ABCG2 in Acute Myeloid Leukemia: Old and New Perspectives.
Daniela DamianiMario TiribelliPublished in: International journal of molecular sciences (2023)
Despite recent advances, prognosis of acute myeloid leukemia (AML) remains unsatisfactory due to poor response to therapy or relapse. Among causes of resistance, over-expression of multidrug resistance (MDR) proteins represents a pivotal mechanism. ABCG2 is an efflux transporter responsible for inducing MDR in leukemic cells; through its ability to extrude many antineoplastic drugs, it leads to AML resistance and/or relapse, even if conflicting data have been reported to date. Moreover, ABCG2 may be co-expressed with other MDR-related proteins and is finely regulated by epigenetic mechanisms. Here, we review the main issues regarding ABCG2 activity and regulation in the AML clinical scenario, focusing on its expression and the role of polymorphisms, as well as on the potential ways to inhibit its function to counteract drug resistance to, eventually, improve outcomes in AML patients.
Keyphrases
- acute myeloid leukemia
- allogeneic hematopoietic stem cell transplantation
- multidrug resistant
- poor prognosis
- end stage renal disease
- ejection fraction
- cancer stem cells
- induced apoptosis
- newly diagnosed
- chronic kidney disease
- gene expression
- prognostic factors
- peritoneal dialysis
- dna methylation
- type diabetes
- binding protein
- risk assessment
- mesenchymal stem cells
- oxidative stress
- cell death
- acute lymphoblastic leukemia
- cell therapy
- climate change
- weight loss
- chemotherapy induced