Activation of the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway has been strongly linked with prostate cancer progression and metastatic potential.1 Loss of the inhibitory phosphatase, PTEN, leading to hyperactivation of PI3K/AKT/mTOR oncogenic signaling, occurs in 40-50% of metastatic castration-resistant prostate cancer.1,2 Not surprising is the fact that PTEN loss in patients with metastatic castration-resistant prostate cancer is associated with a worse prognosis and less benefit from androgen receptor (AR) blockade.3 Likewise, PTEN loss and subsequent Akt activation confer radiation4 and chemotherapy5, 6 resistance.
Evan Yu, MD
Evan Yu, a medical oncologist, treats prostate, bladder, and testicular cancer, and is passionate about providing a personalized medical approach to a selection of novel therapies as well as understanding biologic mechanism of drug sensitivity and resistance.
Medical Oncology, Translational Research, Novel molecular targeted agents, Biomarkers, Imaging (PET scans, MRI), Bone health.
- Professor, Department of Medicine, Division of Oncology, University of Washington School of Medicine
- Member, Clinical Research Division, Fred Hutchinson Cancer Research Center
- Clinical Research Director, Genitourinary Oncology, Seattle Cancer Care Alliance
- Medical Director, Clinical Research Service, Fred Hutchinson Cancer Research Consortium
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