Single-dose DSS-induced inflammation enhances colorectal tumorigenesis in APC and KRAS mutant mice

Colorectal cancer (CRC) arises through interactions between driver mutations, such as in APC and KRAS, and the tumor microenvironment (TME), including inflammatory factors. While chronic inflammation is a known risk factor, the role of transient mild inflammation in tumorigenesis remains unclear. This study assessed the impact of mild inflammation on CRC development using genetically modified KRAS mutant (mut), APC mut, and APC;KRAS double mut mouse models. Mice received tamoxifen at six weeks and were evaluated with or without a 5-day administration of 1.5% dextran sulfate sodium (DSS). Mice were sacrificed at 20 weeks, and tumor number, size, location, histology, immunofluorescence, and RNA sequencing were analyzed.