揭示p16基因沉默的新途径：对肺癌的治疗意义
Uncovering a novel pathway for p16 silencing: Therapeutic implications for lung cancer.
作者信息
Gamell C, Gulati T, Solomon B, Haupt S, Haupt Y
机构信息
The Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, VIC, Australia.
Tumor Suppression Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
出版信息
Mol Cell Oncol. 2017 Mar 7;4(5):e1299273. doi: 10.1080/23723556.2017.1299273. eCollection 2017.
Abstract
A key step during onset of most cases of non-small cell lung cancer (NSCLC) is the loss of the tumor suppressor p16 (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.
摘要
在大多数非小细胞肺癌（NSCLC）病例发病过程中的一个关键步骤是肿瘤抑制因子p16（最为人所知的是p16）的缺失，这通常是由于启动子高甲基化所致。我们最近报道了一条涉及E6相关蛋白和细胞分裂控制蛋白6的新型调控途径，该途径为一种特别侵袭性形式的NSCLC患者的p16沉默提供了一种不依赖甲基化的机制。
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