Abnormally Activated mTOR May Play a Role in Many Cancers
Mutations in a number of cellular proteins and pathways located upstream from mTOR have been implicated in the development and spread of many types of cancer.1-15
These mutations include:
- Overexpression/amplification of a growth factor or growth factor receptor (e.g., EGF/EGFR, HER2, IGF-1/IGF-1R, TGF, estrogen receptor)
- Constitutive (deregulated) activation of a receptor or other signaling protein (e.g., Bcr-Abl, Ras, PI3K)
- Inactivation of a tumor suppressor or other regulatory protein that normally "turns off" a signaling pathway (e.g., PTEN, TSC1/TSC2)
These mutations and others result in the abnormal activation of mTOR, which may lead to deregulated cell proliferation, tumor angiogenesis, and abnormal cell metabolism.

Selected mutations that may abnormally activate mTOR in cancer
Abnormally activated mTOR may play a role in a wide range of cancers, including renal cell carcinoma, lung cancer, breast cancer, colorectal cancer, and neuroendocrine tumors (NET). Inhibitors of mTOR are currently being evaluated in clinical trials in a number of different tumor types.

mTOR is abnormally activated in many cancers
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