{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE329nnn/GSE329964/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE329964"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Nasopharyngeal Swab Transcriptomics Reveals Distinct Pathogenic Mechanisms in Adenoid Hypertrophy and Allergic Rhinitis","description":"Adenoid hypertrophy (AH) frequently coexists with allergic rhinitis (AR) in children, yet the molecular mechanisms underlying this comorbidity remain unclear. Using nasopharyngeal swab-based transcriptomics—enabling inclusion of healthy pediatric controls previously precluded by ethical constraints—this study aimed to characterize the transcriptomic landscape of AH with and without AR and identify disease-specific pathogenic pathways. We performed RNA sequencing on nasopharyngeal swab samples from 25 pediatric subjects, including healthy controls (HC, n=6), children with AH (n=10), and children with AH accompanied by AR (AHAR, n=9). This study underscores the need for individualized therapeutic strategies tailored to distinct disease mechanisms in pediatric upper airway disorders.","dates":{"publication":"2026/08/19"},"accession":"GSE329964","cross_references":{"GSM":["GSM9714135","GSM9714134","GSM9714137","GSM9714136","GSM9714139","GSM9714138","GSM9714131","GSM9714130","GSM9714133","GSM9714132","GSM9714124","GSM9714123","GSM9714126","GSM9714125","GSM9714128","GSM9714127","GSM9714129","GSM9714140","GSM9714142","GSM9714120","GSM9714141","GSM9714144","GSM9714122","GSM9714121","GSM9714143"],"GPL":["24676"],"GSE":["329964"],"taxon":["Homo sapiens"],"PMID":["[42591655]"]}}