Treatment of metastatic renal cell carcinoma and renal pelvic cancer

Abstract

A better understanding of the molecular biology of renal cell carcinoma (RCC) and the emergence of molecular targeted drugs have revolutionized the treatment for patients with metastatic RCC (mRCC). Multi-targeted tyrosine kinase inhibitors (sorafenib and sunitinib) and mammalian target of rapamycin inhibitors (temsirolimus and everolimus) have recently shown superiority over interferon-α or placebo. However, while the molecular targeted drugs have demonstrated encouraging results, these drugs have also sometimes induced unexpected adverse events. Control of adverse events is important to obtain the maximum effectiveness and sustain quality of life for patients. Because renal pelvic cancer has many similarities in pathogenesis with urinary bladder cancer, the same chemotherapeutic regimen is often proposed for patients with metastatic renal pelvic cancer. Combined chemotherapy with gemcitabine and cisplatin is now widely considered to be first-line chemotherapy against these metastatic diseases; however, there are still unresolved problems with this treatment, including the limited survival benefit. To select new therapeutic modalities, a more profound understanding of the molecular biology of renal pelvic cancer is crucial. The purpose of this review is to summarize the current evidence supporting the role and activities of new chemotherapeutic agents and to reveal potential future directions in the management of mRCC and renal pelvic cancer.

Sperm-Associated Antigen 4, a Novel Hypoxia-Inducible Factor 1 Target, Regulates Cytokinesis, and Its Expression Correlates with the Prognosis of Renal Cell Carcinoma

“…47 Half of the patients who undergo resection with a curative intent are expected to have a relapse during the course of the disease, and metastatic RCC is one of the most treatment-resistant malignancies. 48 HIF-1a and HIF-2a are overexpressed in the majority of (E and F). *P < 0.05, **P < 0.01, ***P < 0.001, and y P < 0.0001 versus control siRNA or normoxia.…”

Endothelial follicle stimulating hormone receptor in primary kidney cancer correlates with subsequent response to sunitinib

“…There is a critical need for strategies to increase complete responses (now rare). One strategy is to combine sunitinib with other agents available for RCC therapy [15][16][17][18], but trials have revealed difficulties with combination therapy. By combining these agents, the toxicity of one or more can be enhanced [19].…”

Fisetin enhances cisplatin sensitivity in renal cell carcinoma via the CDK6/PI3K/Akt/mTOR signaling pathway

“…Currently, surgery is the main therapeutic approach for RCC; however, ~30% of patients with RCC develop distant metastasis following surgery ( 2 ). Although cisplatin is an effective therapeutic agent for certain types of cancer, RCC often exhibits resistance to cisplatin, and chemotherapy regimens with cisplatin alone are only effective in 4–6% of patients with RCC ( 3 ). Therefore, there is a need to improve the understanding of the underlying reasons for RCC chemoresistance and to identify new insights for RCC treatment.…”