Mutations resulting in overexpression of intracellular Notch1 (ICN1) are frequently observed
in human T cell acute lymphoblastic leukemia (T-ALL). We have determined the …

Hotspot mutations in the PEST-domain of NOTCH1 and NOTCH2 are recurrently identified
in B cell malignancies. To address how NOTCH-mutations contribute to a dismal prognosis …

NOTCH1 is a large type I transmembrane receptor that regulates normal T-cell development
via a signaling pathway that relies on regulated proteolysis. Ligand binding induces …

The identification of activating mutations in NOTCH1 in the majority of T-cell acute
lymphoblastic leukemias and lymphomas (T-ALL) has brought much interest in inhibiting …

Hematopoietic stem cells give rise to progeny that either self-renew in an undifferentiated
state or lose self-renewal capabilities and commit to lymphoid or myeloid lineages. Here we …

The main oncogenic driver in T-lymphoblastic leukemia is NOTCH1, which activates genes
by forming chromatin-associated Notch transcription complexes. Gamma-secretase-inhibitor …

Activating mutations of NOTCH1 (a well-known oncogene in T-cell acute lymphoblastic
leukemia) are present in∼ 4–13% of chronic lymphocytic leukemia (CLL) cases, where they …

Constitutive Notch activation is required for the proliferation of a subgroup of T-cell acute
lymphoblastic leukemia (T-ALL). Downstream pathways that transmit pro-oncogenic signals …

Constitutive NOTCH signaling in lymphoid progenitors promotes the development of
immature T-cell lymphoblastic neoplasms (T-ALLs). Although it is clear that Notch signaling …

Notch1 activation is essential for T-lineage specification of lymphomyeloid progenitors
seeding the thymus. Progression along the T cell lineage further requires cooperative …