Blood consult: acute myeloid leukemia and the t(8;21)(q22;22).

Geographic Heterogeneity of the AML1-ETO Fusion Gene in Iranian Patients with Acute Myeloid Leukemia

Background: The human AML1 gene, located on chromosome 21, can be fused to the AML1- eight-twenty-one (ETO) oncoprotein on chromosome eight, resulting in a t(8;21)(q22;q22) translocation. Acute myeloid leukemia (AML) associated with this translocation is considered a distinct AML with a favorable prognosis. Due to the various incidences of the translocation, which is associated with geographic ...

The 8;21 chromosome translocation in acute myeloid leukemia is always detectable by molecular analysis using AML1.

The AML1 gene was rearranged in leukemic cells with t(8;21)(q22;q22) or its variant, complex t(8;V;21) translocations from 33 acute myeloid leukemia (AML) patients. The AML1 rearrangement was also detected in three AML patients without t(8;21); two had a normal diploid karyotype, and one had a karyotype of 45,X, - X. The AML1 rearrangement in the t(8;21) breakpoint cluster region was not detect...

Immunophenotypic features of t(8;21) (q22;q22) acute myeloid leukemia in adults.

Therapy-related acute leukemia associated with t(11q23) after primary acute myeloid leukemia with t(8;21): a report of two cases.

Differentiation therapy for the treatment of t(8;21) acute myeloid leukemia using histone deacetylase inhibitors.

Epigenetic modifying enzymes such as histone deacetylases (HDACs), p300, and PRMT1 are recruited by AML1/ETO, the pathogenic protein for t(8;21) acute myeloid leukemia (AML), providing a strong molecular rationale for targeting these enzymes to treat this disease. Although early phase clinical assessment indicated that treatment with HDAC inhibitors (HDACis) may be effective in t(8;21) AML pati...