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FASEB J ; 36(10): e22562, 2022 10.
Artigo em Inglês | MEDLINE | ID: mdl-36125067

RESUMO

Oncoprotein AML1-ETO (AE) derived from t(8;21)(q22;q22) translocation is typically present in a portion of French-American-British-M2 subtype of acute myeloid leukemia (AML). Although these patients have relatively favorable prognoses, substantial numbers of them would relapse after conventional therapy. Here, we explored whether reinforcing the endogenous differentiation potential of t(8;21) AML cells would diminish the associated malignancy. In doing so, we noticed an expansion of immature erythroid blasts featured in both AML1-ETO9a (AE9a) and AE plus c-KIT (N822K) (AK) murine leukemic models. Interestingly, in the AE9a murine model, a spontaneous step-wise erythroid differentiation path, as characterized by the differential expression of CD43/c-Kit and the upregulation of several key erythroid transcription factors (TFs), accompanied the decline or loss of leukemia-initiating potential. Notably, overexpression of one of the key erythroid TFs, Ldb1, potently disrupted the repopulation of AE9a leukemic cells in vivo, suggesting a new promising intervention strategy of t(8;21) AML through enforcing their erythroid differentiation.


Assuntos
Leucemia Mieloide Aguda , Proteínas de Fusão Oncogênica , Animais , Cromossomos Humanos Par 21 , Cromossomos Humanos Par 8 , Proteínas de Ligação a DNA/metabolismo , Humanos , Proteínas com Domínio LIM , Proteínas com Homeodomínio LIM , Leucemia Mieloide Aguda/metabolismo , Camundongos , Proteínas de Fusão Oncogênica/genética , Proteínas de Fusão Oncogênica/metabolismo , Proteína 1 Parceira de Translocação de RUNX1/genética , Translocação Genética
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