Ontology highlight
ABSTRACT: Background
Chronic myeloid leukemia stem cells (CML-LSCs), which exhibit resistance to tyrosine kinase inhibitors (TKIs), are the leading cause of treatment failure and recurrence in chronic myeloid leukemia (CML). This highlights the urgent need for novel therapies aimed at eliminating these CML-LSCs. Chimeric antigen receptor macrophages (CAR-M) not only perform phagocytosis on target cells but also function as antigen-presenting cells, thereby activating the anti-tumor immune response.CD26 (dipeptidyl peptidase 4, DPP IV) is abundantly expressed in CML-LSCs and functions as a tumor-specific antigen (TSA) in CAR-M treatment. The purpose of this study is to evaluate CAR-M's efficacy in targeting CD26-positive CML cells and to develop a novel strategy for CML treatment.Methods<
SUBMITTER: Guoyun J
PROVIDER: S-EPMC11823019 | biostudies-literature | 2025 Feb
REPOSITORIES: biostudies-literature