Concise reportAcute myeloblastic leukemia (ANLL-M2) with t(8;21)(q22;q22) variant expressing lymphoid but not myeloid surface antigens with a high number of G-CSF receptors
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Surrogate marker profiles for genetic lesions in acute leukemias
2010, Best Practice and Research: Clinical HaematologyCitation Excerpt :The low expression of CD11a in t(8;21) AML is explained by the inhibition of CD11a promoter activity through the AML1/ETO fusion product [29]. Due to the high degree of myeloid immaturity, CD19POS t(8;21) cases can be misdiagnosed as ALL [2,28,30]. It is imperative, therefore, to test all cases of acute leukemia simultaneously for cCD22 (or cCD3) and myeloperoxidase in the same cell aliquot.
AML1-MTG8 leukemic protein induces the expression of granulocyte colony- stimulating factor (G-CSF) receptor through the up-regulation of CCAAT/enhancer binding protein epsilon
2000, BloodCitation Excerpt :This difference in response to G-CSF between AML1-MTG8–expressing cells and G-CSFR–expressing cells suggests that additional factor(s) may be required for the continuous proliferation of cells and for the inhibition of morphologic terminal differentiation. Case reports have shown that high expression levels of G-CSFR can be found in leukemic cells from M2 AML patients.49, 50 To determine the relationship between AML with a t(8;21) translocation and G-CSFR expression, we measured G-CSFR activity in leukemic cells from M2 AML patients who were positive or negative for t(8;21).
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