Abstract

The management of metastatic renal cell carcinoma (mRCC) has evolved considerably in the last decade. A number of different systemic molecular targeted agents that have been recently approved have improved the survival of patients with mRCC. This mini-review focuses on the implementation of multi-modality therapy in the management of mRCC and the approved indications of the various available novel agents. These novel agents have expanded our armamentarium and improved clinical outcomes of this challenging disease that has considerable biological heterogeneity and clinical variability.

Highlights

  • Kidney cancer is the twelfth most common cancer worldwide - 338,000 new cases were diagnosed in 2012 [1]

  • In the era of vascular endothelial growth factor (VEGF) targeted therapy, another prognostic model was derived from patients treated with the tyrosine kinase inhibitors (TKIs) sorafenib, Sunitinib, and bevacizumab with IFN [7]

  • Sorafenib has a mechanism of action similar to sunitinib and, in addition to inhibiting VEGF receptor (VEGFR), FLT-3, c-kit, RET, PDGF receptors (PDGFR) a and b, inhibits serine and threonine and ras kinases

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Summary

Introduction

Kidney cancer is the twelfth most common cancer worldwide - 338,000 new cases were diagnosed in 2012 [1]. The highest incidence of kidney cancer is seen in Northern America and Europe while the lowest incidence is seen in Africa and Asia. Renal cell carcinoma (RCC) accounts for more than 90% of cases and represents about 2-3% of adult malignancies. Despite recent scientific advances in diagnosis and management almost 25-30% RCC patients are metastatic at diagnosis [2], and another 2030% of patients with localized disease who undergo nephrectomy develop metastasis, with a median time to relapse of 15-18 months [3]

Prognostic models
Role of surgery
Role of Radiation Therapy
Systemic Therapy
Role of Cytokine Therapy and Immunotherapy
Role of Targeted Therapy
VEGF Inhibitors and TKIs
Role of Chemotherapy
Bone metastasis and supportive care
Findings
Conclusion
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