Rech Andrew J, Vonderheide Robert H
1Abramson Family Cancer Research Institute; 2Abramson Cancer Center; 3Division of Hematology-Oncology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Cancer Discov. 2013 Dec;3(12):1330-2. doi: 10.1158/2159-8290.CD-13-0775.
Tumor-infiltrating T cells have recently been found to upregulate immunosuppressive pathways, such as programmed cell death protein 1 ligand 1 (PD-L1), in a paracrine fashion on tumor cells, but tumor cell-intrinsic regulation of PD-L1 is another potential mechanism. In this issue of Cancer Discovery, Akbay and colleagues show that signaling via mutant EGF receptor (EGFR) in murine lung tumor cells directly upregulates tumor PD-L1 and that therapeutic blockade of this pathway improves survival in EGFR-driven preclinical models-highlighting the dynamic interplay and therapeutic opportunities of cancer cell biology and immune biology.
最近发现肿瘤浸润性T细胞以旁分泌方式上调肿瘤细胞上的免疫抑制途径，如程序性细胞死亡蛋白1配体1（PD-L1），但肿瘤细胞对PD-L1的内在调节是另一种潜在机制。在本期《癌症发现》中，阿克贝及其同事表明，小鼠肺肿瘤细胞中突变型表皮生长因子受体（EGFR）的信号传导直接上调肿瘤PD-L1，并且该途径的治疗性阻断可提高EGFR驱动的临床前模型中的生存率，这突出了癌细胞生物学和免疫生物学的动态相互作用及治疗机会。
