de Biase, Maria Stella, Massip, Florian, Wei, Tzu-Ting, Giorgi, Federico M.
ORCID: 0000-0002-7325-9908, Stark, Rory, Stone, Amanda, Gladwell, Amy, O’Reilly, Martin, Schütte, Daniel
ORCID: 0000-0002-4746-537X, de Santiago, Ines, Meyer, Kerstin B.
ORCID: 0000-0001-5906-1498, Markowetz, Florian, Ponder, Bruce A. J., Rintoul, Robert C.
ORCID: 0000-0003-3875-3780 and Schwarz, Roland F.
ORCID: 0000-0001-9155-4268
(2024).
Smoking-associated gene expression alterations in nasal epithelium reveal immune impairment linked to lung cancer risk.
Genome Medicine, 16 (1).
pp. 1-19.
Springer Nature.
ISSN 1756-994X
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s13073-024-01317-4.pdf Bereitstellung unter der CC-Lizenz: Creative Commons Attribution. Download (3MB) |
Abstract
[Artikel-Nr.: 54] Background: Lung cancer is the leading cause of cancer-related death in the world. In contrast to many other cancers, a direct connection to modifiable lifestyle risk in the form of tobacco smoke has long been established. More than 50% of all smoking-related lung cancers occur in former smokers, 40% of which occur more than 15 years after smoking cessation. Despite extensive research, the molecular processes for persistent lung cancer risk remain unclear. We thus set out to examine whether risk stratification in the clinic and in the general population can be improved upon by the addition of genetic data and to explore the mechanisms of the persisting risk in former smokers. Methods: We analysed transcriptomic data from accessible airway tissues of 487 subjects, including healthy volunteers and clinic patients of different smoking statuses. We developed a computational model to assess smoking-associated gene expression changes and their reversibility after smoking is stopped, comparing healthy subjects to clinic patients with and without lung cancer. Results: We find persistent smoking-associated immune alterations to be a hallmark of the clinic patients. Integrating previous GWAS data using a transcriptional network approach, we demonstrate that the same immune- and interferon-related pathways are strongly enriched for genes linked to known genetic risk factors, demonstrating a causal relationship between immune alteration and lung cancer risk. Finally, we used accessible airway transcriptomic data to derive a non-invasive lung cancer risk classifier. Conclusions: Our results provide initial evidence for germline-mediated personalized smoke injury response and risk in the general population, with potential implications for managing long-term lung cancer incidence and mortality.
| Item Type: | Article |
| Creators: | Creators Email ORCID ORCID Put Code de Biase, Maria Stella UNSPECIFIED UNSPECIFIED UNSPECIFIED Massip, Florian UNSPECIFIED UNSPECIFIED UNSPECIFIED Wei, Tzu-Ting UNSPECIFIED UNSPECIFIED UNSPECIFIED Stark, Rory UNSPECIFIED UNSPECIFIED UNSPECIFIED Stone, Amanda UNSPECIFIED UNSPECIFIED UNSPECIFIED Gladwell, Amy UNSPECIFIED UNSPECIFIED UNSPECIFIED O’Reilly, Martin UNSPECIFIED UNSPECIFIED UNSPECIFIED de Santiago, Ines UNSPECIFIED UNSPECIFIED UNSPECIFIED Markowetz, Florian UNSPECIFIED UNSPECIFIED UNSPECIFIED Ponder, Bruce A. J. UNSPECIFIED UNSPECIFIED UNSPECIFIED |
| URN: | urn:nbn:de:hbz:38-815331 |
| Identification Number: | 10.1186/s13073-024-01317-4 |
| Journal or Publication Title: | Genome Medicine |
| Volume: | 16 |
| Number: | 1 |
| Page Range: | pp. 1-19 |
| Number of Pages: | 19 |
| Date: | 8 April 2024 |
| Publisher: | Springer Nature |
| ISSN: | 1756-994X |
| Language: | English |
| Faculty: | Faculty of Medicine |
| Divisions: | Faculty of Medicine > Weitere > Centrum für integrierte Onkologie (CIO) |
| Subjects: | Medical sciences Medicine |
| ['eprint_fieldname_oa_funders' not defined]: | Publikationsfonds UzK |
| Refereed: | Yes |
| URI: | http://kups.ub.uni-koeln.de/id/eprint/81533 |
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https://orcid.org/0000-0002-7325-9908