated in cancer cells. However, the extent to which Rad18 shapes cancer genomes and impacts tumorigenesis is unclear. The impact of Rad18 in a mutant KRAS-induced tumorigenesis model on genomic mutations is tested in this project. Whole exome sequencing of resulting mouse lung adenocarcinomas after the activation of a latent KrasG12D allele was done in the presence and absence of Rad18.