| Rapid growth of invasive metastatic melanoma in carcinogen-treated hepatocyte growth factor/scatter factor-transgenic mice carrying an oncogenic CDK4 mutation. | skin, |
| Early G(1) cyclin-dependent kinases as prognostic markers and potential therapeutic targets in esophageal adenocarcinoma. | esophageal, |
| Loss of keratinocytic RXRalpha combined with activated CDK4 or oncogenic NRAS generates UVB-induced melanomas via loss of p53 and PTEN in the tumor microenvironment. | skin, |
| LMP1 of Epstein-Barr virus induces proliferation of primary mouse embryonic fibroblasts and cooperatively transforms the cells with a p16-insensitive CDK4 oncogene. | None |
| Cellular response to oncogenic ras involves induction of the Cdk4 and Cdk6 inhibitor p15(INK4b). | None |
| data identify a new role for oncogenic Ras in CDK4 regulation and highlight the functional importance of CDK4 suppression in preventing uncontrolled growth | None |
| Cdk4 disruption renders primary mouse cells resistant to oncogenic transformation, leading to Arf/p53-independent senescence. | None |
| Design and characterization of a hyperstable p16INK4a that restores Cdk4 binding activity when combined with oncogenic mutations. | None |
| Crystallization of gankyrin, an oncoprotein that interacts with CDK4 and the S6b (rpt3) ATPase of the 19S regulator of the 26S proteasome. | None |
| Dissection of protein-protein interaction and CDK4 inhibition in the oncogenic versus tumor suppressing functions of gankyrin and P16. | None |
| both CDK4 and CDK6 are prognostic markers and bona fide oncogenes in EAC. | None |