1 Flashcards
APML
t(15;17) PML-RARA
tx: ATRA+arsenic
complications: DIC
very good prognosis
Good prognoses - AML chromosomal abnormalities
t(8;21) RUNX1
t(16;16) or inv(16) CBFB
Good markers for AML
NPM1 and CEBPA mutations
Bad marker for AML
FLT3 internal tandem duplications
t-AML causes
alkylating agents -> lose Chr5/7
topoisomerase II inhibitors -> rearrange 11q23 MLL
Poor prognoses - AML chromosomal abnormalities
t(1;22) RBM15-MLK1 (megakaryoblasts)
11q23 MLL abnormalities
CML
t(9;22) BCR-ABL 210kD protein
Tx: Gleevec
Good prognosis
Good prognosis - B-ALL chromosomal abnormalities
t(12;21) RUNX1
Otherwise, best if ages 1-10, if B-ALL vs T-ALL, and with hyperdiploidy
Bad prognoses - B-ALL chromosomal abnormalities
t(9;22) BCR-ABL 190kD protein
11q23; MLL
Classical Hodgkins - best prognosis and worst prognosis
Best prognosis is lymphocyte-rich Hodgkins
Worst is lymphocyte-poor
Defining feature of Nodular Lymphocyte-Predominant Hodgkins
Popcorn cells - multilobated nuclei
Mantle cell Non-Hodgkin’s B-CLL
t(11;14) IgH -> Cyclin D (G1->S)
“small”
Marginal zone Non-Hodgkin’s B-CLL
Associated with chronic infl., marginal zone only exists if B cells are proliferating ya dummy
“small”
Follicular Non-Hodgkin’s B-CLL
t(14;18) IgH -> BCL2 -|apoptosis
“small”
Burkitt’s lymphoma
Non-Hodgkin’s B-CLL, intermediate size
IgH -> c-myc (oncogene)
defining features: in Africans, see a jaw mass
Starry sky appearance of blood slides