{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lai X"],"funding":["National Science Foundation of China | National Natural Science Foundation of China-Yunnan Joint Fund","National Science Foundation of China | National Natural Science Foundation of China-Yunnan Joint Fund (NSFC-Yunnan Joint Fund)","National Natural Science Foundation of China","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["45"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11055880"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(1)"],"pubmed_abstract":["Patients with chronic myeloid leukemia (CML) who receive tyrosine kinase inhibitors (TKIs) have been known to achieve treatment-free remission (TFR) upon discontinuing treatment. However, the underlying mechanisms of this phenomenon remain incompletely understood. This study aims to elucidate the mechanism of TFR in CML patients, focusing on the feedback interaction between leukemia stem cells and the bone marrow microenvironment. We have developed a mathematical model to explore the interplay between leukemia stem cells and the bone marrow microenvironment, allowing for the simulation of CML progression dynamics. Our proposed model reveals a dichotomous response following TKI discontinuation, with two distinct patient groups emerging: one prone to early molecular relapse and the other cap"],"journal":["NPJ systems biology and applications"],"pubmed_title":["Computational modeling reveals key factors driving treatment-free remission in chronic myeloid leukemia patients."],"pmcid":["PMC11055880"],"funding_grant_id":["12171478","12331018","11831015"],"pubmed_authors":["Lai X","Lei J","Zhang H","Jiao X"],"additional_accession":[]},"is_claimable":false,"name":"Computational modeling reveals key factors driving treatment-free remission in chronic myeloid leukemia patients.","description":"Patients with chronic myeloid leukemia (CML) who receive tyrosine kinase inhibitors (TKIs) have been known to achieve treatment-free remission (TFR) upon discontinuing treatment. However, the underlying mechanisms of this phenomenon remain incompletely understood. This study aims to elucidate the mechanism of TFR in CML patients, focusing on the feedback interaction between leukemia stem cells and the bone marrow microenvironment. We have developed a mathematical model to explore the interplay between leukemia stem cells and the bone marrow microenvironment, allowing for the simulation of CML progression dynamics. Our proposed model reveals a dichotomous response following TKI discontinuation, with two distinct patient groups emerging: one prone to early molecular relapse and the other cap","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2026-07-15T14:04:55.665Z","creation":"2026-07-05T03:12:26.286Z"},"accession":"S-EPMC11055880","cross_references":{"pubmed":["38678088"],"doi":["10.1038/s41540-024-00370-4"]}}