| Literature DB >> 29057301 |
C Gamell1,2, T Gulati1,2, B Solomon1,3, S Haupt1,2, Y Haupt1,2,4,5.
Abstract
A key step during onset of most cases of non-small cell lung cancer (NSCLC) is the loss of the tumor suppressor p16INK4a (best known as p16), commonly due to promoter hypermethylation. We recently reported a novel regulatory pathway involving E6-associated protein and cell division control protein 6, which provides a methylation-independent mechanism for p16 silencing in patients with a particularly aggressive form of NSCLC.Entities:
Keywords: CDC6; E6AP; INK4/ARF; NSCLC; p16; tumor suppression
Year: 2017 PMID: 29057301 PMCID: PMC5644485 DOI: 10.1080/23723556.2017.1299273
Source DB: PubMed Journal: Mol Cell Oncol ISSN: 2372-3556