Department of Radiation Oncology, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
Department of Molecular, Cellular and Developmental Biology, University of Colorado Boulder, Colorado.
Radiat Res. 2020 Nov 10;194(5):519-531. doi: 10.1667/RR15480.1.
Head and neck squamous cell carcinoma (HNSCC) is a challenging cancer with little change in five-year overall survival rate of 50-60% over the last two decades. Radiation with or without platinum-based drugs remains the standard of care despite limited benefit and high toxicity. HNSCCs often overexpress epidermal growth factor receptor (EGFR) and inhibition of EGFR signaling enhances radiation sensitivity by interfering with repair of radiation-induced DNA breaks. Poly (adenosine diphosphate-ribose) polymerase-1 (PARP1) also participates in DNA damage repair, but its inhibition provides benefit in cancers that lack DNA repair by homologous recombination (HR) such as BRCA-mutant breast cancer. HNSCCs in contrast are typically BRCA wild-type and proficient in HR repair, making it challenging to apply anti-PARP1 therapy in this model. A recently published study showed that a combination of EGFR and PARP1 inhibition induced more DNA damage and greater growth control than each single agent in HNSCC cells. This led us to hypothesize that a combination of EGFR and PARP1 inhibition would enhance the efficacy of radiation to a greater extent than each single agent, providing a rationale for paradigm-shifting combinatorial approaches to improve the standard of care in HNSCC. Here, we report a proof-of-concept study using Detroit562 HNSCC cells, which are proficient for DNA repair by both HR and non-homologous end joining (NHEJ) mechanisms. We tested the effect of adding cetuximab and/or olaparib (inhibitors of EGFR and PARP1, respectively) to radiation and compared it to that of cisplatin and radiation combination, which is the standard of care. Our results demonstrate that the combination of cetuximab and olaparib with radiation was superior to the combination of any single drug with radiation in terms of induction of unrepaired DNA damage, induction of senescence, apoptosis and clonogenic death, and tumor growth control in mouse xenografts. Combined with our recently published phase I safety data on cetuximab/olaparib/radiation triple combination, the data reported here demonstrate a potential for combining biologically-based therapies that might optimize radiosensitization in HNSCC.
头颈部鳞状细胞癌(HNSCC)是一种具有挑战性的癌症,在过去二十年中,其五年总生存率仅略有变化,为 50-60%。尽管存在局限性益处和高毒性,但仍使用放化疗联合铂类药物作为标准治疗方法。HNSCC 常过度表达表皮生长因子受体(EGFR),抑制 EGFR 信号通路通过干扰辐射诱导的 DNA 断裂修复来增强辐射敏感性。聚(二磷酸腺苷核糖)聚合酶-1(PARP1)也参与 DNA 损伤修复,但在缺乏同源重组(HR)修复的癌症(如 BRCA 突变型乳腺癌)中,PARP1 抑制剂具有益处。相比之下,HNSCC 通常为 BRCA 野生型,且 HR 修复功能良好,因此在该模型中应用抗 PARP1 治疗具有挑战性。最近发表的一项研究表明,在 HNSCC 细胞中,EGFR 和 PARP1 抑制的联合作用比单独使用任一药物诱导更多的 DNA 损伤和更强的生长抑制。这使我们假设,EGFR 和 PARP1 抑制的联合作用将比单独使用任一药物更能增强辐射的疗效,为改变范式的组合方法提供了合理依据,以改善 HNSCC 的标准治疗。在这里,我们报告了一项使用 Detroit562 HNSCC 细胞的概念验证研究,这些细胞均通过 HR 和非同源末端连接(NHEJ)机制进行 DNA 修复。我们测试了添加西妥昔单抗和/或奥拉帕利(分别为 EGFR 和 PARP1 的抑制剂)与辐射联合的效果,并将其与顺铂联合辐射的标准治疗方法进行比较。我们的结果表明,在诱导未修复的 DNA 损伤、诱导衰老、凋亡和克隆形成死亡以及肿瘤生长控制方面,西妥昔单抗和奥拉帕利与辐射的联合作用优于任何单一药物与辐射的联合作用。结合我们最近发表的西妥昔单抗/奥拉帕利/放疗三联组合的 I 期安全性数据,这里报告的数据表明,联合使用基于生物学的治疗方法可能优化 HNSCC 的放射增敏作用。