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A prognostic signature for lung adenocarcinoma in people who have never smoked. 2025
Wei Zhao, and
Tongwu Zhang, and
Xing Hua, and
Phuc H Hoang, and
Mona Miraftab, and
Monjoy Saha, and
John P McElderry, and
Jian Sang, and
Olivia W Lee, and
Caleb Hartman, and
Azhar Khandekar, and
Sunandini Sharma, and
Frank J Colón-Matos, and
Samuel Anyaso-Samuel, and
Difei Wang, and
Kristine Jones, and
Amy Hutchinson, and
Belynda Hicks, and
Jennifer Rosenbaum, and
Xiaoming Zhong, and
Yang Yang, and
Angela Pesatori, and
Dario Consonni, and
David C Christiani, and
Kin Chung Leung, and
Maria Pik Wong, and
Marta Manczuk, and
Jolanta Lissowska, and
Beata Świątkowska, and
Anush Mukeria, and
Oxana Shangina, and
David Zaridze, and
Ivana Holcatova, and
Dana Mates, and
Sasa Milosavljevic, and
Simona Ognjanovic, and
Milan Savic, and
Millica Kontic, and
Valerie Gaborieau, and
Paul Brennan, and
Oscar Arrieta, and
Yohan Bossé, and
Eric S Edell, and
Matthew B Schabath, and
Paul Hofman, and
Luis Mas, and
Sai S Yendamuri, and
Chih-Yi Chen, and
I-Shou Chang, and
Chao Agnes Hsiung, and
Geoffrey Liu, and
Jacobo Martínez Santamaría, and
Bonnie E Gould Rothberg, and
Karun Mutreja, and
Scott Lawrence, and
Nathaniel Rothman, and
Ludmil B Alexandrov, and
Charles Leduc, and
Marina K Baine, and
Philippe Joubert, and
Lynette M Sholl, and
William D Travis, and
Robert Homer, and
Qing Lan, and
Stephen J Chanock, and
Lixing Yang, and
Soo-Ryum Yang, and
Jianxin Shi, and
Maria Teresa Landi
Knowledge of tumor cell dynamics can inform prognosis and treatment yet is largely lacking for lung adenocarcinoma in people who have never smoked (NS-LUAD). With RNA-seq data from 684 NS-LUAD and validation in an independent dataset, we identified three subtypes with distinct phenotypic traits and cell compositions. Additional genomic and histological data further characterized the subtypes. 'Steady' , marked by low proliferation, high alveolar cell fraction, moderate-to-well differentiation, and fewer driver genes' alterations, is linked to prolonged survival and low immune evasion. 'Proliferative ' shows high proliferation markers, TP53 mutations, and gene fusions. 'Chaotic' , with high epithelial-to-mesenchymal transition markers, has the worst prognosis even within stage I tumors. Lacking known molecular or histological characteristics, this aggressive subtype is solely identified by transcriptomic data. A 60-gene signature recapitulates the overall classification and strongly predicts survival even within subgroups based on tumor stage or known genomic features, emphasizing its potential for improving NS-LUAD prognostication in clinical settings. The transcriptome of 684 lung adenocarcinomas in people who have never smoked (NS-LUAD) identifies three subtypes with different cellular dynamics, and genomic and morphologic features. A 60-gene signature accurately stratifies subjects for mortality risk, even in stage I, offering a clinically applicable tool for treatment decision making in NS-LUAD patients.
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