ArticleBMC cancer2024
Beyond tobacco: genomic disparities in lung cancer between smokers and never-smokers.
Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- Ginkgetin inhibits non-small cell lung cancer via the HSP90-AKT signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Sex Differences in Cancer Immunotherapy-Clinical Evidence and Mechanisms With a Focus on NSCLC.Immunological reviews · 2026Review
- The Landscape of Clinical Trials in Never-Smoker Non-Small-Cell Lung Cancer: Registered Evidence and Persistent Gaps.Cancers · 2026Article
- Maintaining momentum: the history and future of lung cancer disparities in the United States.Frontiers in oncology · 2026Review
- CLIC6 and ANLN: novel exosome-related prognostic markers and therapeutic targets in lung adenocarcinoma.Frontiers in immunology · 2026Article
- Pharmacogenetic landscape of epidermal growth factor receptor mutations in Kurdish non-small cell lung cancer patients: implications for precision oncology.Ecancermedicalscience · 2026Article
- Survival patterns and mutation profiles in never- and light-smokers with stage IV NSCLC.BMC cancer · 2025Article
- Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia associated with lung adenocarcinoma: clinical, pathological and oncological outcomes from a multicentre analysis.ERJ open research · 2025Article
- Lung cancer in non-smoking women (LCINSW): from risk factors to precision therapy.Cancer metastasis reviews · 2025Review
- A cost-effectiveness analysis model of actionable genomic alteration testing strategies incorporating different modalities and sizes of next-generation sequencing panels in non-small-cell lung cancer.Therapeutic advances in medical oncology · 2025Article
- Downregulation of tRNA methyltransferase FTSJ1 by PM2.5 promotes glycolysis and malignancy of NSCLC via facilitating PGK1 expression and translation.Cell death & disease · 2024Article
- SLC7A11 Expression Is Up-Regulated in HPV- and Tobacco-Associated Lung Cancer.International journal of molecular sciences · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
34 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTobacco use is one of the main risk factors for Lung Cancer (LC) development. However, about 10-20% of those diagnosed with the disease are never-smokers. For Non-Small Cell Lung Cancer (NSCLC) there are clear differences in both the clinical presentation and the tumor genomic profiles between smokers and never-smokers. For example, the Lung Adenocarcinoma (LUAD) histological subtype in never-smokers is predominately found in young women of European, North American, and Asian descent. While the clinical presentation and tumor genomic profiles of smokers have been widely examined, never-smokers are usually underrepresented, especially those of a Latin American (LA) background. In this work, we characterize, for the first time, the difference in the genomic profiles between smokers and never-smokers LC patients from Chile.
methodsWe conduct a comparison by smoking status in the frequencies of genomic alterations (GAs) including somatic mutations and structural variants (fusions) in a total of 10 clinically relevant genes, including the eight most common actionable genes for LC (EGFR, KRAS, ALK, MET, BRAF, RET, ERBB2, and ROS1) and two established driver genes for malignancies other than LC (PIK3CA and MAP2K1). Study participants were grouped as either smokers (current and former, n = 473) or never-smokers (n = 200) according to self-report tobacco use at enrollment.
resultsOur findings indicate a higher overall GA frequency for never-smokers compared to smokers (58 vs. 45.7, p-value < 0.01) with the genes EGFR, KRAS, and PIK3CA displaying the highest prevalence while ERBB2, RET, and ROS1 the lowest. Never-smokers present higher frequencies in seven out of the 10 genes; however, smokers harbor a more complex genomic profile. The clearest differences between groups are seen for EGFR (15.6 vs. 21.5, p-value: < 0.01), PIK3CA (6.8 vs 9.5) and ALK (3.2 vs 7.5) in favor of never-smokers, and KRAS (16.3 vs. 11.5) and MAP2K1 (6.6 vs. 3.5) in favor of smokers. Alterations in these genes are comprised almost exclusively by somatic mutations in EGFR and mainly by fusions in ALK, and only by mutations in PIK3CA, KRAS and MAP2K1.
conclusionsWe found clear differences in the genomic landscape by smoking status in LUAD patients from Chile, with potential implications for clinical management in these limited-resource settings.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.