Medizinische Klinik und Poliklinik IV, Klinikum der Universität, LMU München, Munich, Germany.
Institute for Clinical Chemistry and Laboratory Medicine, University Hospital Carl Gustav Carus at Technische Universität Dresden, Dresden, Germany.
Endocrinology. 2019 Nov 1;160(11):2600-2617. doi: 10.1210/en.2019-00410.
There are no officially approved therapies for metastatic pheochromocytomas apart from ultratrace 131I-metaiodbenzylguanidine therapy, which is approved only in the United States. We have, therefore, investigated the antitumor potential of molecular-targeted approaches in murine pheochromocytoma cell lines [monocyte chemoattractant protein (MPC)/monocyte chemoattractant protein/3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)], immortalized mouse chromaffin Sdhb-/- cells, three-dimensional pheochromocytoma tumor models (MPC/MTT spheroids), and human pheochromocytoma primary cultures. We identified the specific phosphatidylinositol-3-kinase α inhibitor BYL719 and the mammalian target of rapamycin inhibitor everolimus as the most effective combination in all models. Single treatment with clinically relevant doses of BYL719 and everolimus significantly decreased MPC/MTT and Sdhb-/- cell viability. A targeted combination of both inhibitors synergistically reduced MPC and Sdhb-/- cell viability and showed an additive effect on MTT cells. In MPC/MTT spheroids, treatment with clinically relevant doses of BYL719 alone or in combination with everolimus was highly effective, leading to a significant shrinkage or even a complete collapse of the spheroids. We confirmed the synergism of clinically relevant doses of BYL719 plus everolimus in human pheochromocytoma primary cultures of individual patient tumors with BYL719 attenuating everolimus-induced AKT activation. We have thus established a method to assess molecular-targeted therapies in human pheochromocytoma cultures and identified a highly effective combination therapy. Our data pave the way to customized combination therapy to target individual patient tumors.
除了仅在美国获得批准的超痕量 131I-间碘苄胍治疗外,转移性嗜铬细胞瘤尚无官方批准的治疗方法。因此,我们研究了在鼠嗜铬细胞瘤细胞系[单核细胞趋化蛋白(MPC)/单核细胞趋化蛋白/3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴盐(MTT)]、永生化小鼠嗜铬粒蛋白 Sdhb-/-细胞、三维嗜铬细胞瘤肿瘤模型(MPC/MTT 球体)和人嗜铬细胞瘤原代培养物中,分子靶向方法的抗肿瘤潜力。我们确定了特定的磷脂酰肌醇-3-激酶α抑制剂 BYL719 和雷帕霉素靶蛋白抑制剂依维莫司是所有模型中最有效的组合。单独用临床相关剂量的 BYL719 和依维莫司治疗可显著降低 MPC/MTT 和 Sdhb-/-细胞活力。两种抑制剂的靶向联合显着降低了 MPC 和 Sdhb-/-细胞活力,并且对 MTT 细胞具有相加作用。在 MPC/MTT 球体中,单独用临床相关剂量的 BYL719 或与依维莫司联合治疗非常有效,导致球体明显缩小甚至完全塌陷。我们通过 BYL719 减弱依维莫司诱导的 AKT 激活,证实了临床相关剂量的 BYL719 加依维莫司的协同作用在个体患者肿瘤的人嗜铬细胞瘤原代培养物中。因此,我们建立了一种评估人嗜铬细胞瘤培养中分子靶向治疗的方法,并确定了一种高效的联合治疗方法。我们的数据为针对个体患者肿瘤的定制联合治疗铺平了道路。