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Common morphologic features include the following: Most cases with this genetic abnormality have been identified as AMML Eo, but occasional cases have been reported to lack eosinophilia.
As is found in rare cases of AML with t(8; 21), the bone marrow blast percentage in this AML is occasionally less than 20%.
Data suggest that once attained, duration of remission may be shorter in older patients.
Increased morbidity and mortality during induction appear to be directly related to age.
Rarely, AML with this translocation presents with a bone marrow blast percentage less than 20%. The translocation t(8; 21)(q22; q22) involves the fusion transcript is consistently detected in patients with t(8; 21) AML.
This type of AML is usually associated with a good response to chemotherapy and a high complete remission (CR) rate with long-term survival when treated with high-dose cytarabine in the postremission phase as in the Cancer and Leukemia Group B (CLB-9022 and CLB-8525) trials.[17-20] Additional chromosome abnormalities are common, for example, loss of a sex chromosome and del(9)(q22).
Among 36 live offspring of survivors, 2 congenital problems occurred. The differentiation of AML from acute lymphocytic leukemia has important therapeutic implications.
Histochemical stains and cell surface antigen determinations aid in discrimination.
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Many of these translocations are detected by reverse transcriptase–polymerase chain reaction (RT–PCR) or fluorescence hybridization (FISH), which has a higher sensitivity than cytogenetics.
Other recurring cytogenetic abnormalities are less common and described below in AML not otherwise categorized.
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Distinct subsets can be identified using GEP that correspond to known cytogenetic and molecular abnormalities.