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 …

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 …

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 …

The NOTCH1 signaling pathway directly links extracellular signals with transcriptional
responses in the cell nucleus and plays a critical role during T cell development and in the …

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 …

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 …

Notch signaling controls cell fate decisions of hematopoietic progenitors by inhibiting certain
steps of differentiation and inducing either self-renewal or differentiation toward lymphoid or …

Signaling through the Notch1 receptor has a pivotal role in early thymocyte development.
Gain of Notch1 function results in the development of T‐cell acute lymphoblastic leukemia in …

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 …

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