Authors
Azhar Khandekar, Phuc H Hoang, Jens Luebeck, Marcos Díaz-Gay, Wei Zhao, John P McElderry, Caleb Hartman, Mona Miraftab, Olivia W Lee, Kara M Barnao, Kristine Jones, Amy Hutchinson, Belynda Hicks, Erik N Bergstrom, Yang Yang, Martin A Nowak, Nathaniel Rothman, Angela C Pesatori, Dario Consonni, Robert Homer, Marina K Baine, Lynette M Sholl, Philippe Joubert, Charles Leduc, William D Travis, Soo-Ryum Yang, Qing Lan, David C Wedge, Lixing Yang, Stephen J Chanock, Tongwu Zhang, Ludmil B Alexandrov, Maria Teresa Landi
Published in
Journal of the National Cancer Institute. Aug 05, 2026. Epub Aug 05, 2026.
Abstract
The role of extrachromosomal DNA (ecDNA) in lung cancer, particularly in subjects who never smoked (LCINS), remains unclear. Examination of over 1200 whole-genome-sequenced lung cancers identified ecDNA in 18.9% of patients. Recurrent amplification of MDM2 and other oncogenes via ecDNA possibly drives a LCINS subset. Tumors harboring ecDNA showed worse overall survival than tumors harboring other focal amplifications. A strong association with whole-genome doubling suggests most ecDNA reflects genomic instability in treatment-naïve lung cancer.
PMID:
42554978
Bibliographic data and abstract were imported from PubMed on 06 Aug 2026.
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