Description
The Ink4a/Arf tumor supressors play crucial roles in inhibiting cell cycle progression at the G1/S checkpoint. Activating mutations in the KrasG12D oncogene is one of the most frequent changes in human cancer, with resultant constitutive mitogenic signaling within the cell. We generated cohorts of CD19Cre; KrasG12D/+; Ink4a/ArfL/+ mice to evaluate the combined contributions of Ink/Arf loss and KrasG12D activation in pre-B ALL lymphomas.