期刊
BRAIN PATHOLOGY
卷 19, 期 1, 页码 112-120出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1750-3639.2008.00233.x
关键词
glioblastoma; PI3 kinase; kinase inhibitors; Akt; metabolism; apoptosis; combination therapy
资金
- NIH
- Burroughs Wellcome Fund
- American Brain Tumor Association
- Brain Tumor Society
- Alex's Lemonade Stand
- Children's National Brain Tumor
- Wallace H. Coulter, Katie Dougherty
- Pediatric Brain Tumor, Samuel G. Waxman and V Foundations
- UC-Genentech Discovery
- NATIONAL CANCER INSTITUTE [R01CA133091, P01CA081403, R01CA102321, R01CA148699] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS055750] Funding Source: NIH RePORTER
The PI3 kinase (PI3K) family plays a complex role in cell biology and metabolism. Signaling through the PI3Ks is frequently activated in many human cancers, including glioblastoma, because of gain-of-function mutations in PIK3CA or loss of PTEN. Experiments involving genetic mouse models and small molecule inhibitors have helped to elucidate the roles of the regulatory and catalytic subunits of PI3K in metabolism and cancer. Downstream of PI3K is Akt, a critical effector of growth, proliferation and survival. The suggested dependence of glioblastoma tumors on PI3K signaling implies that PI3K inhibitors should lead to effective killing of these cancer cells, but that has been shown not to be the case. The engagement of other survival pathways in response to PI3K inhibition prompts the need to develop combination therapies that promote cytotoxicity in cancer cells.
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