ArticleGenome medicine2026
Somatic copy number alterations profiling in non-small cell lung cancer and their correlation with clinical efficacy in first-line treatment.
Article in Genome medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors.
Funding
Abstract
backgroundImmune checkpoint inhibitors (ICI) are the current standard-of-care first-line treatment for advanced non-small cell lung cancer (NSCLC) without actionable genomic alterations. Yet some patients do not achieve clinical benefit, underscoring the need for predictive biomarkers. High burden of somatic copy number alterations (SCNAs), including chromosomal arm- and whole-chromosome-level changes, has been linked to reduced benefit from ICI. However, its predictive value in chemotherapy or combination regimens remains largely unexplored. Here, we evaluated SCNA burden across multiple first-line treatment strategies in a cohort of patients with NSCLC.
methodsWe assembled a cohort of 258 patients with advanced NSCLC treated with first-line ICI (n = 86), chemotherapy (ChT; n = 107), or a combination of both (ICI + ChT; n = 65). Tumor DNA was analyzed using shallow whole-genome sequencing (sWGS). SCNA burden was quantified as the fraction of the genome altered at the chromosomal arm and whole-chromosome level (FGAa+c). We performed Kaplan-Meier and Cox regression analyses to assess its value across treatment groups. Additionally, we examined associations between recurrent SCNAs, clinical efficacy, and tumor microenvironment (TME) features using data from The Cancer Genome Atlas (TCGA).
resultsHigh SCNA burden (FGAa+c > 4.25) was significantly associated with diminished progression-free survival (PFS) in patients treated with ICI (p-val = 0.0097). In contrast, FGAa+c did not associate with PFS following ChT (p-val = 0.9566) or ICI + ChT (p-val = 0.6472). Specific SCNAs in chromosome 9p were independently associated with reduced ICI benefit (p-val = 0.0469), even after adjusting for FGAa+c (p-val = 0.0229). This SCNA was negatively associated with immune infiltration in the TME and was linked to differences in the immune cell type composition.
conclusionsOur findings suggest that FGAa+c may help identify patients with differential benefit from ICI monotherapy in advanced NSCLC, without evidence of a prognostic role in other treatment modalities. These findings warrant prospective studies to validate its clinical utility in guiding treatment selection.
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.