Targeting RTK Signaling Pathways in Cancer

被引:292
作者
Regad, Tarik [1 ]
机构
[1] Nottingham Trent Univ, John Van Geest Canc Res Ctr, Sch Sci & Technol, Clifton Lane, Nottingham NG11 8NS, England
关键词
RTK; MAP kinase; PI3K; AKT; small molecule inhibitors; cancer; GROWTH-FACTOR-RECEPTOR; SQUAMOUS-CELL CARCINOMA; COMPARATIVE GENOMIC HYBRIDIZATION; GASTROINTESTINAL STROMAL TUMORS; METASTATIC BREAST-CANCER; TYROSINE KINASE DOMAIN; AFATINIB BIBW 2992; C-MET; LUNG-CANCER; PROTEIN-KINASE;
D O I
10.3390/cancers7030860
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The RAS/MAP kinase and the RAS/PI3K/AKT pathways play a key role in the regulation of proliferation, differentiation and survival. The induction of these pathways depends on Receptor Tyrosine Kinases (RTKs) that are activated upon ligand binding. In cancer, constitutive and aberrant activations of components of those pathways result in increased proliferation, survival and metastasis. For instance, mutations affecting RTKs, Ras, B-Raf, PI3K and AKT are common in perpetuating the malignancy of several types of cancers and from different tissue origins. Therefore, these signaling pathways became prime targets for cancer therapy. This review aims to provide an overview about the most frequently encountered mutations, the pathogenesis that results from such mutations and the known therapeutic strategies developed to counteract their aberrant functions.
引用
收藏
页码:1758 / 1784
页数:27
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