{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE332nnn/GSE332556/"]},"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=GSE332556"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Tumor-associated Macrophage GnT-V Enhances Sensitivity to Antitumor Immunotherapy through Branched N-Glycosylation to Promote M1 Polarization","description":"Tumor tissues with differential sensitivity to immunotherapy were sequenced using The DNBelab C4 /DNBelab TaiM4 Series Single-Cell Library Prep Set (MGI) was used for sequencing and sequenced on the DNBSEQ-T7 sequencer with pair-end sequencing. Immunotherapy based on immune checkpoint inhibitors (ICIs) has become one of the most successful clinical treatment strategies and has marked a milestone in the field of cancer therapy. Regrettably, the complex immunosuppressive network within the tumor microenvironment (TME), characterized by imbalanced immune cell subsets and suppressed immune cell function, represents a major cause of ICI treatment failure. This study, through single-cell analysis, provides mechanistic insights into TAM polarization and establishes the therapeutic feasibility of targeting this regulatory axis, thereby introducing a novel treatment strategy to benefit cancer patients.","dates":{"publication":"2026/05/25"},"accession":"GSE332556","cross_references":{"GSM":["GSM9750658","GSM9750659"],"GPL":["29480"],"GSE":["332556"],"taxon":["Homo sapiens"]}}