Evidence map›Paper›PMID 41665314›Full record

ArticleInternational journal of cancer2026

Somatic copy number variation as a prognostic marker for recurrence in never-smokers with early-stage lung adenocarcinoma.

Stijn Vanstraelen, Allison Reiner, Kay See Tan, Brooke Mastrogiacomo, Elizabeth G Dunne, Cameron N Fick, Joseph Dycoco, Aqib Abass, Matthew J Bott, Francisco Sanchez-Vega and 2 more

Abstract read
In one paragraph

Article in International journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Stijn VanstraelenThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Allison ReinerDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Kay See TanDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Brooke MastrogiacomoDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Elizabeth G DunneThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Cameron N FickThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Joseph DycocoThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Aqib AbassDepartment of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Matthew J BottThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Francisco Sanchez-VegaDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
David R JonesThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Gaetano RoccoThoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA.ORCID https://orcid.org/0000-0003-4150-8604

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Lung cancer in never-smokers has a distinct genomic profile characterized by lower tumor mutational burden, more tumor-promoting mutations, and fewer somatic copy number variations (CNVs) compared to smokers. While CNVs are linked to poor outcomes in advanced-stage cancer, their role in early-stage lung adenocarcinoma remains unclear. In a cohort of 210 treatment-naive never-smokers with early-stage lung adenocarcinoma, hierarchical clustering of CNVs identified three distinct groups: CNV low (n = 86 [41%]), CNV moderate (n = 75 [36%]), and CNV high (n = 49 [23%]). CNV low tumors had minimal CNV burden, CNV moderate tumors exhibited loss of heterozygosity in chromosomes 3, 9, 13, 15, and 18, and CNV high tumors showed genome-wide amplifications and whole-genome doubling. Recurrence occurred in 42 patients (20%), with a significantly lower 5-year cumulative incidence in the CNV low group (14% [95% CI, 7%-25%]) compared to the CNV moderate (31% [95% CI, 18%-44%]) and CNV high group (48% [95% CI, 27%-66%]) (p = .004). Adjusted hazard ratios for recurrence were 2.30 (p = .074) and 2.65 (p = .037) for CNV moderate and CNV high, respectively. These findings suggest CNV status is an independent predictor of recurrence, with CNV low tumors being associated with the most favorable prognosis.

Indexed as

AdenocarcinomaAdenocarcinoma of LungBiomarkers, TumorDNA Copy Number VariationsLung NeoplasmsNeoplasm Recurrence, LocalAgedFemaleHumansLoss of HeterozygosityMaleMiddle AgedNeoplasm StagingNon-SmokersPrognosisBiomarkers, Tumorcopy number variationearly‐stagelung cancernever‐smokersrecurrence

Identifiers

PMID41665314
PMCPMC13479557

What OpenQuestion holds

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Registered trials

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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.