{"title":"Brief Report: The Immune Profiles of the Molecular Subtypes of EGFR-Mutant Lung Adenocarcinomas in a Large Real-World Cohort","authors":"","doi":"10.1016/j.cllc.2024.04.016","DOIUrl":null,"url":null,"abstract":"<div><div><ul><li><span>•</span><span><div>EGFR-mutant tumors with exon 19 deletions, L858R mutations, or exon 20 insertions were less likely to be PD-L1 high (TPS ≥ 50%) or TMB high (≥10 mut/MB) as compared to wild-type (WT) tumors. Among EGFR-mutant tumors, those with uncommon alterations in L861Q and G719X had greater rates of TMB high and TP53 co-mutations.</div></span></li><li><span>•</span><span><div>Utilizing bulk<span> RNA sequencing<span> data to characterize the immune tumor microenvironment<span> (TME), exon 19 deletion and L858R mutation tumors were found to have lower median percent fractions of CD8+ T cells versus WT. However, a wide range of values for CD8+ T cells was observed and a subset of exon 19 deletion and L858R tumors had higher values comparable to WT.</span></span></span></div></span></li><li><span>•</span><span><div><span>Exon 19 deletion, L858R, and exon 20 insertion tumors were enriched with immunosuppressive<span> M2 macrophages and </span></span>neutrophils as compared to WT. In contrast, L861Q and G719X tumors had levels of M2 macrophages similar to WT.</div></span></li><li><span>•</span><span><div>A small subset of EGFR-mutant tumors, particularly those with uncommon alterations, bear characteristics that may render them more immunogenic. Continued research is needed to evaluate biomarkers, including the specific subtype of EGFR<span>, as predictors of immunotherapy response to better identify the small subgroup of patients with EGFR-mutant disease that benefit from checkpoint inhibitors.</span></div></span></li></ul></div></div>","PeriodicalId":10490,"journal":{"name":"Clinical lung cancer","volume":"25 7","pages":"Pages e312-e315.e1"},"PeriodicalIF":3.3000,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical lung cancer","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1525730424000767","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
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EGFR-mutant tumors with exon 19 deletions, L858R mutations, or exon 20 insertions were less likely to be PD-L1 high (TPS ≥ 50%) or TMB high (≥10 mut/MB) as compared to wild-type (WT) tumors. Among EGFR-mutant tumors, those with uncommon alterations in L861Q and G719X had greater rates of TMB high and TP53 co-mutations.
•
Utilizing bulk RNA sequencing data to characterize the immune tumor microenvironment (TME), exon 19 deletion and L858R mutation tumors were found to have lower median percent fractions of CD8+ T cells versus WT. However, a wide range of values for CD8+ T cells was observed and a subset of exon 19 deletion and L858R tumors had higher values comparable to WT.
•
Exon 19 deletion, L858R, and exon 20 insertion tumors were enriched with immunosuppressive M2 macrophages and neutrophils as compared to WT. In contrast, L861Q and G719X tumors had levels of M2 macrophages similar to WT.
•
A small subset of EGFR-mutant tumors, particularly those with uncommon alterations, bear characteristics that may render them more immunogenic. Continued research is needed to evaluate biomarkers, including the specific subtype of EGFR, as predictors of immunotherapy response to better identify the small subgroup of patients with EGFR-mutant disease that benefit from checkpoint inhibitors.
期刊介绍:
Clinical Lung Cancer is a peer-reviewed bimonthly journal that publishes original articles describing various aspects of clinical and translational research of lung cancer. Clinical Lung Cancer is devoted to articles on detection, diagnosis, prevention, and treatment of lung cancer. The main emphasis is on recent scientific developments in all areas related to lung cancer. Specific areas of interest include clinical research and mechanistic approaches; drug sensitivity and resistance; gene and antisense therapy; pathology, markers, and prognostic indicators; chemoprevention strategies; multimodality therapy; and integration of various approaches.