Oncogenic PI3K deregulates transcription and translation
There have long been indications of a role for PI3K (phosphatidylinositol 3-kinase) in cancer
pathogenesis. Experimental data document a requirement for deregulation of both
transcription and translation in PI3K-mediated oncogenic transformation. The recent
discoveries of cancer-specific mutations in PIK3CA, the gene that encodes the catalytic
subunit p110α of PI3K, have heightened the interest in the oncogenic potential of this lipid
kinase and have made p110α an ideal drug target.
pathogenesis. Experimental data document a requirement for deregulation of both
transcription and translation in PI3K-mediated oncogenic transformation. The recent
discoveries of cancer-specific mutations in PIK3CA, the gene that encodes the catalytic
subunit p110α of PI3K, have heightened the interest in the oncogenic potential of this lipid
kinase and have made p110α an ideal drug target.
Abstract
There have long been indications of a role for PI3K (phosphatidylinositol 3-kinase) in cancer pathogenesis. Experimental data document a requirement for deregulation of both transcription and translation in PI3K-mediated oncogenic transformation. The recent discoveries of cancer-specific mutations in PIK3CA, the gene that encodes the catalytic subunit p110α of PI3K, have heightened the interest in the oncogenic potential of this lipid kinase and have made p110α an ideal drug target.
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