The AML1-ETO fusion transcription factor is generated by the t(8;21)translocation,which is present in approximately 4%-12% of adult and 12%-30% of pediatric acute myeloid leukemia(AML)patients.Both human and mouse mod...The AML1-ETO fusion transcription factor is generated by the t(8;21)translocation,which is present in approximately 4%-12% of adult and 12%-30% of pediatric acute myeloid leukemia(AML)patients.Both human and mouse models of AML have demonstrated that AML1-ETO is insufficient for leukemogenesis in the absence of secondary events.In this review,we discuss the pathogenetic insights that have been gained from identifying the various events that can cooperate with AML1-ETO to induce AML in vivo.We also discuss potential therapeutic strategies for t(8;21)positive AML that involve targeting the fusion protein itself,the proteins that bind to it,or the genes that it regulates.Recently published studies suggest that a targeted therapy for t(8;21)positive AML is feasible and may be coming sometime soon.展开更多
基金supported by a Leukemia Lymphoma Society SCOR grant(S.D.N.)a Leukemia Lymphoma Society fellowship(L.W.)+1 种基金an Empire State Stem Cell Scholar award(L.W.)a New York State Stem Cell Science grant(S.D.N.).
文摘The AML1-ETO fusion transcription factor is generated by the t(8;21)translocation,which is present in approximately 4%-12% of adult and 12%-30% of pediatric acute myeloid leukemia(AML)patients.Both human and mouse models of AML have demonstrated that AML1-ETO is insufficient for leukemogenesis in the absence of secondary events.In this review,we discuss the pathogenetic insights that have been gained from identifying the various events that can cooperate with AML1-ETO to induce AML in vivo.We also discuss potential therapeutic strategies for t(8;21)positive AML that involve targeting the fusion protein itself,the proteins that bind to it,or the genes that it regulates.Recently published studies suggest that a targeted therapy for t(8;21)positive AML is feasible and may be coming sometime soon.
