Abstract
Renal cell carcinomas make up 3% of all cancers and one in four patients is metastatic at time of diagnosis. This cancer is one of the most resistant to cytotoxic chemotherapy. Studies have shown that the efficiency of interferon-alpha and/or interleukin-2 based immune therapies is limited in patients with metastatic renal cell carcinoma but latest advances in molecular biology and genetic science have resulted in better understanding of its biology. Tumor angiogenesis, tumor proliferation and metastasis develop by the activation of signal message pathways playing a role in the development of renal cell carcinomas. Better definition of these pathways has caused an increase in preclinic and clinical studies into target directed treatment of renal cell carcinoma. Many recent studies have shown that numerous anti-angiogenic agents have marked clinical activity. In this article, the focus is on general characteristics of molecular pathways playing a major role in renal cell carcinoma, reviewing clinical information onagents used in the target directed treatment of metastatic lesions.
Highlights
Renal and renal pelvis tumors make up approximately 3% of all malignancies
Renal cell carcinomas make up 3% of all cancers and one in four patients is metastatic at time of diagnosis
Studies have shown that the efficiency of interferon-alpha and/or interleukin-2 based immune therapies is limited in patients with metastatic renal cell carcinoma but latest advances in molecular biology and genetic science have resulted in better understanding of its biology
Summary
Renal and renal pelvis tumors make up approximately 3% of all malignancies. Most of these cases are renal cell carcinoma (RCC) which are genetically and histologically different from renal pelvis tumors. The most important of these pathways is the angiogenesis pathway which includes von Hippel-Lindau (VHL) gene in its regulation, and important targets in RCC treatment are growth factors associated with this pathway. VHL gene which is located on the chromosome 3p25-26 is the gene responsible for the regulation of hypoxia-inducible factor-1 (HIF-1) (Yazici et al, 2011). The products of this gene control cellular response which develops as a response against oxygen decrease. In the majority of patients with clear cell RCC, tumor suppressing VHL gene has become inactivated by deletion, mutation or methylation (Rini, 2005). General characteristics of the targeted molecules in RCC pathogenesis and clinic data about the drugs targeting these molecules are reviewed
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