Cooperativity between MAPK and PI3K signaling activation is required for glioblastoma pathogenesis.

ABSTRACT:

Background

Glioblastoma (GBM) genomes feature recurrent genetic alterations that dysregulate core intracellular signaling pathways, including the G1/S cell cycle checkpoint and the MAPK and PI3K effector arms of receptor tyrosine kinase (RTK) signaling. Elucidation of the phenotypic consequences of activated RTK effectors is required for the design of effective therapeutic and diagnostic strategies.

Methods

Genetically defined, G1/S checkpoint-defective cortical murine astrocytes with constitutively active Kras and/or Pten deletion mutations were used to systematically investigate the individual and combined roles of these 2 RTK signaling effectors in phenotypic hallmarks of glioblastoma pathogenesis, including growth, migration, and invasion in vitro. A novel syngeneic orth

SUBMITTER: Vitucci M 

PROVIDER: S-EPMC3779038 | biostudies-literature | 2013 Oct

REPOSITORIES: biostudies-literature