<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/GSE284nnn/GSE284668/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</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=GSE284668</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>S100A4 inhibition alters pre-metastatic niche formation in 4T1 lung metastasis model</name><description>Cancer metastasis poses a major clinical challenge and is responsible for ~90% of cancer-associated deaths. However, progress in treating metastatic disease is limited. S100A4/FSP1 has long been associated with cancer metastasis, including breast cancer. In this study, we report preclinical efficacy data of a novel S100A4 blocking antibody that suppresses breast cancer metastasis. 4T1 and MMTV-PyMT breast cancer metastasis to the lung is greatly attenuated by S100A4 blocking antibody treatment. Immunohistochemistry analysis shows that neutrophil infiltration is significantly reduced in the anti-S100A4 treated mice. Single-cell RNA sequence analysis of the premetastatic niche treated with either isotype control or anti-S100A4 antibody from the 4T1 model show that NK and T cell activation in the lung. In this study, we report that S100A4 promotes premetastatic niche formation by promoting neutrophil infiltration and suppressing the function of cytotoxic NK and T cells.</description><dates><publication>2026/05/15</publication></dates><accession>GSE284668</accession><cross_references><GSM>GSM8690315</GSM><GSM>GSM8690316</GSM><GPL>28457</GPL><GSE>284668</GSE><taxon>Mus musculus</taxon><PMID>[41962622]</PMID></cross_references></HashMap>