Characterization of activating mutations of NOTCH3 in T-cell acute lymphoblastic leukemia and anti-leukemic activity of NOTCH3 inhibitory antibodies.

doi:10.1038/onc.2016.133

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Characterization of activating mutations of NOTCH3 in T-cell acute lymphoblastic leukemia and anti-leukemic activity of NOTCH3 inhibitory antibodies.

Oncogene - 24 Nov 2016

Bernasconi-Elias P, Hu T, Jenkins D, Firestone B, Gans S, Kurth E, Capodieci P, Deplazes-Lauber J, Petropoulos K, Thiel P, Ponsel D, Hee Choi S, LeMotte P, London A, Goetcshkes M, Nolin E, Jones M D, Slocum K, Kluk M J, Weinstock D M, Christodoulou A, Weinberg O, Jaehrling J, Ettenberg S A, Buckler A, Blacklow S C, Aster J C, Fryer C J

Abstract excerpt

Notch receptors have been implicated as oncogenic drivers in several cancers, the most notable example being NOTCH1 in T-cell acute lymphoblastic leukemia (T-ALL). To characterize the role of activated NOTCH3 in cancer, we generated an antibody that detects the neo-epitope created upon gamma-secretase cleavage of NOTCH3 to release its intracellular domain (ICD3), and sequenced the negative regulatory region (NRR)...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amino Acid Substitution

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Antibodies, Monoclonal

Share to Antineoplastic Agents

Share to Codon

Share to Epitopes

Share to Precursor T-Cell Lymphoblastic Leukemia-Lymphoma

Share to Receptor, Notch3

Share to Xenograft Model Antitumor Assays

Source

Open in PubMed Open full text

Identifiers

PMID: 27157619
DOI: 10.1038/onc.2016.133
PMCID: PMC5102827

Genes

NOTCH3
NOTCH1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Characterization of activating mutations of NOTCH3 in T-cell acute lymphoblastic leukemia and anti-leukemic activity of NOTCH3 inhibitory antibodies.PMID 27157619Read ↗

Oncogenic Notch signaling in T-cell and B-cell lymphoproliferative disordersSemantic proximity Read ↗

A novel Monoclonal Antibody against Notch1 Targets Leukemia-associated Mutant Notch1 and Depletes Therapy Resistant Cancer Stem Cells in Solid Tumors.Semantic proximity Read ↗

Notch signaling as a therapeutic target for acute lymphoblastic leukemiaSemantic proximity Read ↗

Characterization of Notch1 antibodies that inhibit signaling of both normal and mutated Notch1 receptors.Semantic proximity Read ↗

Recent advances on NOTCH signaling in T-ALL.Semantic proximity Read ↗

Deregulated NOTCH signaling in acute T-cell lymphoblastic leukemia/lymphoma: new insights, questions, and opportunities.Semantic proximity Read ↗

Activating mutations of NOTCH1 in human T cell acute lymphoblastic leukemia.Semantic proximity Read ↗

Targeting NOTCH1 in hematopoietic malignancy.Semantic proximity Read ↗

Oncogenic NOTCH1 control of MYC and PI3K: challenges and opportunities for anti-NOTCH1 therapy in T-cell acute lymphoblastic leukemias and lymphomas.Semantic proximity Read ↗

LAG Time in the Era of Immunotherapy—New Molecular Insights Into the Immunosuppression Mechanism of Lymphocyte Activation Gene‐3Semantic proximity Read ↗

T cell acute lymphoblastic leukemia/lymphoma: a human cancer commonly associated with aberrant NOTCH1 signaling.Semantic proximity Read ↗

Development and characterization of Novel Small Molecule Inhibitors Targeting LAG-3 ProteinSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.