ArticleClinical and translational medicine2026
The landscape of responses to neoadjuvant immunotherapy in resectable Kirsten rat sarcoma viral oncogene homolog-mutant lung adenocarcinoma: Clinical heterogeneity and correlative immunologic analysis.
Article in Clinical and translational medicine, 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
backgroundKirsten rat sarcoma viral oncogene homolog (KRAS)-mutant lung adenocarcinoma (LUAD) typically demonstrates limited response to neoadjuvant immunotherapy (NIT). Elucidating the immune determinants that differentiate responders from non-responders was critical for optimizing immunotherapy strategies. This study aimed to characterize the tumour microenvironment features of KRAS-mutant LUAD following neoadjuvant programmed death protein 1 (PD-1) inhibitor therapy by integrating clinical outcomes with single-cell RNA sequencing (scRNA-seq).
methodsA total of 143 patients with resectable LUAD were consecutively enrolled in this study, including 106 cases in the KRAS-wildtype cohort and 37 cases in the KRAS-mutant cohort. We systematically compared the pathological response rates, survival outcomes and recurrence patterns between the two cohorts. We performed scRNA-seq on tumour specimens from 234 real-world patients with non-small cell lung cancer. From this cohort, 48 LUAD cases were identified and stratified by KRAS mutation status (13 KRAS-mutant and 35 KRAS-wildtype patients). Cellular compositions, transcriptional features and intercellular communication networks were analysed.
resultsClinical analysis revealed that the KRAS-mutant group exhibited significantly poorer pathological responses (p = .032) and inferior long-term survival compared to the KRAS-wildtype group. We identified an immunosuppressive tumour necrosis factor receptor superfamily member 4 (TNFRSF4)-expressing regulatory T-cell (CD4T_Treg_TNFRSF4) subset enriched in non-responders, whereas responders showed increased frequencies of T helper 1 cells (Th1 cells) and a previously unrecognized exhausted-like B-cell state (Bex). Bex cells displayed impaired metabolic activity yet retained antigen presentation potential and showed extensive cellular interactions with Th1 cells, suggesting a supportive role in Th1-mediated antitumour immunity.
conclusionKRAS-mutant patients exhibited significantly poorer pathological responses, and KRAS-mutant status may independently predict survival outcomes after NIT in LUAD patients. Additionally, our study unveiled the cellular and molecular architecture underlying differential responses to NIT in KRAS-mutant LUAD, emphasizing the opposing roles of immunosuppressive Tregs and synergistic Bex-Th1 networks. HIGHLIGHTS: KRAS-mutant LUAD patients exhibit inferior pathological responses and survival after neoadjuvant immunotherapy compared to KRAS-wildtype patients. A CD4T_Treg_TNFRSF4 subset is enriched in non-responders, defining an immunosuppressive microenvironment. Responders are characterized by a synergistic network between Th1 cells and a novel exhausted-like B-cell (Bex) state. The balance between immunosuppressive Tregs and the Th1/Bex axis determines therapeutic efficacy in KRAS-mutant LUAD.
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