Oncogenic driver mutations underlie the spatial tumour immune landscape of non-small cell lung cancer

Saskia Hartner, Hanie Abolfathi, Morteza Rezanejad, Bridget Liu, Elham Karimi, Dakota Rogers, Mark Sorin, Samuel Doré, Lysanne Desharnais, Michèle Orain, William Enlow, Andréanne Gagné, Yuhong Wei, Yohan Bossé, Daniela F. Quail, Philippe Joubert () and Logan A. Walsh ()
Additional contact information
Saskia Hartner: McGill University
Hanie Abolfathi: Université Laval
Morteza Rezanejad: McGill University
Bridget Liu: McGill University
Elham Karimi: McGill University
Dakota Rogers: McGill University
Mark Sorin: McGill University
Samuel Doré: McGill University
Lysanne Desharnais: McGill University
Michèle Orain: Institut universitaire de cardiologie et de pneumologie de Québec – Université Laval
William Enlow: Institut universitaire de cardiologie et de pneumologie de Québec – Université Laval
Andréanne Gagné: Institut universitaire de cardiologie et de pneumologie de Québec – Université Laval
Yuhong Wei: McGill University
Yohan Bossé: Institut universitaire de cardiologie et de pneumologie de Québec – Université Laval
Daniela F. Quail: McGill University
Philippe Joubert: Institut universitaire de cardiologie et de pneumologie de Québec – Université Laval
Logan A. Walsh: McGill University

Nature Communications, 2025, vol. 16, issue 1, 1-10

Abstract: Abstract Lung adenocarcinoma (LUAD) is a molecularly diverse form of lung cancer characterized by distinct oncogenic driver mutations that influence both tumour biology and clinical outcomes. Understanding the interplay between these oncogenic drivers and the tumour microenvironment (TME) is crucial for improving therapeutic strategies and patient management. Here, we investigate the impact of driver mutations on the composition and spatial architecture of the TME in LUAD. Using imaging mass cytometry (IMC), we analyse tumour samples from 157 LUAD patients, integrating genomic and clinical data to link specific mutations with tumour characteristics. Unique patterns are associated with mutated KRAS and EGFR tumours with TP53 co-mutations, suggesting these co-mutations reshape the TME and promote resistance to tyrosine kinase inhibitors (TKIs). Overall, our findings highlight the complex interplay between oncogenic driver mutations and the TME in LUAD, underscoring the importance of integrating genomic and cellular data to understand the underlying tumour behaviour and prognosis.

Date: 2025
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DOI: 10.1038/s41467-025-63465-4

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