Exploring a mutation-based signature to predict the benefits of immune checkpoint inhibitors in oncogene-addicted subsets of non-small cell lung cancer: a retrospective study

探索基于突变的特征来预测免疫检查点抑制剂对非小细胞肺癌癌基因依赖亚群的疗效:一项回顾性研究

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Abstract

BACKGROUND: Despite the effectiveness of immune checkpoint blockade (ICB) therapy in cancer treatment, oncogene-addicted subsets of non-small cell lung cancer (NSCLC) typically derive limited benefits. Herein, we established and evaluated a mutation-based signature to predict ICB efficacy in patients with both non-mutant and oncogene-mutant NSCLC. METHODS: The predictive power of the signature was evaluated and validated across advanced NSCLCs cases with or without targetable oncogene alterations, using four public and one in-house immunotherapy cohort. NSCLC cohorts from The Cancer Genome Atlas were used to explore the underlying mechanisms of the signature. Herein, we defined a gene mutation number (GMN) based on the signature and classified patients into high and low GNM groups (GMN-H and GMN-L, respectively). RESULTS: The GMN-H group exhibited significantly improved overall survival (OS) (hazard ratio [HR], 0.23; 95% confidence interval [CI]: 0.14-0.37; P < 0.001 in the discovery cohort) and progression-free survival (HR, 0.43; 95% CI: 0.28-0.65; P < 0.001 in the discovery cohort; HR, 0.41; 95% CI: 0.26-0.66; P = 0.0011 in the validation cohort) after ICB therapy. The survival advantage of GMN-H persisted in patients with KRAS mutations, whereas only trends toward improved survival outcomes were observed in those with EGFR, HER2, or MET alterations. Moreover, in the KRAS(G12C)- and KRAS(G12V)-mutant subgroups, patients with GMN-H exhibited a better OS. Compared with GMN-L, GMN-H was associated with higher levels of neoantigens, enrichment of WNT and MAPK pathways, and increased intra-tumoral CD8 + T cell infiltration. CONCLUSIONS: The mutation-based signature established herein represents a robust biomarker for identifying patients with advanced NSCLCs who are most likely to benefit from ICB therapy, including those with targetable oncogene alterations.

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