Search Tips
of 1 Next >
Results Found: 3
  • PI3K inhibition activates SGK1 via a feedback loop to promote chromatin-based regulation of ER-dependent gene expression

    Authors
    Toska, Eneda
    Koche, Richard Patrick
    Description

    Summary from GEO: "The phosphoinositide 3-kinase (PI3K) pathway integrates extracellular stimuli to phosphorylate and activate key downstream effectors such as AKT and serum-and glucocorticoid-inducible kinase (SGK1). We have previously reported that the PI3K pathway regulates ER-dependent transcription in breast cancer through the phosphorylation of the epigenetic regulator KMT2D by AKT. Here, we...

    Subject
    Chromatin Assembly and Disassembly
    Phosphatidylinositol 3-Kinase
    Phosphoinositide-3 Kinase Inhibitors
    Phosphorylation
    Receptors, Estrogen
    Access Rights
    Free to All
  • A paracrine IGF1/IGF1R-PI3K signaling loop underlies resistance to CSF-1R inhibition in GBM

    Authors
    Bowman, Robert L.
    Quail, Daniela F.
    Joyce, Johanna A.
    Description

    Summary from GEO: "Glioblastoma multiforme (GBM) is the most aggressive form of glioma, and is notorious for its terminal prognosis and lack of responsiveness to current treatment approaches. The brain tumor microenvironment (TME) represents a largely untapped reservoir of therapeutic target options in GBM. Here we have focused on the interplay between glioma cells and tumor-associated macrophages/...

    Subject
    Drug Therapy, Combination
    Glioblastoma
    Macrophages
    Neoplasm Recurrence, Local
    Phosphoinositide-3 Kinase Inhibitors
    Receptor, IGF Type 1
    Tumor Microenvironment
    Access Rights
    Free to All
  • Microenvironment-driven IGF-1R/PI3K signaling underlies acquired resistance to CSF1R inhibition in gliomas (CGH)

    Authors
    Bowman, Robert L.
    Quail, Daniela F.
    Schuhmacher, Alberto J.
    Joyce, Johanna A.
    Description

    Summary form GEO: "Macrophages accumulate with glioblastoma multiforme (GBM) progression, and can be acutely targeted via inhibition of colony stimulating factor-1 receptor (CSF-1R) to regress high-grade tumors in animal models. However, whether and how resistance emerges in response to sustained CSF-1R blockade is unknown. Here, we investigate whether long-term CSF-1R inhibition can stably regress...

    Subject
    Drug Therapy, Combination
    Glioblastoma
    Macrophages
    Neoplasm Recurrence, Local
    Phosphoinositide-3 Kinase Inhibitors
    Receptor, IGF Type 1
    Tumor Microenvironment
    Access Rights
    Free to All