MAML3
Overview
MAML3 (Mastermind Like Transcriptional Coactivator 3) is a transcriptional co-activator in the NOTCH signalling pathway, homologous to MAML1 and MAML2. In pancreatic ductal adenocarcinoma (PAAD), MAML3 is part of recurrent NOTCH-pathway alterations that collectively affect 31% of cases and nominate γ-secretase inhibitors as candidate therapies.
Alterations observed in the corpus
- MAML3 part of NOTCH-pathway alterations (NOTCH1–4, JAG1/JAG2, MAML1–3) totalling 31% of cases in a 109-case PDA WES cohort; amplification/mutation patterns nominate γ-secretase inhibitor MK0752 as a candidate therapy. PMID:25855536
- Recurrent in-frame UBTF–MAML3 and TCF4–MAML3 fusions (10 fusion-positive tumors) in pheochromocytoma/paraganglioma; 2.7-fold overexpression (p<5e-6); drives DNA hypomethylation and Wnt/Hedgehog signaling; defines the Wnt-altered subtype and is a clinical marker of metastasis and poor aggressive-disease-free survival PMID:28162975
Cancer types (linked)
- PAAD: Part of the NOTCH-pathway alteration cluster in a 109-case whole-exome sequencing cohort of resected pancreatic ductal adenocarcinoma. PMID:25855536
Co-occurrence and mutual exclusivity
- Co-altered with NOTCH1–4, JAG1, JAG2, and MAML1/MAML2 as part of the broader NOTCH-pathway alteration cluster in PDA. PMID:25855536
Therapeutic relevance
- NOTCH-pathway alterations including MAML3 in 31% of PDA cases nominate γ-secretase inhibitor MK0752 as a candidate therapy. PMID:25855536
Open questions
- Specific alteration types (amplification vs. mutation) and frequencies of individual MAML family members in PDA are not broken out per gene. PMID:25855536
Sources
This page was processed by crosslinker on 2026-05-14. - PMID:28162975
This page was processed by entity-page-writer on 2026-05-15.