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Asthma, chronic obstructive pulmonary disease (COPD) and obstructive sleep apnoea (OSA) are the most common respiratory disorders worldwide. Given demographic and environmental changes, prevalence for each is likely to increase. Although exact numbers are not known, based on chance alone, many people will be affected by both lower airways obstruction and concomitant upper airway obstruction during sleep. Some recent studies suggest that there is a reciprocal interaction, with chronic lung disease predisposing to OSA, and OSA worsening control and outcomes from chronic lung disease. Thus, the combination of wake and sleep respiratory disorders can create an overlap syndrome with unique pathophysiological, diagnostic and therapeutic concerns. Although much work needs to be done, given the above, Respirologists, Sleep Medicine and Primary Care providers must be vigilant for overlap syndromes. Accurate diagnosis of, for example, OSA as a cause of nocturnal symptoms in a patient with asthma is likely to limit further ineffective titration of medications for asthma. Moreover, prompt treatment of OSA in the overlap syndromes will not only offer symptomatic benefit of OSA, but also improve symptoms and healthcare resource utilization attributable to obstructive lung disease, and in COPD, it may reduce mortality.
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http://dx.doi.org/10.1111/resp.13107 | DOI Listing |
Stem Cell Rev Rep
September 2025
Department of Medical Genetics and Prenatal Diagnostics, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
The emergence of organoid models has significantly bridged the gap between traditional cell cultures/animal models and authentic human disease states, particularly for genetic disorders, where their inherent genetic fidelity enables more biologically relevant research directions and enhances translational validity. This review systematically analyzes established organoid models of genetic diseases across organs (e.g.
View Article and Find Full Text PDFJ Cancer Res Clin Oncol
September 2025
Inner Mongolia Medical University Affiliated Hospital, Hohhot, 010030, Inner Mongolia, China.
Purpose: Lung cancer is currently the most common malignant tumor worldwide and one of the leading causes of cancer-related deaths, posing a serious threat to human health. MicroRNAs (miRNAs) are a class of endogenous non-coding small RNA molecules that regulate gene expression and are involved in various biological processes associated with lung cancer. Understanding the mechanisms of lung carcinogenesis and detecting disease biomarkers may enable early diagnosis of lung cancer.
View Article and Find Full Text PDFMol Syst Biol
September 2025
Department of Medicine, Division of Cardiovascular Medicine, Stanford University, Stanford, CA, USA.
Vascular sites have distinct susceptibility to atherosclerosis and aneurysm, yet the epigenomic and transcriptomic underpinning of vascular site-specific disease risk is largely unknown. Here, we performed single-cell chromatin accessibility (scATACseq) and gene expression profiling (scRNAseq) of mouse vascular tissue from three vascular sites. Through interrogation of epigenomic enhancers and gene regulatory networks, we discovered key regulatory enhancers to not only be cell type, but vascular site-specific.
View Article and Find Full Text PDFNat Genet
September 2025
Cancer Research UK Lung Cancer Centre of Excellence, University College London Cancer Institute, London, UK.
Aberrant DNA methylation has been described in nearly all human cancers, yet its interplay with genomic alterations during tumor evolution is poorly understood. To explore this, we performed reduced representation bisulfite sequencing on 217 tumor and matched normal regions from 59 patients with non-small cell lung cancer from the TRACERx study to deconvolve tumor methylation. We developed two metrics for integrative evolutionary analysis with DNA and RNA sequencing data.
View Article and Find Full Text PDFBr J Cancer
September 2025
Department of Genetics, Institut Curie, PSL Research University, Paris, France.
Background: Identifying molecular alterations specific to advanced lung adenocarcinomas could provide insights into tumour progression and dissemination mechanisms.
Method: We analysed tumour samples, either from locoregional lesions or distant metastases, from patients with advanced lung adenocarcinoma from the SAFIR02-Lung trial by targeted sequencing of 45 cancer genes and comparative genomic hybridisation array and compared them to early tumours samples from The Cancer Genome Atlas.
Results: Differences in copy-number alterations frequencies suggest the involvement in tumour progression of LAMB3, TNN/KIAA0040/TNR, KRAS, DAB2, MYC, EPHA3 and VIPR2, and in metastatic dissemination of AREG, ZNF503, PAX8, MMP13, JAM3, and MTURN.