Molecular basis for the treatment of renal cell carcinoma

被引:17
|
作者
Suarez, Cristina [1 ]
Morales, Rafael [1 ]
Munoz, Eva [1 ]
Rodon, Jordi [1 ]
Valverde, Claudia M. [1 ]
Carles, Joan [1 ]
机构
[1] Vall Hebron Univ Hosp, Dept Med Oncol, ES-08035 Barcelona, Spain
来源
CLINICAL & TRANSLATIONAL ONCOLOGY | 2010年 / 12卷 / 01期
关键词
Renal cell carcinoma; Molecular basis; Targeted therapies; Key pathways; ENDOTHELIAL GROWTH-FACTOR; TUMOR-SUPPRESSOR GENE; RECEPTOR ANTIBODY C225; INTERFERON-ALPHA; PHASE-II; HEREDITARY LEIOMYOMATOSIS; FUMARATE-HYDRATASE; ANTITUMOR-ACTIVITY; INVASIVE GROWTH; DOUBLE-BLIND;
D O I
10.1007/s12094-010-0461-4
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Renal cell carcinoma (RCC) is a heterogeneous malignancy whose incidence rate has notably increased in recent years without any evident reason. Traditionally, RCC has been resistant to classic treatments ( chemotherapy, radiotherapy and hormonal therapy), with only a small percentage of patients benefiting from cytokine therapy. Different hereditary syndromes have been associated with RCC, Von Hippel Lindau (VHL) being the most important syndrome. Understanding key molecular pathways implicated in the tumorigenesis of RCC has crystallised in the development of more effective therapies. Specifically, drugs targeting VEGF (bevacizumab, sunitinib, sorafenib, axitinib, pazopanib) and PI3K-mTOR (temsirolimus and everolimus) have become the cornerstone of renal cancer treatment.
引用
收藏
页码:15 / 21
页数:7
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