Publications by authors named "Fetta Mazed"
Article Synopsis
- Recent advances in targeted therapies for acute myeloid leukemia (AML) have not significantly addressed many cases, especially those lacking actionable therapy targets.
- In a study of 127 AML cases, 40% showed alterations in RAS pathway genes, which correlated with worse outcomes and survival rates for patients.
- The combination of the MEK inhibitor trametinib and the anti-helminthic drug pyrvinium pamoate showed promising antileukemic effects in both laboratory tests and mouse models, suggesting a potential new treatment strategy for RAS+ AML.
Article Synopsis
- AMPK is a key regulator of energy balance in cells, influencing growth and survival, and activation of AMPK has shown potential anti-cancer effects, particularly in acute myeloid leukemia (AML).
- The study reveals that the AMPK activator GSK621 triggers the unfolded protein response (UPR) in AML cells, causing changes in energy metabolism that promote cell death.
- Combining GSK621 with the Bcl-2 inhibitor venetoclax enhances the effectiveness of treatment, suggesting that AMPK activation could be a promising strategy for AML therapy through reshaping mitochondrial processes.
Relapses driven by chemoresistant leukemic cell populations are the main cause of mortality for patients with acute myeloid leukemia (AML). Here, we show that the ectonucleotidase CD39 (ENTPD1) is upregulated in cytarabine-resistant leukemic cells from both AML cell lines and patient samples and . CD39 cell-surface expression and activity is increased in patients with AML upon chemotherapy compared with diagnosis, and enrichment in CD39-expressing blasts is a marker of adverse prognosis in the clinics.
View Article and Find Full Text PDFFms-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD) is frequently detected in acute myeloid leukemia (AML) patients and is associated with a dismal long-term prognosis. FLT3 tyrosine kinase inhibitors provide short-term disease control, but relapse invariably occurs within months. Pim protein kinases are oncogenic FLT3-ITD targets expressed in AML cells.
View Article and Find Full Text PDF