Contribution of the dual coding capacity of the p16INK4a/MTS1/CDK2 locus to human malignancies

摘要: During the three last years, so-called p16 locus on human chromosome band 9p21 has been increasingly implicated in different cancers by a variety of alterations abolishing both copies p16INK4a/MTS1/CDKN2 gene and adjacent p15INK4b gene, two members family specific inhibitors cyclin D 1-3-CDK4/6 complexes that control cell cycle progression G1 to S phase. While these properties are characteristic tumor suppressor genes, abundant experimental data have clearly identified link between loss function p16INK4a tumorigenic processes. The role onset natural tumors is less obvious. New light may be shed development recent finding an alternative transcript from encodes p19ARF, negative regulator which unrelated p15 does not act binding any CDK. Hence, this protein appears element novel mechanism, whose impairing might involved tumorigenesis.