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. Author manuscript; available in PMC: 2013 Sep 2.
Published in final edited form as: Semin Cutan Med Surg. 2010 Sep;29(3):190–195. doi: 10.1016/j.sder.2010.06.002

Figure 1.

Figure 1

High-risk melanoma predisposition loci. The schematic represents the signaling pathways controlled by CDKN2A loci. The 2 different protein products encoded by the splice variants - p14Arf and p16Ink4a, converge on the same cellular function—cell-cycle regulation. The p14Arf regulates the p53 tumor suppressor network and the P16Ink4a regulates the Rb network. Variants in p14Arf, p16Ink4a, Cdk4, and Rb contribute to deregulated signaling and uncontrolled cell proliferation.