Table I.

Dual role of Notch signaling in cancer

Tumor type	Role of Notch signaling	Genes mutated	Putative or observed effect	References
T-ALL	Oncogene	NOTCH1	Ligand independent activation	Ellisen et al., 1991
		FBXW7	Stabilization of N1-IC	Weng et al., 2004
				Malyukova et al., 2007
				Maser et al., 2007
				O’Neil et al., 2007
				Thompson et al., 2007
CLL	Oncogene	NOTCH1	Stabilization of N1-IC	Fabbri et al., 2011
			Correlated with reduced survival	Puente et al., 2011
NSCLC	Oncogene	NOTCH1	Stabilization of N1-IC	Westhoff et al., 2009
			Correlated with reduced survival
PDAC	Oncogene	none	Loss of NOTCH1 decreased tumor latency	Hanlon et al., 2010
	Tumor suppressor		Loss of NOTCH2 increased tumor latency	Mazur et al., 2010
HCC	Tumor suppressor	none	Endogenous activation of Notch induces growth arrest and apoptosis	Viatour et al., 2011
			Activated Notch pathway correlated with better survival
CMML	Tumor suppressor	NCSTN	Loss of function mutations	Klinakis et al., 2011
		MAML1	Activated Notch signaling inhibits myeloid progenitor differentiation.
		APH1A
		NOTCH2
HNSCC	Tumor suppressor	NOTCH1	Truncated or ligand-binding inefficient receptors	Stransky et al., 2011
		NOTCH2	Predicted to impair differentiation	Agrawal et al., 2011
		NOTCH3
B-ALL	Tumor suppressor	none	Endogenous or exogenous activation of Notch induces growth arrest and apoptosis	Zweidler-McKay et al., 2005

PDAC: pancreatic ductal adenocarcinoma; B-ALL: B cell acute lymphoblastic leukemia.