Systems-pharmacology dissection of a drug synergy in imatinib-resistant CML

Nat Chem Biol. 2012 Nov;8(11):905-912. doi: 10.1038/nchembio.1085. Epub 2012 Sep 30.

Abstract

Occurrence of the BCR-ABL(T315I) gatekeeper mutation is among the most pressing challenges in the therapy of chronic myeloid leukemia (CML). Several BCR-ABL inhibitors have multiple targets and pleiotropic effects that could be exploited for their synergistic potential. Testing combinations of such kinase inhibitors identified a strong synergy between danusertib and bosutinib that exclusively affected CML cells harboring BCR-ABL(T315I). To elucidate the underlying mechanisms, we applied a systems-level approach comprising phosphoproteomics, transcriptomics and chemical proteomics. Data integration revealed that both compounds targeted Mapk pathways downstream of BCR-ABL, resulting in impaired activity of c-Myc. Using pharmacological validation, we assessed that the relative contributions of danusertib and bosutinib could be mimicked individually by Mapk inhibitors and collectively by downregulation of c-Myc through Brd4 inhibition. Thus, integration of genome- and proteome-wide technologies enabled the elucidation of the mechanism by which a new drug synergy targets the dependency of BCR-ABL(T315I) CML cells on c-Myc through nonobvious off targets.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aniline Compounds / pharmacology*
  • Animals
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology*
  • Apoptosis / drug effects
  • Benzamides / pharmacology*
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Dose-Response Relationship, Drug
  • Down-Regulation / drug effects
  • Drug Resistance, Neoplasm / drug effects*
  • Drug Synergism
  • Fusion Proteins, bcr-abl / antagonists & inhibitors
  • Fusion Proteins, bcr-abl / genetics
  • Imatinib Mesylate
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • Mice
  • Nitriles / pharmacology*
  • Piperazines / pharmacology*
  • Protein Kinase Inhibitors / pharmacology*
  • Proteomics
  • Proto-Oncogene Proteins c-myc / antagonists & inhibitors
  • Proto-Oncogene Proteins c-myc / metabolism
  • Pyrazoles / pharmacology*
  • Pyrimidines / pharmacology*
  • Quinolines / pharmacology*
  • Structure-Activity Relationship
  • Systems Biology

Substances

  • Aniline Compounds
  • Benzamides
  • Nitriles
  • Piperazines
  • Protein Kinase Inhibitors
  • Proto-Oncogene Proteins c-myc
  • Pyrazoles
  • Pyrimidines
  • Quinolines
  • bosutinib
  • Imatinib Mesylate
  • Fusion Proteins, bcr-abl
  • danusertib