Table 2.

Genes deregulated by MLL-AF9 and prioritized as potentially druggable targets in MLL-AF9 leukemia

Gene	log 2 FC	Protein class	Official full name
			Biological role
AHR	0.44	Nuclear receptor	Aryl hydrocarbon receptor
			Upregulated by AML associated fusion gene AML1-ETO. Differentiation of myeloblastic leukemia cells. Estrogen receptor degradation. AHR knockout mice display CML.
ATP2B2	−0.69	Transporter	ATPase, Ca++ transporting, plasma membrane 2
			Lowers intracellular calcium; protects from apoptosis.
DRD5	−0.96	Receptor	Dopamine receptor D5
			Raised after G-CSF treatment; dopamine receptor agonists activate Wnt signaling, induce migration and increase clonogenic capacity and repopulation of CD34+ cells.
HIPK2	0.5	Enzyme	Homeodomain interacting protein kinase 2
			Phosphorylates transcription (co-) factors (e.g. c-Myb); may trigger (myeloid) differentiation and apoptosis. Mutations found in AML cases.
PARP8	−0.63	Enzyme	Poly (ADP-ribose) polymerase family, member 8
			Phosphorylated upon DNA damage. Upregulated in MLL rearranged AML patients.
ROR2	0.81	Receptor/enzyme	Receptor tyrosine kinase-like orphan receptor 2
			Mediates noncanonical Wnt signaling. Putative tumor suppressor in leukemia, presumably via inhibition of Wnt canonical signaling.
TAS1R3	−2.01	Receptor	Taste receptor, type 1, member 3
			Glucose absorption/energy supply. Heterodimers sense extracellular amino acids, activate MTORC1 and inhibit autophagy.

Details to biological roles and references are given in Additional file 3: Table S2. Log₂FC: log₂ fold change in MLL-AF9 knockdown relative to control.