Pharmacological targeting of -catenin in normal karyotype acute myeloid leukemia blasts
Open Access
- 7 November 2014
- journal article
- Published by Ferrata Storti Foundation (Haematologica) in Haematologica
- Vol. 100 (2) , e49-e52
Abstract
Over 11,000 people in the US are diagnosed with acute myeloid leukemia (AML) each year, and despite attempts to improve therapy, the overall 5-year survival remains 26%, largely due to a high rate of relapse. Defining the mechanisms responsible for persistence of the malignant clone is essential toKeywords
This publication has 13 references indexed in Scilit:
- Genomic impact of transient low-dose decitabine treatment on primary AML cellsBlood, 2013
- Quantifying nuclear p65 as a parameter for NF‐κB activation: Correlation between ImageStream cytometry, microscopy, and Western blotCytometry Part A, 2011
- An RNAi-based chemical genetic screen identifies three small-molecule inhibitors of the Wnt/ wingless signaling pathwayProceedings of the National Academy of Sciences, 2011
- Heterogeneous sensitivity of human acute myeloid leukemia to β-catenin down-modulationLeukemia, 2011
- β-Catenin Mediates the Establishment and Drug Resistance of MLL Leukemic Stem CellsCancer Cell, 2010
- The Wnt/β-Catenin Pathway Is Required for the Development of Leukemia Stem Cells in AMLScience, 2010
- Tankyrase inhibition stabilizes axin and antagonizes Wnt signallingNature, 2009
- Clinical significance of nuclear non‐phosphorylated beta‐catenin in acute myeloid leukaemia and myelodysplastic syndromeBritish Journal of Haematology, 2008
- Expression of β-catenin by acute myeloid leukemia cells predicts enhanced clonogenic capacities and poor prognosisLeukemia, 2006
- Constitutive activation of the Wnt/β-catenin signalling pathway in acute myeloid leukaemiaOncogene, 2005