Molecular mechanisms of tumor resistance to PI3K-mTOR-targeted therapy.
- Author:
Jing TAN
1
;
Qiang YU
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents; pharmacology; therapeutic use; Drug Resistance, Neoplasm; Genes, myc; Humans; Molecular Targeted Therapy; methods; Neoplasms; drug therapy; metabolism; Phosphatidylinositol 3-Kinases; antagonists & inhibitors; metabolism; Phosphorylation; Proto-Oncogene Proteins c-myc; metabolism; Signal Transduction; Sirolimus; pharmacology; therapeutic use; TOR Serine-Threonine Kinases; antagonists & inhibitors; metabolism
- From:Chinese Journal of Cancer 2013;32(7):376-379
- CountryChina
- Language:English
- Abstract: Deregulation of the phosphatidylinositide 3-kinase (PI3K) and mammalian target of rapamycin (mTOR) signaling pathway occurs frequently in a wide range of human cancers and is a major driving force in tumorigenesis. Thus, small molecules targeting this pathway are under active development as anticancer therapeutics. Although small-molecule inhibitors of the PI3K-mTOR pathway have shown promising clinical efficacy against human cancers, the emergence of drug resistance may limit their success in the clinic. To date, several resistance mechanisms, including both PI3K-dependent and -independent mechanisms, have been described. Here, we summarize the current understanding of resistance mechanisms to PI3K-mTOR inhibitors and discuss potential strategies for overcoming resistance for potential clinical application.
