1999年9月23日 · 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 ...

1999年9月23日 · 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.

2024年2月23日 · We identified 14 HR-HPV negative metastatic HNCUP to either the cervical or parotid gland lymph nodes, of which, 11 (11/14, 79%) had UV signature mutations, including 4 (4/10, 40%) p16 positive cases. All UV signature mutation positive cases had at least one significant TP53 mutation and greater than 20 unique gene mutations.

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...

2004年1月8日 · It is clearly shown that p16-compromised osteosarcoma U2OS cell line and p16−/− mouse embryo fibroblasts are sensitive to UV-induced apoptosis, as compared to their respective isogenic...

2011年3月15日 · The tumor suppressor p16 INK4A, a phosphoprotein that exists in human cells under both phosphorylated and nonphosphorylated forms, plays crucial roles during the cellular response to UV light. However, it is still unclear how this protein is activated in response to this carcinogenic agent.

1999年4月1日 · The results revealed an accumulation of p16, p21 and PCNA proteins by UVB exposure, indicating a concomitant protective or adaptive role of these molecules in UVB carcinogenesis. This is the first report to show that p16 protein may have a role in the response to UVB exposure in human skin.

1999年10月1日 · 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 ...

1999年9月1日 · 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 ...

P16-compromised or P16-deficient cells demonstrated sensitivity to ultraviolet (UV) light-induced apoptosis, suggesting that the absence of functional P16 allows propagation of proapoptotic signaling (28).