LBH-589 (panobinostat) potentiates fludarabine anti-leukemic activity through a JNK- and XIAP-dependent mechanism

This publication has 37 references indexed in Scilit:

• Histone deacetylase inhibitor induces DNA damage, which normal but not transformed cells can repair
  Proceedings of the National Academy of Sciences, 2010
• Histone Deacetylase Inhibitors Activate NF-κB in Human Leukemia Cells through an ATM/NEMO-related Pathway
  Journal of Biological Chemistry, 2010
• Pulsatile Stimulation Determines Timing and Specificity of NF-κB-Dependent Transcription
  Science, 2009
• IAPs contain an evolutionarily conserved ubiquitin-binding domain that regulates NF-κB as well as cell survival and oncogenesis
  Nature Cell Biology, 2008
• Interruption of the Ras/MEK/ERK signaling cascade enhances Chk1 inhibitor–induced DNA damage in vitro and in vivo in human multiple myeloma cells
  Blood, 2008
• A Phase I Study of Intravenous LBH589, a Novel Cinnamic Hydroxamic Acid Analogue Histone Deacetylase Inhibitor, in Patients with Refractory Hematologic Malignancies
  Clinical Cancer Research, 2006
• Nuclear factor-κB in cancer development and progression
  Nature, 2006
• Molecular Linkage Between the Kinase ATM and NF-κB Signaling in Response to Genotoxic Stimuli
  Science, 2006
• Blockade of Histone Deacetylase Inhibitor-Induced RelA/p65 Acetylation and NF-κB Activation Potentiates Apoptosis in Leukemia Cells through a Process Mediated by Oxidative Damage, XIAP Downregulation, and c-Jun N-Terminal Kinase 1 Activation
  Molecular and Cellular Biology, 2005
• MODULATION OF ARABINOSYLNUCLEOSIDE METABOLISM BY ARABINOSYLNUCLEOTIDES IN HUMAN-LEUKEMIA CELLS
  1988