{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Dubourg A"],"funding":["Ligue Contre le Cancer Vienne et Deux-Sèvres"],"pagination":["2791"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11352811"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(16)"],"pubmed_abstract":["<h4>Background</h4>A major issue in Chronic Myeloid Leukemia (CML) is the persistence of quiescent leukemia stem cells (LSCs) in the hematopoietic niche under tyrosine kinase inhibitor (TKI) treatment.<h4>Results</h4>Here, using CFSE sorting, we show that low-proliferating CD34+ cells from CML patients in 3D co-culture hide under HS27A stromal cells during TKI treatment-a behavior less observed in untreated cells. Under the same conditions, Ba/F3p210 cells lose their spontaneous motility. In CML CD34+ and Ba/F3p210 cells, while Rac1 is completely inhibited by TKI, RhoA remains activated but is unable to signal to ROCK. Co-incubation of Ba/F3p210 cells with TKI, SKF-96365 (a calcium channel inhibitor), and EGF restores myosin II activation and amoeboid motility to levels comparable to untre"],"journal":["Cancers"],"pubmed_title":["SKF-96365 Expels Tyrosine Kinase Inhibitor-Treated CML Stem and Progenitor Cells from the HS27A Stromal Cell Niche in a RhoA-Dependent Mechanism."],"pmcid":["PMC11352811"],"funding_grant_id":["None (Nicolas Bourmeyster)"],"pubmed_authors":["Bourmeyster N","Harnois T","Dubourg A","Cousin L","Constantin B"],"additional_accession":[]},"is_claimable":false,"name":"SKF-96365 Expels Tyrosine Kinase Inhibitor-Treated CML Stem and Progenitor Cells from the HS27A Stromal Cell Niche in a RhoA-Dependent Mechanism.","description":"<h4>Background</h4>A major issue in Chronic Myeloid Leukemia (CML) is the persistence of quiescent leukemia stem cells (LSCs) in the hematopoietic niche under tyrosine kinase inhibitor (TKI) treatment.<h4>Results</h4>Here, using CFSE sorting, we show that low-proliferating CD34+ cells from CML patients in 3D co-culture hide under HS27A stromal cells during TKI treatment-a behavior less observed in untreated cells. Under the same conditions, Ba/F3p210 cells lose their spontaneous motility. In CML CD34+ and Ba/F3p210 cells, while Rac1 is completely inhibited by TKI, RhoA remains activated but is unable to signal to ROCK. Co-incubation of Ba/F3p210 cells with TKI, SKF-96365 (a calcium channel inhibitor), and EGF restores myosin II activation and amoeboid motility to levels comparable to untre","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Aug","modification":"2026-04-07T20:21:23.919Z","creation":"2025-04-06T13:43:39.979Z"},"accession":"S-EPMC11352811","cross_references":{"pubmed":["39199564"],"doi":["10.3390/cancers16162791"]}}