{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Laplante P"],"funding":["Ligue Contre le Cancer","Ministère de l'Enseignement Supérieur et de la Recherche","Philanthropia Foundation","Campus France"],"pagination":["101145"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11905862"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["62"],"pubmed_abstract":["Mismatch repair deficiency leads to high mutation rates and microsatellite instability (MSI-H), associated with immune infiltration and responsiveness to immunotherapies. In early stages, MSI-H tumors generally have a better prognosis and lower metastatic potential than microsatellite-stable (MSS) tumors, especially in colorectal cancer. However, in advanced stages, MSI-H tumors lose this survival advantage for reasons that remain unclear. We developed a syngeneic mouse model of MSI cancer by knocking out the MMR gene Msh2 in the metastatic 4T1 breast cancer cell line. This model mirrored genomic features of MSI-H cancers and showed reduction in metastatic incidence compared to their MSS counterparts. In MSI-H tumors, we observed an enrichment of immune gene-signatures that negatively corr"],"journal":["Neoplasia (New York, N.Y.)"],"pubmed_title":["Effect of MisMatch repair deficiency on metastasis occurrence in a syngeneic mouse model."],"pmcid":["PMC11905862"],"funding_grant_id":["12551"],"pubmed_authors":["Rosa R","Kannouche PL","Laplante P","Pouvelle C","Goulas J","Nebot-Bral L","Nikolaev S","Silvin A"],"additional_accession":[]},"is_claimable":false,"name":"Effect of MisMatch repair deficiency on metastasis occurrence in a syngeneic mouse model.","description":"Mismatch repair deficiency leads to high mutation rates and microsatellite instability (MSI-H), associated with immune infiltration and responsiveness to immunotherapies. In early stages, MSI-H tumors generally have a better prognosis and lower metastatic potential than microsatellite-stable (MSS) tumors, especially in colorectal cancer. However, in advanced stages, MSI-H tumors lose this survival advantage for reasons that remain unclear. We developed a syngeneic mouse model of MSI cancer by knocking out the MMR gene Msh2 in the metastatic 4T1 breast cancer cell line. This model mirrored genomic features of MSI-H cancers and showed reduction in metastatic incidence compared to their MSS counterparts. In MSI-H tumors, we observed an enrichment of immune gene-signatures that negatively corr","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2026-06-03T02:33:11.248Z","creation":"2025-04-04T00:32:39.604Z"},"accession":"S-EPMC11905862","cross_references":{"pubmed":["39985912"],"doi":["10.1016/j.neo.2025.101145"]}}