{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE326nnn/GSE326046/"]},"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=GSE326046"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Breast implant associated anaplastic large cell lymphoma is a heterogeneous T cell disease with active pro-tumour cross-talk and immune suppression","description":"Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) is a rare T cell lymphoma in women with textured implants. Little is known about the cell of origin (COO) and whether the tumour immune microenvironment (TIME) is critical for BIA-ALCL survival. Single-cell RNA sequencing revealed BIA-ALCL cells were heterogeneous with unique gene profiles per patient and signature genes BATF3, SERPINS, TNFSFR8, and IL2RA. The COO is a CD4+ or CD8+ memory T cell identified through rearranged TCR and gene expression. The BIA-ALCL TIME included distinct myeloid clusters, dendritic cells (DCs), and monocytes, which may support lymphoma cells. Cytokines IL-13, IL-10, TNF and secretory PDL1 were increased in BIA-ALCL seroma, indicating an immunosuppressive TIME. Interactome analysis revealed a complex network among lymphoma cells, dominated by IL-13, IL-10, and TNF members. Endogenous CD8+ T cells exhibit higher checkpoint expression than benign seromas. No clonal relationship exists between BIA-ALCL and endogenous T cells. Tissue-archetype and gene-expression analysis revealed T-cell exclusion and immunosuppressive TIME in invasive disease. In summary, BIA-ALCL cells are diverse and differ from other CD4+ T cell lymphomas. The TIME provides immunosuppressive signals to activated/exhausted T cells and homeostatic signals that promote BIA-ALCL proliferation. These new findings may offer novel therapeutic targets for advanced disease patients.","dates":{"publication":"2026/09/03"},"accession":"GSE326046","cross_references":{"GSM":["GSM9619758","GSM9619759","GSM9619778","GSM9619756","GSM9619757","GSM9619779","GSM9619776","GSM9619754","GSM9619777","GSM9619755","GSM9619774","GSM9619775","GSM9619753","GSM9619772","GSM9619773","GSM9619770","GSM9619771","GSM9619769","GSM9619767","GSM9619768","GSM9619765","GSM9619766","GSM9619763","GSM9619764","GSM9619761","GSM9619762","GSM9619760","GSM9619780"],"GPL":["20301","30173"],"GSE":["326046"],"taxon":["Homo sapiens"],"PMID":["[42533032]"]}}