<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE326nnn/GSE326046/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE326046</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Breast implant associated anaplastic large cell lymphoma is a heterogeneous T cell disease with active pro-tumour cross-talk and immune suppression</name><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.</description><dates><publication>2026/09/03</publication></dates><accession>GSE326046</accession><cross_references><GSM>GSM9619758</GSM><GSM>GSM9619759</GSM><GSM>GSM9619778</GSM><GSM>GSM9619756</GSM><GSM>GSM9619757</GSM><GSM>GSM9619779</GSM><GSM>GSM9619776</GSM><GSM>GSM9619754</GSM><GSM>GSM9619777</GSM><GSM>GSM9619755</GSM><GSM>GSM9619774</GSM><GSM>GSM9619775</GSM><GSM>GSM9619753</GSM><GSM>GSM9619772</GSM><GSM>GSM9619773</GSM><GSM>GSM9619770</GSM><GSM>GSM9619771</GSM><GSM>GSM9619769</GSM><GSM>GSM9619767</GSM><GSM>GSM9619768</GSM><GSM>GSM9619765</GSM><GSM>GSM9619766</GSM><GSM>GSM9619763</GSM><GSM>GSM9619764</GSM><GSM>GSM9619761</GSM><GSM>GSM9619762</GSM><GSM>GSM9619760</GSM><GSM>GSM9619780</GSM><GPL>20301</GPL><GPL>30173</GPL><GSE>326046</GSE><taxon>Homo sapiens</taxon><PMID>[42533032]</PMID></cross_references></HashMap>