Concomitant AID Expression and BCL7A Loss Associates With Accelerated Phase Progression and Imatinib Resistance in Chronic Myeloid Leukemia
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Dear Editor, The mechanisms involved in chronic myeloid leukemia (CML) progression from the chronic phase (CP) to an accelerated phase (AP) or blast crisis (BC) remain largely undetermined, but generally involve additional molecular changes besides the Philadelphia chromosome [1]. Evidence suggests that secondary BCR (breakpoint cluster region)-ABL1 (Abelson murine leukemia viral oncogene homolog 1)-dependent/independent genetic events play a critical role in blast transformation [2]. Besides BCR-ABL1 point mutations, deletions and/or rearrangements of other cancer-related genes have been associated with CML-BC [2]. Recent studies have demonstrated that aberrant activation-induced cytidine deaminase (AID) expression promotes genetic instability, eventually leading to progression and drug resistance in CML [3].
Abstract
Dear Editor, The mechanisms involved in chronic myeloid leukemia (CML) progression from the chronic phase (CP) to an accelerated phase (AP) or blast crisis (BC) remain largely undetermined, but generally involve additional molecular changes besides the Philadelphia chromosome [1]. Evidence suggests that secondary BCR (breakpoint cluster region)-ABL1 (Abelson murine leukemia viral oncogene homolog 1)-dependent/independent genetic events play a critical role in blast transformation [2]. Besides BCR-ABL1 point mutations, deletions and/or rearrangements of other cancer-related genes have been associated with CML-BC [2]. Recent studies have demonstrated that aberrant activation-induced cytidine deaminase (AID) expression promotes genetic instability, eventually leading to progression and drug resistance in CML [3].
참고문헌 (10)
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