Ontology highlight
ABSTRACT: Background
Chronic-Phase Chronic Myeloid Leukemia (C-PCML) is defined by the presence of the BCR-ABL1 fusion gene, which encodes a tyrosine kinase protein that drives the uncontrolled proliferation and survival of leukemic stem cells (LSCs). Nilotinib, a tyrosine kinase inhibitor, targets the activity of BCR-ABL1 by reducing aberrant signaling pathways, which drive the regeneration of LSCs. Despite nilotinib's action, a population of resilient LSCs persist in the bone marrow (BM) and can indeed drive relapse and progression in CML patients.Methods
Our study investigated the gene expression profiling (GEP) of BM CD34+/lin- cells from 79 CP-CML patients at diagnosis, compared to the BM CD34+/lin- cells from the same patients after 12 months of nilotinib treatment and t
SUBMITTER: Trojani A
PROVIDER: S-EPMC11940473 | biostudies-literature | 2025 Mar
REPOSITORIES: biostudies-literature