AML Flashcards

1
Q

Granulocytic maturation
Extramedullary involvement
Favorable prognosis

A

AML with t(8;21)

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2
Q

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

A

AML with inv(16)

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3
Q
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
A

AML with t(15;17)

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4
Q

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

A

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

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5
Q

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

A

AML with myelodysplasia-related changes

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6
Q

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

A

Therapy-related AML and MDS

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7
Q

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

A

Alkylating agent related AML/MDS

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8
Q

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

A

Topoisomerase II inhibitor-related AML

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9
Q

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

A

Myeloid sarcoma

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10
Q

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

A

FLT3– new prognositic marker in AML

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11
Q
Nucleocytoplasmic shuffling protein 
Mutation in 50-60% of AML with NORMAL karyotype 
Favorable prognosis (in cases w/o mutated FLT3)
A

NPM1

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