[HTML][HTML] Splicing into senescence: the curious case of p16 and p19ARF

DA Haber - Cell, 1997 - cell.com
Cell, 1997cell.com
The study of tumor suppressor genes generates much of its excitement from the
convergence of experiments addressing the genetic basis of cancer, together with the
cellular pathways that regulate cellular proliferation, immortality, and cell cycle progression.
Among the most notable of these gene products is the cyclin-dependent kinase inhibitor p16
(also known as CDKN2, MTS-1, and INK4a), implicated in cell cycle regulation and cellular
senescence, whose loss results in genetic predisposition to malignant melanoma and …
The study of tumor suppressor genes generates much of its excitement from the convergence of experiments addressing the genetic basis of cancer, together with the cellular pathways that regulate cellular proliferation, immortality, and cell cycle progression. Among the most notable of these gene products is the cyclin-dependent kinase inhibitor p16 (also known as CDKN2, MTS-1, and INK4a), implicated in cell cycle regulation and cellular senescence, whose loss results in genetic predisposition to malignant melanoma and pancreatic cancer (for review, see
cell.com