Sep 23, 1999 · Our data demonstrate for the first time the presence of p16 UV induced mutations in non melanoma skin cancer, particularly in the most aggressive SCC type, and support that p16 and p53 are...

P16 INK4A is a tumor suppressor and cell cycle regulator that has been linked to aging and senescence. Extensive research has revealed that p16 expression is significantly increased in senescent cells, as well as during natural aging or age-related pathologies.

P16 INK4A (also known as P16 and MTS1), a protein consisting exclusively of four ankyrin repeats, is recognized as a tumor suppressor mainly due to the prevalence of genetic inactivation of the p16INK4A (or CDKN2A) gene in virtually all types of human cancers.

Sep 23, 1999 · Our data demonstrate for the first time the presence of p16 UV induced mutations in non melanoma skin cancer, particularly in the most aggressive SCC type, and support that p16 and p53 are involved in two independent pathways in skin carcinogenesis.

Apr 1, 1999 · These results indicate that together with p21, p16 protein may play an important role for protective or adaptive response to UVB exposure of human skin. 1. Introduction. Ultraviolet (UV) radiation induces DNA damage in epidermal cells and is thereby responsible for sunlight-induced skin cancer.

Jan 8, 2004 · In the present study, we sought to investigate the role of p16 in apoptosis induced by ultraviolet light (the most important etiological cause of skin cancer) and cisplatin (an anticancer DNA...

Although its canonical pathway through retinoblastoma (RB) is well delineated, RB-independent functions for p16 are beginning to emerge. Here we summarize non-canonical roles of p16, including our recent finding on its role in nucleotide metabolism.

Mar 15, 2011 · We have shown here that UVC upregulates p16 INK4A and the phosphorylated form of the protein at the 4 serine sites; Ser-7, Ser-8, Ser-140, and Ser-152. This accumulation of p16 INK4A occurred through increasing the stability of both forms of the protein.

Our data demonstrate for the ®rst time the presence of p16 UV induced mutations in non melanoma skin cancer, particularly in the most aggressive SCC type, and support that p16 and p53 are...

Sep 1, 1999 · In this report, we demonstrate that when human skin was irradiated with suberythemal doses of UV radiation, levels of p16 were dramatically increased by 16 h postirradiation, peaking at 24 h, and declining by 72 h. p16 was expressed in the nucleus and cytoplasm of melanocytes and keratinocytes within the epidermis, and the pattern of p16 ...