Abstract
Inactivation of the INK4α/ARF (or CDKN2α) locus is a common and critical genetic event in the development of human and mouse melanoma. This locus engages the Rb and p53 tumor suppressor pathways through its capacity to encode two distinct gene products, p16INK4a and p14ARF. This review highlights the body of evidence supporting a role for both p16INK4a and p14ARF in the suppression of melanoma, and speculates as to why this locus is preferentially targeted in this tumor type. In addition, the potential importance of these two pathways in mediating UV-induced melanoma genesis will be addressed via genetic and molecular evidence in the mouse.
Original language | English (US) |
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Pages (from-to) | 3092-3098 |
Number of pages | 7 |
Journal | Oncogene |
Volume | 22 |
Issue number | 20 |
DOIs | |
State | Published - May 19 2003 |
Keywords
- Cell cycle
- Ultraviolet light
- cdk4
- cdk6
- p19
ASJC Scopus subject areas
- Molecular Biology
- Genetics
- Cancer Research