AML Flashcards
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)
NPM1