RRAS2
Overview
RRAS2 (also known as TC21) encodes a member of the RAS superfamily of small GTPases. The RRAS2 Q72 residue is paralogous to the well-characterized Q61 hotspot of canonical RAS genes (HRAS, KRAS, NRAS). Activating mutations at this position lock the protein in a GTP-bound active state, and RRAS2 has been found mutated in primary prostate cancer as part of a broader landscape of RAS-family pathway alterations.
Alterations observed in the corpus
- RRAS2 Q72L mutation in one primary prostate tumor; paralogous to RAS Q61 activating hotspot PMID:26544944
Cancer types (linked)
- PRAD (Prostate Adenocarcinoma): Q72L activating mutation observed in the TCGA prostate adenocarcinoma cohort (n=333), part of a broader ~25% PI3K/MAPK pathway alteration landscape PMID:26544944
Co-occurrence and mutual exclusivity
- Identified alongside HRAS Q61R (3/4 mutant cases) and RAC1 Q61R mutations in prostate cancer; these represent paralogous activating hotspots suggesting convergent RAS-like signaling activation PMID:26544944
Therapeutic relevance
- As part of the ~25% of prostate tumors with actionable PI3K or MAPK pathway lesions, RRAS2-activating mutations may represent candidates for MAPK-pathway inhibitor strategies PMID:26544944
Open questions
- The clinical and functional significance of RRAS2 Q72L in prostate cancer beyond the analogy to canonical RAS hotspots has not been experimentally validated PMID:26544944
Sources
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