Tyrosine Kinase Inhibitor Discontinuation in Chronic Myeloid Leukemia: Strategies to Optimize Success and New Directions.
Delphine ReaSofiane FodilEtienne LenglineEmmanuel RaffouxJean-Michel CayuelaPublished in: Current hematologic malignancy reports (2024)
Patients in treatment-free remission are a minority, and it is believed that some may still retain a reservoir of leukemic stem cells; thus, whether they can be considered as truly cured is uncertain. Strengthening BCR::ABL1 inhibition increases deep molecular responses but is not sufficient to improve treatment-free remission, and we lack biomarkers to identify and specifically target residual cells with aggressive potential. Another level of complexity resides in the intra- and inter-patient clonal heterogeneity of minimal residual disease and characteristics of the bone marrow environment. Finding determinants of deep molecular responses achievement and elucidating varying biological mechanisms enabling either post-tyrosine kinase inhibitor chronic myeloid leukemia control or relapse may help develop innovative and safe therapies. In the light of the increasing prevalence of CML, targeting the residual leukemic stem cell pool is thought to be the key.
Keyphrases
- chronic myeloid leukemia
- stem cells
- bone marrow
- end stage renal disease
- ejection fraction
- acute myeloid leukemia
- newly diagnosed
- induced apoptosis
- risk factors
- chronic kidney disease
- single cell
- mesenchymal stem cells
- cell proliferation
- rheumatoid arthritis
- ulcerative colitis
- single molecule
- cell therapy
- systemic lupus erythematosus
- risk assessment
- cell death