Discover oncology · 2026
p53 expression and NLR could recognize distinct subtypes of lung adenocarcinoma with high expression of PD-L1 (TPS ≥ 50%), defined with 22C3 antibody.
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Li Ming, Huang Mengqi, Huang Yuchen, Zhang Xiaoliang, Wu Haibo, Feng Zhenzhong
Аннотация
BACKGROUND: Lung adenocarcinoma (LUAD) with high expression of PD-L1 (TPS ≥ 50%) is a distinct subset of NSCLC and a potential immunotherapy candidate. An improved understanding of the heterogeneity of PD-L1-high LUAD patients and the recognition of other biomarkers combined with PD-L1 could facilitate more precise use of PD-1 inhibitors in clinical practice.
METHODS: Surgically resected tumour tissues from 69 LUAD patients with a PD-L1 TPS ≥ 50% defined by 22C3 antibody were tested for p53 and IFN-γ protein expression using immunohistochemistry. The densities of CD8 and Granzyme B-positive T cells were evaluated by immunohistochemistry. EGFR mutation was detected by RT‒PCR, ALK rearrangement was examined by a fluorescence in situ hybridization (FISH) assay, and TP53 gene mutations were sequenced using Sanger sequencing.
RESULTS: Differences in clinicopathological features, including age and spread through the air space (STAS), were observed between patients with higher PD-L1 expression (TPS ≥ 50%, < 70%) and those with the highest PD-L1 expression (TPS ≥ 70%). LUAD patients whose PD-L1 TPS was ≥ 70% and whose p53 protein abnormal expression or NLR was < 5 had higher densities of CD8-positive tumour-infiltrating lymphocytes (TILs) and Granzyme B-positive T cells as well as higher IFN-γ protein expression than those whose TPS was < 70%, those whose p53 protein expression was normal, or those whose NLR was ≥ 5.
CONCLUSIONS: The present study is the first to reveal that distinct subtypes of PD-L1-high LUAD can be identified on the basis of p53 protein expression and the NLR. p53 expression and the NLR can recognize a subtype with brisk immune cell cytotoxicity that might potentially respond better to PD-1 inhibitors.
METHODS: Surgically resected tumour tissues from 69 LUAD patients with a PD-L1 TPS ≥ 50% defined by 22C3 antibody were tested for p53 and IFN-γ protein expression using immunohistochemistry. The densities of CD8 and Granzyme B-positive T cells were evaluated by immunohistochemistry. EGFR mutation was detected by RT‒PCR, ALK rearrangement was examined by a fluorescence in situ hybridization (FISH) assay, and TP53 gene mutations were sequenced using Sanger sequencing.
RESULTS: Differences in clinicopathological features, including age and spread through the air space (STAS), were observed between patients with higher PD-L1 expression (TPS ≥ 50%, < 70%) and those with the highest PD-L1 expression (TPS ≥ 70%). LUAD patients whose PD-L1 TPS was ≥ 70% and whose p53 protein abnormal expression or NLR was < 5 had higher densities of CD8-positive tumour-infiltrating lymphocytes (TILs) and Granzyme B-positive T cells as well as higher IFN-γ protein expression than those whose TPS was < 70%, those whose p53 protein expression was normal, or those whose NLR was ≥ 5.
CONCLUSIONS: The present study is the first to reveal that distinct subtypes of PD-L1-high LUAD can be identified on the basis of p53 protein expression and the NLR. p53 expression and the NLR can recognize a subtype with brisk immune cell cytotoxicity that might potentially respond better to PD-1 inhibitors.