TRIO
Overview
TRIO is a guanine nucleotide exchange factor (GEF) with dual RhoGEF domains that activates both RAC1 and RHOA, regulating cytoskeletal dynamics, cell migration, and invasion. In esophageal adenocarcinoma (EAC), TRIO is one of several upstream RAC1-regulatory genes recurrently mutated, consistent with convergent selection on the RAC1 signaling axis in this cancer type.
Alterations observed in the corpus
- Recurrently mutated in EAC (145-tumor WES cohort); identified as one of several upstream regulators of RAC1 alongside TIAM1, VAV2, ECT2, DOCK2, and ELMO1 PMID:23525077.
- TRIO recurrent focal amplification detected in TCC bladder cancer PMID:24121792
- TRIO identified as a recurrent structural-variant partner of CLPTM1L in acral lentiginous melanoma (ACRM); all such rearrangements occurred in BRAF wild-type tumors PMID:28373299.
- Recurrent TRIO-TERT fusions (n=3) drive highest TERT expression in DDLPS sarcoma PMID:29100075
Cancer types (linked)
- EAC: Part of a convergently mutated RAC1-GEF regulatory axis in esophageal adenocarcinoma; downstream effector PAK1 is recurrently amplified at 11q13 PMID:23525077.
Co-occurrence and mutual exclusivity
Therapeutic relevance
- The convergent RAC1-pathway alteration pattern in EAC implicates RAC1/PAK1 signaling as a candidate therapeutic axis, though no TRIO-specific targeting agents are discussed in the corpus PMID:23525077.
Open questions
- Functional validation of TRIO mutations in EAC invasion models has not been reported in this cohort PMID:23525077.
Sources
This page was processed by crosslinker on 2026-05-09. - PMID:24121792
This page was processed by crosslinker on 2026-05-09. - PMID:28373299
This page was processed by wiki-cli on 2026-05-14. - PMID:29100075
This page was processed by wiki-cli on 2026-05-15.