Development of AML with t(8;21)(q22;q22) and RUNX1-RUNX1T1 fusion following Philadelphia-negative clonal evolution during treatment of CML with Imatinib.
Schafhausen
Philippe
P
Dierlamm
Judith
J
Bokemeyer
Carsten
C
Bruemmendorf
Tim H
TH
Bacher
Ulrike
U
Zander
Axel R
AR
Schnittger
Susanne
S
Hochhaus
Andreas
A
D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001549:Benzamides; D002891:Chromosomes, Human, Pair 21 / Q000235:genetics; D002898:Chromosomes, Human, Pair 8 / Q000235:genetics; D050676:Core Binding Factor Alpha 2 Subunit / Q000235:genetics*; D005260:Female; D006801:Humans; D000068877:Imatinib Mesylate; D007621:Karyotyping; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy*; D015470:Leukemia, Myeloid, Acute / Q000235:genetics*; D054438:Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / Q000235:genetics* / Q000473:pathology; D008875:Middle Aged; D015514:Oncogene Proteins, Fusion / Q000235:genetics*; D010879:Piperazines / Q000627:therapeutic use*; D011743:Pyrimidines / Q000627:therapeutic use*; D000075142:RUNX1 Translocation Partner 1 Protein; D014178:Translocation, Genetic / Q000235:genetics*
C107844:AML1-ETO fusion protein, human; D000970:Antineoplastic Agents; D001549:Benzamides; D050676:Core Binding Factor Alpha 2 Subunit; D015514:Oncogene Proteins, Fusion; D010879:Piperazines; D011743:Pyrimidines; D000075142:RUNX1 Translocation Partner 1 Protein; D000068877:Imatinib Mesylate