Solomon David A, Kim Jung-Sik, Jean Walter, Waldman Todd
Department of Oncology, Tumor Biology Training Program, Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, Washington, District of Columbia 20057, USA.
Cancer Res. 2008 Nov 1;68(21):8657-60. doi: 10.1158/0008-5472.CAN-08-2084.
Glioblastoma multiforme (GBM) is one of the most dreaded cancer diagnoses due to its poor prognosis and the limited treatment options. Homozygous deletion of the p16(INK4a)/p14(ARF)/p15(INK4b) locus is among the most common genetic alterations in GBM. Two recent studies have shown that deletion and mutation of another INK4 family member, p18(INK4c), also drives the pathogenesis of GBM. This minireview will discuss the known roles for p18(INK4c) in the initiation and progression of cancer and suggest opportunities for future studies.
多形性胶质母细胞瘤(GBM)因其预后不良和治疗选择有限,是最可怕的癌症诊断之一。p16(INK4a)/p14(ARF)/p15(INK4b)基因座的纯合缺失是GBM中最常见的基因改变之一。最近的两项研究表明,INK4家族的另一个成员p18(INK4c)的缺失和突变也推动了GBM的发病机制。本综述将讨论p18(INK4c)在癌症发生和发展中的已知作用,并提出未来研究的机会。