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Published on: January 22, 2013
Sunitinib resistance in renal cell carcinoma: From molecular mechanisms to predictive biomarkers
Juan Jin1, Yuhao Xie2, Jin-Shi Zhang3
1Department of Nephrology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Traditional Chinese Medicine), Hangzhou, Zhejiang 310003, China.
Abstract:
Currently, renal cell carcinoma (RCC) is the most prevalent type of kidney cancer. Targeted therapy has replaced radiation therapy and chemotherapy as the main treatment option for RCC due to the lack of significant efficacy with these conventional therapeutic regimens. Sunitinib, a drug used to treat gastrointestinal tumors and renal cell carcinoma, inhibits the tyrosine kinase activity of a number of receptor tyrosine kinases, including vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), c-Kit, rearranged during transfection (RET) and fms-related receptor tyrosine kinase 3 (Flt3). Although sunitinib has been shown to be efficacious in the treatment of patients with advanced RCC, a significant number of patients have primary resistance to sunitinib or acquired drug resistance within the 6-15 months of therapy. Thus, in order to develop more efficacious and long-lasting treatment strategies for patients with advanced RCC, it will be crucial to ascertain how to overcome sunitinib resistance that is produced by various drug resistance mechanisms. In this review, we discuss: 1) molecular mechanisms of sunitinib resistance; 2) strategies to overcome sunitinib resistance and 3) potential predictive biomarkers of sunitinib resistance.
Insights
Understanding sunitinib resistance in renal cell carcinoma (RCC) is key. This review explores mechanisms, strategies to overcome resistance, and biomarkers for advanced kidney cancer treatment.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Renal cell carcinoma (RCC) is the most common kidney cancer.
- Targeted therapy, like sunitinib, is the primary treatment for advanced RCC.
- Sunitinib inhibits multiple receptor tyrosine kinases, including VEGFR and PDGFR.
Purpose of the Study:
- To review molecular mechanisms of sunitinib resistance in RCC.
- To discuss strategies for overcoming sunitinib resistance.
- To identify potential predictive biomarkers for sunitinib resistance.
Main Methods:
- Literature review of studies on sunitinib resistance in RCC.
- Analysis of molecular pathways involved in drug resistance.
- Evaluation of emerging therapeutic strategies and biomarkers.
Main Results:
- Sunitinib resistance can be primary or acquired within 6-15 months.
- Various molecular mechanisms contribute to sunitinib resistance.
- Identifying biomarkers may predict treatment response and resistance.
Conclusions:
- Overcoming sunitinib resistance is crucial for effective, long-lasting RCC treatment.
- Further research into resistance mechanisms and biomarkers is needed.
- Developing novel strategies will improve outcomes for advanced RCC patients.
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