Intratumoral administration of the Toll‐like receptor 7/8 agonist 3M‐052 enhances interferon‐driven tumor immunogenicity and suppresses metastatic spread in preclinical triple‐negative breast cancer,Clinical & Translational Immunology

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Intratumoral administration of the Toll‐like receptor 7/8 agonist 3M‐052 enhances interferon‐driven tumor immunogenicity and suppresses metastatic spread in preclinical triple‐negative breast cancer
Clinical & Translational Immunology ( IF 4.6 ) Pub Date : 2020-09-28 , DOI: 10.1002/cti2.1177
Damien J Zanker _{1,

2} , Alex J Spurling ₂ , Natasha K Brockwell _{1,

2} , Katie L Owen _{1,

2} , Jasmine M Zakhour ₃ , Tina Robinson ₃ , Hendrika M Duivenvoorden _{3,

4} , Paul J Hertzog ₅ , Stefanie R Mullins ₆ , Robert W Wilkinson ₆ , Belinda S Parker _{1,

2,

3}

Affiliation

Loss of tumor‐inherent type I interferon (IFN) signalling has been closely linked to accelerated metastatic progression via decreased immunogenicity and antitumor immunity. Previous studies in murine models of triple‐negative breast cancer (TNBC) demonstrate that systemic IFN inducers are effective antimetastatic agents, via sustained antitumor CD8⁺ T‐cell responses. Repeated systemic dosing with recombinant IFNs or IFN inducers is associated with significant toxicities; hence, the use of alternate intratumoral agents is an active area of investigation. It is critical to investigate the impact of intratumoral agents on subsequent metastatic spread to predict clinical impact.

中文翻译：

Toll 样受体 7/8 激动剂 3M-052 的瘤内给药可增强干扰素驱动的肿瘤免疫原性并抑制临床前三阴性乳腺癌的转移扩散

肿瘤固有的 I 型干扰素 (IFN) 信号传导的丧失与通过降低免疫原性和抗肿瘤免疫力而加速转移进展密切相关。先前对三阴性乳腺癌 (TNBC) 小鼠模型的研究表明，全身性 IFN 诱导剂通过持续的抗肿瘤 CD8 ⁺ T 细胞反应是有效的抗转移剂。重组 IFN 或 IFN 诱导剂的重复全身给药与显着毒性相关；因此，使用替代瘤内药物是一个活跃的研究领域。研究肿瘤内药物对随后转移扩散的影响以预测临床影响至关重要。

更新日期：2020-09-28

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