Restoring the Long Noncoding RNA MEG3 Indicates a Potential Role for JAK-STAT Signaling in Chronic Myeloid Leukemia

摘要

Chronic Myeloid Leukemia (CML) is associated with a somatic rearrangement,the Philadelphia chromosome [1], which results in the formationof a fusion gene between the breakpoint cluster (BCR) andAbelson murine leukemia viral oncogene homolog 1 (ABL1). As BCRABLis a constitutively active tyrosine kinase, the treatment of choice isone of several tyrosine kinase inhibitors (TKI), which have beenshown to be quite effective in increasing the 5-year survival rate ofthis disease. There are many factors including side effects, patient dosingpreferences, and molecular and clinical staging that determine theTKI of choice. Not all patients will tolerate a TKI and these also showlower efficacy in advanced stages of CML [2] including the acceleratedphase (CML-AP) where cells multiply more rapidly and blast phase(CML-BP) that more closely resembles an acute leukemia. It is in thisspace of TKI intolerant or non-responsive CML that Li et al. have performedtheir work.