Division of Oncology, Department of Medicine, Stanford University, Stanford, California.
Department of Pathology, Stanford University, Stanford, California.
Cancer Res. 2020 Sep 15;80(18):3799-3802. doi: 10.1158/0008-5472.CAN-20-0787. Epub 2020 Jul 30.
Myc and Ras are two of the most commonly activated oncogenes in tumorigenesis. Together and independently they regulate many cancer hallmarks including proliferation, apoptosis, and self-renewal. Recently, they were shown to cooperate to regulate host tumor microenvironment programs including host immune responses. But, is their partnership always cooperative or do they have distinguishable functions? Here, we provide one perspective that Myc and Ras cooperation depends on the genetic evolution of a particular cancer. This in turn, dictates when they cooperate via overlapping and identifiably distinct cellular- and host immune-dependent mechanisms that are cancer type specific.
Myc 和 Ras 是肿瘤发生中最常被激活的两种癌基因。它们共同和独立地调节许多癌症特征,包括增殖、凋亡和自我更新。最近,它们被证明合作调节宿主肿瘤微环境程序,包括宿主免疫反应。但是,它们的伙伴关系总是合作的吗?还是它们有可区分的功能?在这里,我们提供了一种观点,即 Myc 和 Ras 的合作取决于特定癌症的遗传进化。这反过来又决定了它们何时通过重叠和可识别的独特的细胞和宿主免疫依赖性机制合作,这些机制是癌症类型特异性的。