Ontology highlight
ABSTRACT: Background
Chronic myeloid leukemia (CML) is a clonal malignancy propelled by the BCR::ABL1 fusion gene originating from the Philadelphia chromosome. This gene activates ABL tyrosine kinase, which enhances the survival of leukemic cells. Although tyrosine kinase inhibitors (TKIs) have significantly advanced the treatment of CML, resistance to these inhibitors presents a substantial hurdle. Consequently, novel therapeutic strategies targeting resistance mechanisms independent of BCR::ABL1 are urgently needed.Methods
This study investigated the potential impact of combining WEE1 inhibitors, particularly MK-1775, with vitamin K2 (VK2) in treating CML. To analyze differentially expressed and spliced transcripts in CML, we examined mRNA profiles from peripheral blo
SUBMITTER: Okabe S
PROVIDER: S-EPMC12394061 | biostudies-literature | 2025 Oct
REPOSITORIES: biostudies-literature