Oncology - break-points, probes, therapies Flashcards Preview

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Flashcards in Oncology - break-points, probes, therapies Deck (15):
1

inv(3) or t(3;3)

AML

inv(3)(q21.3q26.2)

t(3;3)(q21.3;q26)

GATA2;MECOM

ELN adverse

2

t(8;21)

AML

t(8;21)(q22;q22.1)

RUNX1-RUNX1T1

ELN favourable

3

inv(16)

AML

inv(16)(p13.1q22)

CBFB-MYH11

ELN favourable

4

t(9;11)

AML

t(9;11)(p21.3;q23.3)

MLLT3-KMT2A

ELN Intermediate

5

t(6;9)

AML

t(6;9)(p23;q34.1)

DEK-NUP214

ELN Adverse

6

t(15;17)

APL

t(15;17)(q24;q21)

PML-RARA

Favourable if treated with ATRA

7

NPM1 mutation

Favourable

8

FLT3-ITD

Poor

9

NPM1 mutation with no/low FLT-ITD

Favourable

10

NPM1 mutation and FLT3-ITD high

Intermediate

FLT3 inhibitors = midostaurin

11

Wild type NPM1 with no/low FLT3-ITD

Intermediate

12

Wild type NPML with high FLT3-ITD

Adverse

FLT3 inhibitors = midostaurin

13

-5 or del(5q), -7, -17/abn(17p)

Adverse

14

Mutated RUNX1 or ASXL1 or TP53

Adverse

15

Novel therapies for AML

FLT3 inhibitors

Epigenetic therapies that target the metabolic enzymes IDH1 and IDH2 that are frequently mutated in AML

Targeted immunotherapy CD33, CD123,
CLEC12A (AML antigenic targets)

Engineered chimeric antigen receptor T (CAR-T) cells target CD33 and CD123 are in early trials