1 to these carcinogens and inactivation of the p16INK4A gene.

2      Ultraviolet light and deficiency of the p16ink4a gene are known factors that predispose one to t

3 ich is an important transcription factor for p16INK4a gene expression, thereby reducing the level of

4 , it has been unclear how LMP1 represses the p16INK4a gene expression.

5 mors or cell lines, and all deletions of the p16INK4a gene extended into exon 2, which would be expec

6 l lines, and intragenic mutations within the p16INK4a gene have been detected in familial melanoma ki

7 s led to the identification of mutations the p16INK4a gene in two tumors.

8  lung epithelial cell lines for p15INK4b and p16INK4a gene inactivation.

9  in this pathway, homozygous deletion of the p16INK4A gene, is commonly observed in head and neck squ

10 h homozygous deletions limited to either the p16INK4a gene only (20%; 2 of 10), both the p16INK4a and

11                                              p16INK4a gene product expression was also demonstrated i

12  potential therapeutic role of re-expressing p16INK4a gene product in mesothelioma cells and tumors.

13               These results demonstrate that p16INK4a gene transfer may play a therapeutic role in th

14                                          The p16INK4a gene uniquely consists of alternative first exo

15                         Neither p15INK4b nor p16INK4a gene was individually deleted in any of the tum

16 he 5' CpG islands of the murine p15INK4b and p16INK4a genes was found to be highly frequent.

17 encing analyses, intragenic mutations in the p16INK4a gene were also revealed in two (10%; 2 of 21) m

18 ructure indicates that most mutations to the p16Ink4a gene, which result in loss of function, are due