ArticleClinical lung cancer2026
High Programmed Death-Ligand 1 Expression is Associated With a Shorter Progression Free Survival in ALK-Rearranged Lung Cancer Patients Treated With First Line Tyrosine Kinase Inhibitors.
Article in Clinical lung cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAlthough ALK-positive non-small cell lung cancer (NSCLC) derives limited benefit from immune checkpoint inhibitors, PD-L1 expression is frequently elevated at diagnosis. The clinical relevance of PD-L1 expression for the efficacy and durability of response to ALK tyrosine kinase inhibitors (TKIs) remains unclear. We investigated the association between tumor PD-L1 expression and outcomes with first-line ALK TKIs and used complementary preclinical models to explore potential biological mechanisms.
methodsClinical, pathologic, molecular, and treatment outcomes were evaluated among patients with ALK-rearranged NSCLC treated at the University of Colorado. PD-L1 expression was assessed by tumor proportion score (TPS). Murine EML4-ALK lung cancer cell lines were engineered to overexpress PD-L1, and effects on ALK TKI response were evaluated in vitro and in immune-competent mouse models.
resultsAmong 130 TKI-naïve patients treated with first-line ALK TKIs, 57 (44%) had high PD-L1 expression (TPS ≥ 50%). After multivariable adjustment, high PD-L1 expression was associated with significantly shorter progression-free survival (PFS) compared with low PD-L1 expression (11 vs. 21 months; HR 2.29, 95% CI, 1.51-3.49; P ≤ .001), with no difference in overall survival (91 vs. 107 months; HR 1.16, 95% CI, 0.62-2.17). Objective response rates were similar between PD-L1-high and -low tumors (81.8% vs. 83.3%; Pearson r = -0.20, 95% CI, -0.40-0.07). In preclinical EML4-ALK models, tumor cell PD-L1 overexpression did not alter alectinib sensitivity, depth, or durability of response in vitro or in vivo
conclusionsHigh PD-L1 expression is associated with shorter PFS to first-line ALK TKIs without affecting the initial radiographic response. Preclinical findings suggest that PD-L1-intrinsic tumor cell signaling does not directly impair ALK TKI efficacy, implicating tumor microenvironment-mediated mechanisms in reduced response durability.
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