AML/ALL Flashcards
AML – Acute myeloid leukemia
leukemic cells resemble cells of one or more myeloid lineages
ALL – Acute lymphoblastic leukemia
Leukemic cells - resemble precursor/immature lymphocytes
Etiology acute leukemia
Chromosomal abnormality, in PCR - block ability to differentiate/increase autonomy of growth signalling pathway
Risk factors for acute leukemia
Chemo (alkylating agent, topoisomerase II), ionizing, tabacco smoke, benzene, genetic syndrome
Acute leukemia clinical presentation
Anemia (fatigue, malaise, pallor, dyspnea)
Thrombocytopenia (brusing, petechiae, hemorrhage)
Neutropenia (fever, infection)
Rare: thrombotic events, DIC, skin/gum/tissues
___% of cases of ALL occur in children less than ___ y/o
75%; 6 y/o
Immaturity markers
CD34
Common immature lymphoblasts markers
TdT
B cell linage markers
CD19, CD22
T cell lineage markers
CD3, CD7
B cell mature markers
CD20, surface immunoglobulin
B-ALL accounts for _______ % of ALL, typically ALL of ____(age)___
80-85; childhood
BCR-ABL1 B-ALL
cytogenetics, distribution, prognosis
t(9;22) - philadelphia chromosome
“Ph+ALL”
25% of adult ALL, 2% childhood ALL
Poor prognosis
B-ALL MLL
translocation 11q23
Neonates/young infants
poor prognosis
B-ALL ETV6-RUNX1
t(12;21)
25% childhood B-ALL
Favorable prognosis
T-ALL traits
25% of ALL Adolescent/young adults Mediastinal mass High WBC Favors males
T-ALL prognosis general trends in children vs adults
Good - kids >95%, cure80% Poor adults Remission 60-80 Cure<50%
Poor ALL prognosis factors
< 1 y/o; >10 y/o Very high WBC T-lymphoblastic hypodiploidy Slow response to rx Min residual disease
AML - Acute myeloid leukemia occurs in what age?
adults (65 avg); 10% of childhood leukemia are AML
AML diagnosis
> 20% myeloblasts in marrow/peripheral blood
- morphologic appearance
- flow cytometric
- immunohistochemistry
Common myeloid markers
CD117 (C-Kit)
Myeloperoxidase
AML/APL - PML-RARA/M3 AML
t(15;17) Blocked at promyeloctyes (not at blasts) Hypergranular morphology Auer rods DIC
APL treatment
- RARA - retinotic acid receptor alpha protein - does not signal well –> accumulation of promyelocyte
Give high doses of ATRA to overcome
AML RUNX1-RUNX1T1
t(8;21)
5% AML - younger patient
Good prognosis
APL secondary risk
Disseminated intravascular coagulation (DIC)
AML CBFB - MYH11
inv(16) or t(16;16) 5-10% AML Younger patients Baso Eos Good prognosis
AML RBM15 - MKL 1
Megakaryoblastic differenation
Infants with downs
Good prognosis
AML MLL - 11q23
abnormalities of MLL - some monocytic differentiation
Poor prognosis
t-AML alkylating agent latency
2-8 years
t-AML alkylation agent cytogenetics
whole/partial deletion of 5 and 7
t-AML topoisomerase inhibitor
1-2 years
MLL 11q23 rearrangement
NOS
Not otherwise specified
AML NOS subtype
undifferentiated - myeloblasts
Myelomonocytic
Monoblasts/monocytic -> skin/gum lesion
Megakaryoblastics –> marrow fibrosis
AML NOS molecular abnormality
FLT3 - poor
NPM1 - good
CEBPA - good
Hematopoietic stem cell transplant depends on
Younger patient
High risk disease
Relapse disease
Current health standing
which t-AML will be de novo?
topoisomerase II
Prognosis of t-AML?
very poor
Auer Rodes are?
fused azurophilic granules
