靶向表观基因组克服 PI3K 抑制耐药性。
Tackling Resistance to PI3K Inhibition by Targeting the Epigenome.
机构信息
Department of Biomedicine, University of Basel, University Hospital Basel, 4031 Basel, Switzerland.
Department of Biomedicine, University of Basel, University Hospital Basel, 4031 Basel, Switzerland.
出版信息
Cancer Cell. 2017 May 8;31(5):616-618. doi: 10.1016/j.ccell.2017.04.010.
Phosphoinositide-3-kinase (PI3K) pathway inhibitors have emerged as promising therapeutic agents for estrogen receptor (ERα)-positive breast cancers. However, incipient resistance limits the clinical benefit. Toska and colleagues identified that the epigenetic regulator KMT2D enhances ERα activity in BYL719-treated PIK3CA mutant breast cancer, leading to a rationale for targeting the epigenome and PI3K signaling.
磷酸肌醇 3-激酶 (PI3K) 通路抑制剂已成为治疗雌激素受体 (ERα) 阳性乳腺癌的有前途的治疗剂。然而，初步的耐药性限制了临床获益。Toska 及其同事发现，表观遗传调节剂 KMT2D 增强了 BYL719 处理的 PIK3CA 突变型乳腺癌中的 ERα 活性，为靶向表观基因组和 PI3K 信号提供了依据。
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