Discover Community Create You

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

Article

t(11;19)(q21;p13) translocation in mucoepidermoid carcinoma creates a novel fusion product that disrupts a Notch signaling pathway.

Nature genetics - 1 Feb 2003

Tonon Giovanni, Modi Sanjay, Wu Lizi, Kubo Akihito, Coxon Amy B, Komiya Takefumi, O'Neil Kevin, Stover Kristen, El-Naggar Adel, Griffin James D, Kirsch Ilan R, Kaye Frederic J

Abstract excerpt

Truncation of Notch1 has been shown to cause a subtype of acute leukemia, and activation of Notch4 has been associated with mammary and salivary gland carcinomas of mice. Here we identify a new mechanism for disrupting Notch signaling in human tumorigenesis, characterized by altered function of a new ortholog of the Drosophila melanogaster Notch co-activator molecule Mastermind. We cloned the t(11;19)...

Read the complete abstract on PubMed

Topics

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

Share to Artificial Gene Fusion
Share to Chromosomes, Human, Pair 11

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chromosomes, Human, Pair 19

Share to Neoplasms, Glandular and Epithelial

Share to Receptors, Notch

Share to Ribonuclease, Pancreatic

Share to Salivary Gland Neoplasms

Share to Transcription Factor HES-1

Source

Identifiers

PMID: 12539049
DOI: 10.1038/ng1083

Genes

MAML2
HES1
MAML1

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

t(11;19)(q21;p13) translocation in mucoepidermoid carcinoma creates a novel fusion product that disrupts a Notch signaling pathway.PMID 12539049Read ↗

CRTC1/MAML2 gain-of-function interactions with MYC create a gene signature predictive of cancers with CREB–MYC involvementSemantic proximity Read ↗

<i>MECT1-MAML2</i> Fusion Transcript Defines a Favorable Subset of Mucoepidermoid CarcinomaSemantic proximity Read ↗

Molecular classification of mucoepidermoid carcinomas—Prognostic significance of the <i>MECT1</i> – <i>MAML2</i> fusion oncogeneSemantic proximity Read ↗

The CRTC1-MAML2 fusion is the major oncogenic driver in mucoepidermoid carcinomaSemantic proximity Read ↗

Mect1-Maml2 Fusion Oncogene Linked to the Aberrant Activation of Cyclic AMP/CREB Regulated GenesSemantic proximity Read ↗

Recurrent rearrangements of the Myb/SANT-like DNA-binding domain containing 3 gene (MSANTD3) in salivary gland acinic cell carcinomaSemantic proximity Read ↗

Targeting Notch and EGFR signaling in human mucoepidermoid carcinomaSemantic proximity Read ↗

Gene expression profiling analysis of CRTC1-MAML2 fusion oncogene-induced transcriptional program in human mucoepidermoid carcinoma cellsSemantic proximity Read ↗

The landscape of gene fusions and somatic mutations in salivary gland neoplasms - Implications for diagnosis and therapy.Semantic proximity Read ↗

Identification of a novel fusion gene <i>MLL‐MAML2</i> in secondary acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(q21q23)Semantic proximity Read ↗

Whole-Exome Sequencing of Salivary Gland Mucoepidermoid Carcinoma.Semantic proximity Read ↗

Multi-dimensional genomic analysis of myoepithelial carcinoma identifies prevalent oncogenic gene fusionsSemantic proximity Read ↗

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