Analysis of BCR-ABL1 tyrosine kinase domain mutational spectra in primitive chronic myeloid leukemia cells suggests a unique mutator phenotype.
Grant
H
H
Jiang
X
X
Stebbing
J
J
Foroni
L
L
Craddock
C
C
Griffiths
M
M
Clark
R E
RE
O'Brien
S
S
Khorashad
J S
JS
Gerrard
G
G
Wang
L
L
Irving
J A E
JA
Wang
M
M
Karran
L
L
Dyer
M J S
MJ
Forrest
D
D
Page
K
K
Eaves
C J
CJ
Woolfson
A
A
D000970:Antineoplastic Agents / Q000627:therapeutic use; D001549:Benzamides; D019008:Drug Resistance, Neoplasm / Q000235:genetics*; D016044:Fusion Proteins, bcr-abl / Q000235:genetics*; D015894:Genome, Human; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D008962:Models, Theoretical; D010641:Phenotype; D010879:Piperazines / Q000627:therapeutic use; D017354:Point Mutation / Q000235:genetics*; D011379:Prognosis; D017434:Protein Structure, Tertiary; D011743:Pyrimidines / Q000627:therapeutic use
D000970:Antineoplastic Agents; D001549:Benzamides; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl