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Flashcards in AML Deck (11):

Granulocytic maturation
Extramedullary involvement
Favorable prognosis

AML with t(8;21)


Immunophenotypic features of myelomonocytic leukemia (dual differentiation towards granulocytes and monocytes)
Eosinophils with dysplastic features
Extramedullary involvement
Favorable prognosis

AML with inv(16)


Atypical promyelocytes -- Hypergranular
Have reniform nuclei
Multiple prominent Auer rods
Hypergranular cases show leukopenia
Microgranular cases show leukocytosis
Commonly manifests as DIC at diagnosis
Responds to ATRA

AML with t(15;17)


Infantile AML
Monocytic features and presents with hyperleukocytosis
Exramedullary tissue infiltration is common
Can have several translocation partners

AML with 11q23 (MLL) rearrangements
t(9;11) has intermediate prognosis
Others involving MLL gene have intermediate to poor prognosis


Characterized by dysplasia in >50% of two or more lineages
And/or myelodysplasia-associated cytogenetic abnormalities -- Monosomy 7/del(7q), Monosomy 5/del(5q) or complex karyotypes
Predominantly in older individuals
Unfavorable prognosis

AML with myelodysplasia-related changes


Occurs in patients previously treated with chemo/radiotherapy
Can be caused by either alkylating agents or topoisomerase II inhibitors

Therapy-related AML and MDS


Occur a median of 5 years after treatment
Risk due to total dose and patient age
Multi-lineage dysplasia
Abberrancies of Chr 5 and 7

Alkylating agent related AML/MDS


Tend to occur sooner than 5 years after treatment (median 2.5-3 years)
Usually monocytic or myelomonocytic
11q23 (MLL) balanced translocations are common
Poor prognosis
Resembles de novo AML with 11q23 (MLL) gene arrangements

Topoisomerase II inhibitor-related AML


Extramedullary tumor of immature myeloid cells
Can occur after, concurrent or preceding AML diagnosis
Usually treated in same fashion as AML

Myeloid sarcoma


Receptor tyrosine kinase with important role in hematopoietic progenitor survival and proliferation
Activating mutation caused by internal tandem duplications of the juxtamembrane domain confers poor prognosis

FLT3-- new prognositic marker in AML


Nucleocytoplasmic shuffling protein
Mutation in 50-60% of AML with NORMAL karyotype
Favorable prognosis (in cases w/o mutated FLT3)