Mammalian target of rapamycin inhibitors for the targeted therapy of non-small cell lung cancer.
10.3881/j.issn.1000-503X.2010.02.025
- Author:
Yi LIN
1
;
Li ZHANG
Author Information
1. Department of Medical Oncology, PUMC Hospital, CAMS and PUMC, Beijing 100730, China.
- Publication Type:Journal Article
- MeSH:
Carcinoma, Non-Small-Cell Lung;
drug therapy;
metabolism;
Humans;
Lung Neoplasms;
drug therapy;
metabolism;
Sirolimus;
therapeutic use;
TOR Serine-Threonine Kinases;
antagonists & inhibitors;
metabolism
- From:
Acta Academiae Medicinae Sinicae
2010;32(2):239-242
- CountryChina
- Language:Chinese
-
Abstract:
The mammalian target of rapamycin (mTOR), a master regulator of translation initiation, has recently emerged as an attractive therapeutic target for cancer therapy. It has been demonstrated that mTOR inhibitors activate several cell survival pathways including phosphatidyl inositol 3-kinase/serine or threonine-specific protein kinase Akt and mitogen-activated protein kinase or extracellular signal-regulated kinase kinase/extracellular signal-regulated kinase while suppressing mTOR signaling in different types of cancer cell lines and human tumor samples and thus make the cancer cells acquire resistance to the mTOR-targeted therapy. However, these cancer cells may be more dependent on (or addicted to) these survival pathways after receiving the mTOR-targeted therapy. It can be assumed that the combination of mTOR inhibitor and the suppressor of these survival pathways might achieve greater efficacy in inhibiting the growth of cancer cells. In this article we discuss the results of many pre-clinical and clinical studies of mTOR targeted therapy, with an emphasis of its effect against the non-small cell lung cancer.
