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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%.Other adverse prognostic factors include central nervous system involvement with leukemia, systemic infection at diagnosis, elevated white blood cell count (), treatment-induced AML, and history of myelodysplastic syndromes or another antecedent hematological disorder.Patients with leukemias that express the progenitor cell antigen CD34 and/or the P-glycoprotein ( Cytogenetic analysis provides some of the strongest prognostic information available, predicting outcome of both remission induction and postremission therapy, as seen in a trial from the Southwest Oncology Group (SWOG) and the Eastern Cooperative Oncology Group (ECOG) (E-3489).[8] Cytogenetic abnormalities that indicate a good prognosis include t(8; 21), inv(16) or t(16;16), and t(15;17). Patients with AML that is characterized by deletions of the long arms or monosomies of chromosomes 5 or 7; by translocations or inversions of chromosome 3, t(6; 9), t(9; 22); or by abnormalities of chromosome 11q23 have particularly poor prognoses with chemotherapy.More than 25% of adults with AML (about 45% of those who attain CR) can be expected to survive 3 or more years and may be cured.Remission rates in adult AML are inversely related to age, with an expected remission rate of more than 65% for those younger than 60 years.Both inv(16)(p13; q22) and t(16; 16)(p13; q22) result in the fusion of the CBF-beta (.[15] The use of FISH and RT–PCR methods may be necessary to document this fusion gene because its presence cannot be reliably documented by traditional cytogenetics banding techniques.[24] Patients with this type of AML may achieve higher CR rates when treated with high-dose cytarabine in the postremission phase.[17,18,20] APL [AML with t(15; 17)(q22; q12); () and variants] (FAB Classification M3) APL AML with t(15; 17)(q22; q12) is an AML in which promyelocytes predominate.APL exists as two types, hypergranular or typical APL and microgranular (hypogranular) APL.

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The positive predictive value appears to be sufficiently powerful to be clinically useful only for patients with the t(8;21) and inv(16) (now referred to as core-binding factor [CBF] leukemias) and acute promyelocytic leukemia (APL) with the t(15;17).This category is characterized by characteristic genetic abnormalities and frequently high rates of remission and favorable prognoses with the notable exception of those with 11q23 abnormalities.[14] The reciprocal translocations t(8; 21), inv(16) or t(16;16), t(15; 17), and translocations involving the 11q23 breakpoint are the most commonly identified genetic abnormalities.These structural chromosome rearrangements result in the formation of fusion genes that encode chimeric proteins that may contribute to the initiation or progression of leukemogenesis.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.GEP identified several cases of CBF leukemias that were not diagnosed using conventional cytogenetics.[10-12] Next-generation sequencing of AML genomes has identified an average of 13 mutations per case.Mutated genes include transcription-factor fusions, nucleophosmin-1, tumor-suppressor, DNA-methylation-related, signaling, chromatin-modifying, myeloid transcription-factor, cohesion-complex, and spliceosome-complex.[13] In the following outline and discussion, the older FAB classifications are noted where appropriate.The decision to treat should be based on other factors including patient age, previous history of MDS, clinical findings, disease progression, in addition to the blast percentage, and most importantly, patient preference.Several groups have begun to investigate the use of gene expression profiling (GEP) using microarrays to augment current diagnostic and prognostic studies for AML.Among 36 live offspring of survivors, 2 congenital problems occurred.[14] The differentiation of AML from acute lymphocytic leukemia has important therapeutic implications.Histochemical stains and cell surface antigen determinations aid in discrimination.