{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE292nnn/GSE292700/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":[" Other","Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE292700"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Molecular architecture of the tumor microenvironment caused by BRCA1 and BRCA2 somatic mutations in human lung adenocarcinoma","description":"We have employed a single cell sequencing approach using 10x Genomics scRNAseq and scTCR-seq to study the heterogeneity and molecular architecture of tumor microenvironment (TME) caused by BRCA1 and BRCA2 somatic mutations in lung adenocarcinoma (LUAD). LUADs are considered to be a heterogeneity population in the lung epithelium. Homologous recombination repair (HRR) deficiency has been linked to enhanced immunotherapy responses in non-small cell lung cancer patients. The HRR genes BRCA1 and BRCA2 are key regulators of DNA repair, yet their impact on the TME in LUAD remains unclear.This study provides a comprehensive characterization of the BRCA-mutant TME in LUAD patients, uncovering distinct immune response mechanisms and potential therapeutic strategies. These findings enhance our understanding of BRCA1/2-driven molecular architecture and offer novel insights into improving therapy efficacy in LUAD.","dates":{"publication":"2026/05/07"},"accession":"GSE292700","cross_references":{"GSM":["GSM8863840","GSM8863841","GSM8863830","GSM8863839","GSM8863837","GSM8863838","GSM8863835","GSM8863836","GSM8863833","GSM8863834","GSM8863831","GSM8863832"],"GPL":["34284"],"GSE":["292700"],"taxon":["Homo sapiens"]}}