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Metastasis and Carcinoma Case Studies / Lung Cancer Diagnosis and Treatment · Journal article
BMC Pulmonary Medicine · September 10, 2026
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This is a retrospective descriptive case series of 8 patients with driver gene-positive advanced NSCLC who developed sarcomatoid transformation after TKI therapy. The study reports increased PD-L1 expression in all three evaluable paired cases and enhanced intratumoral lymphocyte infiltration in most patients, but provides no comparative evidence, clinical outcomes, or mechanistic validation.
Retrospective single-centre case series. Patients with driver gene-positive advanced NSCLC who developed sarcomatoid transformation following TKI therapy treated at a single hospital. Intervention: Sarcomatoid transformation after tyrosine kinase inhibitor therapy (observational). n = 8.
Eight patients with advanced NSCLC harbouring driver gene mutations developed sarcomatoid transformation after TKI therapy Paired PD-L1 testing in all three evaluable cases showed increased PD-L1 expression after transformation Enhanced intratumoral lymphocyte infiltration observed in most patients after transformation
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This descriptive series identifies a potential immune phenotype shift (increased PD-L1, enhanced lymphocyte infiltration) in a rare resistance mechanism to TKI therapy. The findings are exploratory and would require validation in larger cohorts and experimental models before informing therapeutic strategy.
Single-centre retrospective case series of 8 patients describing clinicopathological features and immune markers after sarcomatoid transformation; no control group, no comparative analysis, and no clinical outcomes reported.
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This descriptive series identifies a potential immune phenotype shift (increased PD-L1, enhanced lymphocyte infiltration) in a rare resistance mechanism to TKI therapy. The findings are exploratory and would require validation in larger cohorts and experimental models before informing therapeutic strategy.
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In patients with driver gene-positive advanced non-small cell lung cancer (NSCLC), acquired resistance following targeted therapy remains a major clinical challenge. This resistance can arise through various mechanisms, such as point mutations, activation of bypass pathways, and transformation of cancer cells. Among these mechanisms, neuroendocrine differentiation is relatively common, whereas epithelial–mesenchymal transition (EMT) is also involved, though to a lesser extent. In contrast, sarcomatoid transformation is comparatively rare. In this study, we retrospectively analyzed eight patients with advanced NSCLC harboring driver gene mutations who developed sarcomatoid transformation after tyrosine kinase inhibitor (TKI) therapy at our hospital. We comprehensively examined their clinical characteristics, genomic profiles, and changes in the tumor immune microenvironment. Notably, paired PD-L1 testing revealed that all three evaluable cases showed increased PD-L1 expression after transformation, along with enhanced intratumoral lymphocyte infiltration in most patients. These findings provide valuable insights into the resistance mechanisms and potential therapeutic strategies for this challenging patient population.
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