KRAS allelic imbalance drives a MAPK dependent tumour initiation programme inefficient at rewiring the tumour microenvironment to provoke metastasis

Murine small intestinal tumours, adjacent normal tissues and tumour organoids, following Kras mutation under the control of VilCreER, alone or in combination with p53 and Notch mutation, in the presence or absence of a wild type Kras allele. Overall design: Expression data from whole intestinal tumours, normal intestine, or tumour derived organoids.