The MYC proto-oncogenes encode a family of transcription factors that are among the most commonly activated oncoproteins in human neoplasias. Indeed, MYC aberrations or upregulation of MYC-related pathways by alternate mechanisms occur in the vast majority of cancers. MYC proteins are master regulators of cellular programmes. Thus, cancers with MYC activation elicit many of the hallmarks of cancer required for autonomous neoplastic growth. In preclinical models, MYC inactivation can result in sustained tumour regression, a phenomenon that has been attributed to oncogene addiction. Many therapeutic agents that directly target MYC are under development; however, to date, their clinical efficacy remains to be demonstrated. In the past few years, studies have demonstrated that MYC signalling can enable tumour cells to dysregulate their microenvironment and evade the host immune response. Herein, we discuss how MYC pathways not only dictate cancer cell pathophysiology but also suppress the host immune response against that cancer. We also propose that therapies targeting the MYC pathway will be key to reversing cancerous growth and restoring antitumour immune responses in patients with MYC-driven cancers.

MYC _原癌基因编码一个转录因子家族，这些转录因子是人类肿瘤中最常被激活的癌蛋白之一。事实上，MYC 畸变或通过替代机制对 MYC 相关通路的上调发生在绝大多数癌症中。MYC 蛋白是细胞程序的主要调节剂。因此，具有 MYC 激活的癌症会引发自主肿瘤生长所需的许多癌症特征。在临床前模型中，MYC 失活可导致持续的肿瘤消退，这种现象已归因于致癌基因成瘾。许多直接针对 MYC 的治疗药物正在开发中；然而，迄今为止，它们的临床疗效仍有待证明。在过去的几年里，研究表明，MYC 信号可以使肿瘤细胞失调其微环境并逃避宿主免疫反应。在此，我们讨论 MYC 通路如何不仅决定癌细胞的病理生理学，而且还抑制宿主针对该癌症的免疫反应。我们还提出，针对 MYC 通路的疗法将是逆转癌症生长和恢复癌症患者抗肿瘤免疫反应的关键。MYC驱动的癌症。