PTEN and PI3K/AKT in non-small-cell lung cancer

被引:205
|
作者
Perez-Ramirez, Cristina [1 ,2 ]
Canadas-Garre, Marisa [1 ]
Angel Molina, Miguel [3 ]
Jose Faus-Dader, Maria [2 ]
Angel Calleja-Hernandez, Miguel [1 ,4 ]
机构
[1] Complejo Hosp Univ Granada, Inst Invest Biosanitaria Granada, UGC Prov Farm Granada, Pharmacogenet Unit, Granada 18014, Spain
[2] Univ Granada, Fac Pharm, Dept Biochem, E-18071 Granada, Spain
[3] SL Hosp Univ Quiron Dexeus, PANGAEA BIOTECH, Barcelona 08028, Spain
[4] Univ Granada, Fac Pharm, Dept Pharmacol, E-18071 Granada, Spain
关键词
EGFR; NSCLC; pharmacogenetics; PI3K; PTEN; resistance; TKI; TUMOR-SUPPRESSOR GENE; FACTOR-RECEPTOR GENE; TYROSINE KINASE INHIBITORS; VINORELBINE PLUS CISPLATIN; HEMATOPOIETIC STEM-CELLS; PHASE-III TRIAL; NF-KAPPA-B; PHOSPHOINOSITIDE; 3-KINASE; MESENCHYMAL TRANSITION; ACQUIRED-RESISTANCE;
D O I
10.2217/pgs.15.122
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Non-small-cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide. In the last years, the identification of activating EGFR mutations, conferring increased sensitivity and disease response to tyrosine kinase inhibitors, has changed the prospect of NSCLC patients. The PTEN/PI3K/AKT pathway regulates multiple cellular functions, including cell growth, differentiation, proliferation, survival, motility, invasion and intracellular trafficking. Alterations in this pathway, mainly PTEN inactivation, have been associated with resistance to EGFR-tyrosine kinase inhibitor therapy and lower survival in NSCLC patients. In this review, we will briefly discuss the main PTEN/PI3K/AKT pathway alterations found in NSCLC, as well as the cell processes regulated by PTEN/PI3K/AKT leading to tumorigenesis.
引用
收藏
页码:1843 / 1862
页数:20
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