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Mechanisms of apoptosis sensitivity and resistance to the BH3 mimetic ABT-737 in acute myeloid leukemia.
ABT-737 effectively kills acute myeloid leukemia blast, progenitor, and stem cells without affecting normal hematopoietic cells, suggesting that ABT- 737 could be a highly effective antileukemia agent when the mechanisms of resistance identified here are considered. Expand
Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia.
Ph-like ALL was found to be characterized by a range of genomic alterations that activate a limited number of signaling pathways, all of which may be amenable to inhibition with approved tyrosine kinase inhibitors. Expand
MDM2 antagonists induce p53-dependent apoptosis in AML: implications for leukemia therapy.
No induction of apoptosis was observed in AML samples harboring mutant p53, and p53 activation by targeting the p53-MDM2 interaction might offer a novel therapeutic strategy for AML that retain wild-type p53. Expand
Abrogation of nuclear receptors Nr4a3 andNr4a1 leads to development of acute myeloid leukemia
A previously unsuspected function of Nor-1 and Nur77 is described—as critical tumor suppressors of myeloid leukemogenesis and potential targets for therapeutic intervention in AML. Expand
Antidiabetic therapies affect risk of pancreatic cancer.
Diabetic patients who had taken metformin had a significantly lower risk of pancreatic cancer compared with those who had not taken met formin, and insulin or insulin secretagogue use was associated with increased risk of Pancreatic cancer in diabetic patients. Expand
Leukemia stem cells and microenvironment: biology and therapeutic targeting.
  • M. Konopleva, C. Jordan
  • Biology, Medicine
  • Journal of clinical oncology : official journal…
  • 10 February 2011
This article reviews both the intrinsic and extrinsic components that are known to influence the survival of human LSCs and new strategies that exploit potentially unique properties of the L SCs and their microenvironment are discussed. Expand
Venetoclax combined with decitabine or azacitidine in treatment-naive, elderly patients with acute myeloid leukemia.
The novel combination of venetoclax with decitabine or azacitidine was effective and well tolerated in elderly patients with AML and achieved complete remission (CR) + CR with incomplete count recovery (CRi). Expand
Mutant FLT3: a direct target of sorafenib in acute myelogenous leukemia.
Sorafenib may have therapeutic efficacy in AML patients whose cells harbor FLT3-ITD mutations and was 1000- to 3000-fold more effective in inducing growth arrest and apoptosis than in Ba/F3 cells with FLT 3-D835Y mutant or wild-typeFLT3 and inhibited the phosphorylation of tyrosine residues in ITD mutant but not wild- type FLT2 protein. Expand
BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia.
These findings demonstrate that BCR-ABL1 compound mutants confer different levels of TKI resistance, necessitating rational treatment selection to optimize clinical outcome, and in vitro resistance profiling was predictive of treatment outcomes in Ph(+) leukemia patients. Expand
Pharmacologic inhibition of fatty acid oxidation sensitizes human leukemia cells to apoptosis induction.
It is demonstrated that pharmacologic inhibition of FAO with etomoxir or ranolazine inhibited proliferation and sensitized human leukemia cells to apoptosis induction by ABT-737, and evidence suggesting that FAO regulates the activity of Bak-dependent mitochondrial permeability transition is generated. Expand