Gain-of-function NOTCH1 mutations are found in 50%–70% of human T cell acute
lymphoblastic leukemia/lymphoma (T-ALL) cases. Gain-of-function NOTCH1 alleles that …

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 …

Recent work with mouse models and human leukemic samples has shown that gain-of-
function mutation (s) in Notch1 is a common genetic event in T-cell acute lymphoblastic …

Human acute T-cell lymphoblastic leukemias and lymphomas (T-ALL) are commonly
associated with gain-of-function mutations in Notch1 that contribute to T-ALL induction and …

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

Notch signaling is often considered a model hematopoietic proto-oncogene because of its
role as the main trigger of T cell acute lymphoblastic leukemia (T-ALL). Although its role in T …

T-cell acute lymphoblastic leukemia (T-ALL) is a highly proliferative hematologic malignancy
that results from the transformation of immature T-cell progenitors. Aberrant cell growth and …

Mammalian Notch homologs were first identified from the involvement of Notch1 in a
recurrent chromosomal translocation in a subset of human T-cell leukemias. The effect of the …

Abstract Purpose: Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic
leukemia (T-ALL), occurring in> 50% of patients. In murine models of T-ALL, Notch-1 …

NOTCH1 pathway activation contributes to the pathogenesis of over 60% of T-cell acute
lymphoblastic leukemia (T-ALL). While Notch is thought to exert the majority of its effects …