Chronic myeloid leukemia and BCR/ABL signal pathways are not associated with AKT1 pleckstrin homology domain (E17K) mutations.
He
Yanli
Y
Zheng
Jine
J
Hu
Yanjie
Y
Xiao
Hong
H
Liu
Jun
J
Li
Xiaoqing
X
Du
Wen
W
Chen
Xiangjun
X
Hu
Yu
Y
Huang
Shiang
S
D019943:Amino Acid Substitution; D000970:Antineoplastic Agents / Q000494:pharmacology; D001549:Benzamides; D019008:Drug Resistance, Neoplasm; D016044:Fusion Proteins, bcr-abl / Q000037:antagonists & inhibitors / Q000502:physiology*; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy / Q000201:enzymology / Q000235:genetics* / Q000473:pathology; D020125:Mutation, Missense; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors / Q000502:physiology*; D010879:Piperazines / Q000627:therapeutic use; D017354:Point Mutation; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D017434:Protein Structure, Tertiary; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics*; D011743:Pyrimidines / Q000627:therapeutic use
D000970:Antineoplastic Agents; D001549:Benzamides; D009363:Neoplasm Proteins; D010879:Piperazines; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl; C494918:AKT1 protein, human; D051057:Proto-Oncogene Proteins c-akt