Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
32 Cards in this Set
- Front
- Back
|
Increased eosinophils -Smudgy Pink neutrophils CD34, CD19 Weakly tdt positive CD 56 in worse Common in young patients with AML 5-10%
|
AML with t(8;21)
|
|
|
AML1 gene encodes -core binding factor alpha-(CBF-alpha RNX1)-ETO(8;21) gene (RUNX1T1)
-KIT mutation associated with poorer prognosis |
AML with t(8;21)
|
|
|
increased marrow eosinophils with “hybrid” basophil granules >3%
Associated with myeloid granulocytic sarcoma |
AML with inv(16) or AML with t(16;16)
|
|
|
-Fusion of -Core binding Factor –B (CBF-beta) at 16;q22 with MYH11(smooth muscle myosin heavy chain gene at 16p13) thought to lock out the CBF gene product from the nucleus
--KIT mutations associated with decreased survival |
AML with inv(16) or AML with t(16;16)
|
|
|
Hypergranular-Low WBC -Low promyeloces -Faggot cells
|
AML with t(15:17) or APL or PML/RAR
|
|
|
Hypogranular--High WBC -high promyelocytes
-very deep central groove |
AML with t(15:17) or APL or PML/RAR
|
|
|
High DIC -Intra cerebral hemorrhage
|
AML with t(15:17) or APL or PML/RAR
|
|
|
AML with t(15:17) or APL or PML/RAR
Treatment? |
ATRA -Blasts are <10%
|
|
|
-PML gene (15q21) with retinoic acid receptor
|
AML with t(15:17) or APL or PML/RAR
|
|
|
Most commonly associated with monoblastic or promocytic morphology -~ 5% of AML
-common in children especially infants |
AML with t(9;11)
|
|
|
-Multiple translocation (>50) involving the 11q23 site -Associated with both ALL & AML
|
AML with t(9;11)
|
|
|
-11q23 is the site of ??
|
Mixed Lineage Leukemia gene
|
|
|
-20% blasts
-< 3% of the blasts react with MPO, SBB, NSE -No Auer Rods CD13,CD 33,CD 14 -React with myeloid lineage abys -Ultrastructural evidence of myeloid differentiation |
AML minimally Diff (FAB M0)
|
|
|
->20% blasts
->3% of the blasts react with MPO, SBB,NSE -<10% of marrow show maturation of promyelocyte stage or beyond |
AML without Maturation
(FAB M1) |
|
|
->20% blasts
->3% of the blasts react with MPO or SBB >10% of the cells mature to promyelocytic stage |
AML with Maturation
|
|
|
>20% blasts Monocytic cells in blood > 5x10^9/L
-presence of 20-80% of both granulocytic and monocytic elements in the blood. -Concurrent proliferation of both Neutrophil & monocyte cell line |
Acute Myelomonocytic Leukemia
M4 |
|
|
M5A > 80%
Commonly associated with Extramedullary tumors: Cutaneous tumors, gingival masses organomegaly Testicular mases |
Monoblast
|
|
|
M5B < 80%
Commonly associated with Extramedullary tumors: Cutaneous tumors, gingival masses organomegaly Testicular mases |
Monocytic
|
|
|
Erythroid cells >50% in marrow
PAS positive |
Erythroleukemias (FAB M6)
|
|
|
>20% blasts
>50% of the blasts are megakaryocytic lineage defined EM |
Acute Megakaryoblastic Leukemia
|
|
|
Associated with Basophilia
Bad prognosis |
t(6;9)
|
|
|
Normal or Elevated Platelet count .
Odd megakartyocyte Bad prognosis |
Inv(3)(q21;q26.2)
|
|
|
Megakaryoblastic Leukemia in children & infants
|
t(1;22)
|
|
|
Point mutations
-Short duplications -Deletions |
BGA
|
|
|
-Activated Flt3 turns on cell division
-mutation occurs in cases such APL,-higher WBC -higher blasts -Normal chrom -Treatment -Small molecule inhibitors in clinical trails. -limited success to date. |
Flt3 ITDs
|
|
|
-AML with Mutated NPM1
-mutated in 40-60% of cytogenetically normal AML -often with monocytic components |
NPM1
|
|
|
-Only provisional
-Not clear what coexistent flt3 muations or chromosomes mean |
AML with mutated CEBPA
|
|
|
-History of bone marrow failure with <20% blasts
|
AML evolving from Myelo-dys-plastic Syndrome
|
|
|
-Dysplasia present in > 50% of at least two cell lines
|
AML with multilineage dysplasia without prior history of MDS
|
|
|
-Loss of 7/7q , 5/5q, 11(q)
-common changes 7, del(7q) , -5,del (5q) sufficient to classify an AML as myelodysplasia related changed Most common in elderly Worse than AML as a whole |
AML with a bad karyotype
|
|
|
-abnormality of chrom 5 & 7 very common
-prominent multilineage dysplasia -Present 5-10 years after treatmet Very poor prognosis |
Alkylating Agent
|
|
|
-11q23 abnormality
-Monocytic morphology -present 1-5 years of treatment with acute onset. |
Epidophyllotoxin (topoisomerase II)
|
