ArticleJournal of the National Cancer Center2026
Exploring the genetic overlap between obstructive sleep apnea and prostate cancer.
Article in Journal of the National Cancer Center, 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
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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.
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Who cites it
1 citing paper in PubMed.
- Work at night, sleep loss, fatigue, and cancer: exposure, mechanisms, and epidemiological evidence.Journal of the National Cancer Center · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Studies have highlighted the possible association between obstructive sleep apnea (OSA) and an increased risk of cancer, especially prostate cancer. However, the extent to which genes that are found in both conditions contribute to their comorbidity is unclear. The aim of this study was to identify risk genes present in both conditions. Methods: Genes common to both conditions were identified and the statistical significance of the overlap was assessed. Pathway enrichment and protein-protein interaction analyses were performed on the intersecting gene set. Results: There were 68 common genes, more than would be expected by random effects. This intersect list was associated mainly with hypoxia, apoptosis, oxidative stress, and cell cycle proliferation, or cell damage. A 17-node protein interaction network highlighted key proteins involved in these enriched pathways. Conclusions: The results of the analysis indicated a common molecular etiology underlying this comorbidity. Proliferation, apoptosis, and hypoxia pathways were significantly enriched among the overlapping genes, suggesting their role in pathophysiological processes.
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