Journal
GENES & DEVELOPMENT
Volume 36, Issue 15-16, Pages 874-875Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.350069.122
Keywords
meningioma; YAP1; NF2; Hippo; YAP1-MAML2; gene fusion
Categories
Funding
- National Cancer Institute (NCI) Intramural Program
- NCI Comprehensive Oncology Network for Evaluating Rare CNS Tumors (NCI-CONNECT)
- Rare Tumor Patient Engagement Network (RTPEN)
- Cancer Moonshot funds
- National Institutes of Health, National Cancer Institute, Center for Cancer Research, Neuro-Oncology Branch
Ask authors/readers for more resources
Loss of NF2 gene and YAP1-MAML2 fusion in meningiomas promote tumor formation through TEAD-dependent YAP1 activity. Pharmacological inhibition of YAP1-TEAD has shown antitumor activity in both YAP1 fusion-positive and NF2 mutant meningiomas. Disruption of the YAP1-TEAD interaction may provide a potential therapeutic option for these tumors.
Loss of the NF2 tumor suppressor gene is a common finding in meningiomas, and more recently YAP1 fusions have been found in a subset of pediatric NF2 wild-type meningiomas. In the previous issue of Genes & Development, Szulzewsky and colleagues (pp. 857-870) showed that TEAD-dependent YAP1 activity by either the loss of the NF2 gene or YAP1-MAML2 fusion is an oncogenic process promoting meningioma tumorigenesis. Furthermore, pharmacological inhibition of YAP1-TEAD resulted in antitumor activity in both YAP1 fusion-positive and NF2 mutant meningiomas. Together, these data indicate that disruption of the YAP1-TEAD interaction raises a potential therapeutic option for these tumors that requires future investigation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available
Share Paper
