MyoD-Cre driven alterations in K-Ras and p53 lead to a mouse model with histological and molecular characteristics of human rhabdomyosarcoma [RMS_GEMM_cell_lines]

We have developed a new conditional genetically engineered mouse model of rhabdomyosarcoma (RMS) with homologous molecular signature to human RMS that provides valuable pre-clinical models for evaluating novel therapies Overall design: Mice expressing MyoD promoter-regulated Cre-recombinase were crossed with germline p53Flox or Lox-Stop-Lox (LSL) knock-in alleles expressing oncogenic p53R172H and/or K-RasG12D mutants. Resulting tumors were isolated and dissociated to establish cell lines.