Imatinib resistance and progression of CML to blast crisis: somatic hypermutation AIDing the way.
Very little is known about how acquired oncogenic mutations arise. In this issue of Cancer Cell, Klemm and colleagues present evidence supporting a role for the antibody diversification enzyme activation-induced deaminase (AID) in the generation of mutations associated with disease progression and drug resistance in chronic myeloid leukemia.
Strout
Matthew P
MP
Yale Cancer Center, Department of Internal Medicine, Section of Hematology, Yale University School of Medicine, New Haven, CT 06520, USA.
Schatz
David G
DG
D000970:Antineoplastic Agents / Q000627:therapeutic use; D001549:Benzamides; D001752:Blast Crisis / Q000188:drug therapy*; D045744:Cell Line, Tumor; D003564:Cytidine Deaminase / Q000378:metabolism*; D018450:Disease Progression; D019008:Drug Resistance, Neoplasm / Q000235:genetics*; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D008954:Models, Biological; D009154:Mutation; D010879:Piperazines / Q000627:therapeutic use*; D011743:Pyrimidines / Q000627:therapeutic use*; D000098830:AICDA (Activation-Induced Cytidine Deaminase)
D000970:Antineoplastic Agents; D001549:Benzamides; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D000098830:AICDA (Activation-Induced Cytidine Deaminase); D003564:Cytidine Deaminase