TRAF3
Overview
TRAF3 is a negative regulator of NF-κB signaling disrupted in U-CLL via a recurrent chr14 deletion.
Alterations observed in the corpus
- TRAF3 is disrupted (together with ZFP36L1 and DICER1) by a recurrent 37-Mb chr14 deletion in U-CLL (4/87 WGS, 4.6%) arising via class-switch recombination PMID:35927489.
- NF-kB regulator; recurrently mutated and homozygously deleted in multiple myeloma (MM); contributes to aberrant NF-kB pathway activation in a subset of MM tumors PMID:24434212
- Recurrent deletions (14%) and truncating mutations (8%) in HPV(+) HNSCC; first reported link between TRAF3 loss and HPV-associated cancer; loss promotes aberrant NF-kB signalling PMID:25631445
- Identified as a novel B-cell activity driver in CLL in a 538-patient WES study; involved in NF-kB signaling pathway in B-cell malignancies PMID:26466571
- Recurrently focally deleted in both lung ADC and lung SqCC (Pan-Lung analysis) in a 1,144-NSCLC exome-sequencing cohort PMID:27158780.
Cancer types (linked)
- CLLSLL — disrupted by the recurrent U-CLL chr14 structural deletion PMID:35927489.
Co-occurrence and mutual exclusivity
- Co-disrupted with ZFP36L1 and DICER1 on the same chr14 deletion PMID:35927489.
Therapeutic relevance
- No direct targeted therapy reported in the corpus.
Open questions
- Functional contribution of TRAF3 loss relative to ZFP36L1/DICER1 co-disruption on the same event is unresolved PMID:35927489.
Sources
This page was processed by crosslinker on 2026-04-08. - PMID:24434212
This page was processed by wiki-cli on 2026-05-09. - PMID:25631445
This page was processed by wiki-cli on 2026-05-14. - PMID:26466571
This page was processed by wiki-cli on 2026-05-14. - PMID:27158780
This page was processed by wiki-cli on 2026-05-14.