Chronic myeloid leukemia and BCR/ABL signal pathways are not associated with AKT1 pleckstrin homology domain (E17K) mutations

Eur J Haematol. 2010 Jan 1;84(1):87-8. doi: 10.1111/j.1600-0609.2009.01350.x. Epub 2009 Sep 10.
No abstract available

Publication types

  • Letter
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Substitution*
  • Antineoplastic Agents / pharmacology
  • Benzamides
  • Drug Resistance, Neoplasm
  • Fusion Proteins, bcr-abl / antagonists & inhibitors
  • Fusion Proteins, bcr-abl / physiology*
  • Humans
  • Imatinib Mesylate
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • Mutation, Missense*
  • Neoplasm Proteins / antagonists & inhibitors
  • Neoplasm Proteins / physiology*
  • Piperazines / therapeutic use
  • Point Mutation*
  • Protein Kinase Inhibitors / pharmacology
  • Protein Structure, Tertiary
  • Proto-Oncogene Proteins c-akt / genetics*
  • Pyrimidines / therapeutic use

Substances

  • Antineoplastic Agents
  • Benzamides
  • Neoplasm Proteins
  • Piperazines
  • Protein Kinase Inhibitors
  • Pyrimidines
  • Imatinib Mesylate
  • Fusion Proteins, bcr-abl
  • AKT1 protein, human
  • Proto-Oncogene Proteins c-akt