The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21287, USA.
J Mammary Gland Biol Neoplasia. 2012 Dec;17(3-4):205-16. doi: 10.1007/s10911-012-9264-2. Epub 2012 Aug 4.
Recent advances in genetics and genomics have revealed new pathways that are aberrantly activated in many breast cancers. Chief among these genetic changes are somatic mutations and/or gains and losses of key genes within the phosphoinositide 3-kinase (PI3K) pathway. Since breast cancer cell growth and progression is often dependent upon activation of the PI3K pathway, there has been intense research interest in finding therapeutic agents that can selectively inhibit one or more constituents of this signaling cascade. Here we review key molecules involved with aberrant PI3K pathway activation in breast cancers and current efforts to target these components for therapeutic gain.
近年来,遗传学和基因组学的进展揭示了许多乳腺癌中异常激活的新途径。这些遗传变化中主要的是磷脂酰肌醇 3-激酶(PI3K)途径中的体细胞突变和/或关键基因的增益和缺失。由于乳腺癌细胞的生长和进展通常依赖于 PI3K 途径的激活,因此人们一直致力于寻找能够选择性抑制这种信号级联反应的一个或多个组成部分的治疗剂。在这里,我们回顾了乳腺癌中异常 PI3K 途径激活所涉及的关键分子,并概述了针对这些成分进行治疗的最新研究进展。