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This study found that KrasG12D mutant cells are typically cleared from adult pancreas tissues through mechanisms involving the EphA2 receptor, suggesting its role as a tumor suppressor in pancreatic cancer.

This study found that injury-induced proliferation of wild-type cells can suppress oncogenic growth in Ras-mosaic skin.

This study found that quiescence in hair follicle stem cells acts as a tumor suppression mechanism for cutaneous squamous cell carcinoma, with Pten activity necessary to maintain this state.

This research found that activating a KrasG12D mutation in mice led to skin thickening, papillomas, and hair growth issues, suggesting that even rare KRAS mutations can mimic human RAS/MAPK syndrome symptoms.

The researchers reported that in mice, the type of tumor suppressor deleted along with oncogenic Kras activation in HFSCs influenced the specific squamous cell carcinoma phenotype that developed.