| Type | Gene Modification | Chromosome rearrangement | Protein expression | Protein Function
|
|---|
| tumoral
| fusion
|
|
|
|
|
with NUP98 in translocation t(7;11),in acute myeloid leukemia (see AML2) |
| tumoral
|
|
|
| gain of function
|
|
coactivated by MEIS1 in acute and chronic myelogenous leukemia and in infant acute lymphoid leukemia |
| tumoral
|
|
| --over
|
|
|
in acute monocytic leukemia |
| tumoral
|
|
| --over
|
|
|
of NUP98-HOXA9 represses myeloid-specific gene transcription, thereby contributing to differentiation block in leukemogenesis |
| constitutional
|
|
| --over
|
|
|
very high expression in haemopoietic cells in adults over sixty |
| constitutional
|
|
| --over
|
|
|
inhibits inflammatory cytokine dependent inducible expression of leukocyte adhesion molecules in endothelial cells |
| tumoral
|
| translocation
|
|
|
|
t(7;17)(p15;q23) with MSI2 may contribute to disease progression in chronic myeloid leukemia |
| tumoral
|
|
| --other
|
|
aberrant expression has been shown to be important to the development of leukemia  |
| tumoral
|
|
| --over
|
|
|
of HOXA9 and HOXA10 and their essential cofactor MEIS1 in cells with the t(4;11) chromosome translocation and MLL-AF4 in acute leukemia |
