Journal
ONCOGENE
Volume 24, Issue 50, Pages 7465-7474Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1209096
Keywords
PTEN; AKT; prostate cancer; phosphoinostide; 3-kinase
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Prostate cancer remains a major cause of cancer-related mortality. Genetic clues to the molecular pathways driving the most aggressive forms of prostate cancer have been limited. Genetic inactivation of PTEN through either gene deletion or point mutation is reasonably common in metastatic prostate cancer and the resulting activation of phosphoinostide 3-kinase, AKT and mTOR provides a major therapeutic opportunity in this disease as mTOR inhibitors, HSP90 inhibitors and PI3K inhibitors begin to enter clinical development.
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