Exploring the genetic overlap between obstructive sleep apnea and prostate cancer.
[BACKGROUND] Studies have highlighted the possible association between obstructive sleep apnea (OSA) and an increased risk of cancer, especially prostate cancer.
APA
Porcacchia AS, Moyses-Oliveira M, et al. (2026). Exploring the genetic overlap between obstructive sleep apnea and prostate cancer.. Journal of the National Cancer Center, 6(2), 204-210. https://doi.org/10.1016/j.jncc.2025.11.004
MLA
Porcacchia AS, et al.. "Exploring the genetic overlap between obstructive sleep apnea and prostate cancer.." Journal of the National Cancer Center, vol. 6, no. 2, 2026, pp. 204-210.
PMID
42007214
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.
[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.