Bopp Anna R, Lamenza Felipe F, Upadhaya Puja, Ryan Nathan M, Kazmierowicz Natalie, Jordanides Pete P, Siddiqui Arham, Pracha Sherefuddin H, Roth Peyton, Iwenofu O Hans, Oghumu Steve
Department of Pathology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, 249 Evans Hall, 520 King Ave., Columbus, OH, 43201, USA.
Cancer Immunol Immunother. 2025 May 30;74(7):227. doi: 10.1007/s00262-025-04081-5.
Head and neck squamous cell carcinoma (HNSCC) is one of the most diagnosed malignancies globally, with a 5-year survival rate of only 40-50%. Current therapies are limited to aggressive chemoradiotherapy combinations and disfiguring resection. Recent research has demonstrated that inhibition of Bruton's tyrosine kinase (BTK) by ibrutinib is an effective treatment for aggressive solid cancers. However, little is known about the effects of ibrutinib on aggressive HNSCC. We tested the efficacy of ibrutinib against HNSCC in vitro and in a metastatic, aggressive MOC2 orthotopic murine model and determined the underlying mechanisms. Ibrutinib decreased cancer cell growth in vitro, reduced tumor burden in vivo, decreased metastasis to the tumor draining lymph nodes and lungs, and enhanced overall survival outcomes. Flow cytometric analysis revealed decreased infiltration of tumor-infiltrating immunosuppressive T cells expressing the co-inhibitory markers PD-1, LAG-3, and IL-10. Furthermore, ibrutinib treatment increased cytotoxic T cell infiltration into the tumor microenvironment. Further analysis demonstrated that the effects on immunosuppressive T cell phenotypes were directly mediated by ibrutinib. Immunosuppressive myeloid cells were also observed to express lower levels of PDL1 in ibrutinib-treated mice. Our study demonstrates the potential of BTK inhibitors, specifically ibrutinib, in the treatment of HNSCC, mediated by its inhibitory effect on HNSCC cancer cell growth and metastasis, as well as modulation of the T cell anti-tumor immune microenvironment.
头颈部鳞状细胞癌(HNSCC)是全球诊断最多的恶性肿瘤之一,其5年生存率仅为40%-50%。目前的治疗方法仅限于积极的放化疗联合以及毁容性切除。最近的研究表明,依鲁替尼抑制布鲁顿酪氨酸激酶(BTK)对侵袭性实体癌是一种有效的治疗方法。然而,依鲁替尼对侵袭性HNSCC的影响知之甚少。我们在体外以及转移性侵袭性MOC2原位小鼠模型中测试了依鲁替尼对HNSCC的疗效,并确定了其潜在机制。依鲁替尼在体外降低了癌细胞的生长,在体内减轻了肿瘤负担,减少了肿瘤引流淋巴结和肺部的转移,并提高了总体生存结果。流式细胞术分析显示,表达共抑制标志物PD-1、LAG-3和IL-10的肿瘤浸润性免疫抑制性T细胞浸润减少。此外,依鲁替尼治疗增加了细胞毒性T细胞向肿瘤微环境的浸润。进一步分析表明,对免疫抑制性T细胞表型的影响是由依鲁替尼直接介导的。在接受依鲁替尼治疗的小鼠中,还观察到免疫抑制性髓样细胞表达较低水平的PDL1。我们的研究证明了BTK抑制剂,特别是依鲁替尼,在治疗HNSCC方面的潜力,这是由其对HNSCC癌细胞生长和转移的抑制作用以及对T细胞抗肿瘤免疫微环境的调节介导的。