EPH receptor signaling as a novel therapeutic target in NF2-deficient meningioma.

ABSTRACT:

Background

Meningiomas are the most common primary brain tumor in adults, and somatic loss of the neurofibromatosis 2 (NF2) tumor suppressor gene is a frequent genetic event. There is no effective treatment for tumors that recur or continue to grow despite surgery and/or radiation. Therefore, targeted therapies that either delay tumor progression or cause tumor shrinkage are much needed. Our earlier work established mammalian target of rapamycin complex mTORC1/mTORC2 activation in NF2-deficient meningiomas.

Methods

High-throughput kinome analyses were performed in NF2-null human arachnoidal and meningioma cell lines to identify functional kinome changes upon NF2 loss. Immunoblotting confirmed the activation of kinases and demonstrated effectiveness of drugs to block the acti

SUBMITTER: Angus SP 

PROVIDER: S-EPMC6071664 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature