MAGI2
Overview
MAGI2 (Membrane-Associated Guanylate Kinase Inverted 2) encodes a scaffolding protein that binds and stabilizes PTEN, thereby promoting PTEN-mediated suppression of PI3K/AKT signaling. Recurrent structural rearrangements in MAGI2 in melanoma effectively mimic PTEN loss, implicating it as an indirect tumor suppressor in PI3K pathway regulation.
Alterations observed in the corpus
- MAGI2 is recurrently rearranged in 3/25 metastatic melanomas (WGS discovery cohort); disruption of MAGI2 destabilizes PTEN and is functionally equivalent to PTEN loss PMID:22622578
- Recurrent disruptive rearrangements identified in prostate adenocarcinoma via chromoplexy, alongside GSK3B and FOXO1, implicating MAGI2 in prostate cancer signaling; functional consequences not experimentally validated PMID:23622249
Cancer types (linked)
- SKCM (Melanoma): Structural rearrangements in 3/25 discovery WGS tumors; co-occurs with PTEN rearrangements across the cohort PMID:22622578
Co-occurrence and mutual exclusivity
- Rearrangements co-occur with other loci disrupted by structural variation in melanoma (PTEN, MACROD2, FHIT, CSMD1, RBFOX1) PMID:22622578
Therapeutic relevance
- MAGI2 loss activates the PI3K/AKT pathway; patients with MAGI2 rearrangements may show functional equivalence to PTEN-null tumors, with potential sensitivity to PI3K or AKT inhibitors, though no direct clinical data are available.
Open questions
- Whether MAGI2 rearrangements are mutually exclusive with direct PTEN mutations or co-occur, and whether combined loss confers additive pathway activation, is not resolved in the current corpus.
Sources
This page was processed by crosslinker on 2026-05-09. - PMID:23622249
This page was processed by crosslinker on 2026-05-09.