Lack of Bcr-Abl point mutations in chronic myeloid leukemia patients in chronic phase before imatinib treatment is not predictive of response.
Agirre
Xabier
X
Fontalba
Ana
A
Andreu
Enrique J
EJ
Odero
Maria Dolores
MD
Larráyoz
María José
MJ
Montiel
Cristina
C
Calasanz
María José
MJ
Fernández-Luna
José Luis
JL
Prósper
Felipe
F
D019943:Amino Acid Substitution; D001549:Benzamides; D002999:Clone Cells / Q000737:chemistry / Q000648:ultrastructure; D004252:DNA Mutational Analysis; D004273:DNA, Neoplasm / Q000235:genetics*; D019008:Drug Resistance, Neoplasm; D016044:Fusion Proteins, bcr-abl / Q000235:genetics*; D016313:Genes, abl; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy / Q000235:genetics*; D015466:Leukemia, Myeloid, Chronic-Phase / Q000188:drug therapy / Q000235:genetics*; D020125:Mutation, Missense; D010879:Piperazines / Q000627:therapeutic use*; D017354:Point Mutation; D016133:Polymerase Chain Reaction; D017434:Protein Structure, Tertiary / Q000235:genetics; D011743:Pyrimidines / Q000627:therapeutic use*; D016896:Treatment Outcome
D001549:Benzamides; D004273:DNA, Neoplasm; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl