Abstract
Lung cancer is the leading cause of cancer-related death in the United States, and 85 to 90% of lung cancer cases are associated with tobacco use. Tobacco components promote lung tumorigenesis through genotoxic effects, as well as through biochemical modulation of signaling pathways such as the Akt/mammalian target of rapamycin (mTOR) pathway that regulates cell proliferation and survival. This review will describe cell surface receptors and other upstream components required for tobacco carcinogen - induced activation of Akt and mTOR. Preclinical studies show that inhibitors of the Akt/mTOR pathway inhibit tumor formation in mouse models of carcinogen-induced lung tumorigenesis. Some of these inhibitors will be highlighted, and their clinical potential for the treatment and prevention of lung cancer will be discussed.
Original language | English (US) |
---|---|
Pages (from-to) | 4-10 |
Number of pages | 7 |
Journal | Clinical Cancer Research |
Volume | 16 |
Issue number | 1 |
DOIs | |
State | Published - Jan 1 2010 |
Externally published | Yes |
ASJC Scopus subject areas
- Oncology
- Cancer Research