scholarly journals Systemic therapy for patients with advanced, unresectable or metastatic renal cell carcinoma: moving to guidelines

2012 ◽  
Vol 1 (2S) ◽  
Author(s):  
Sebastien J. Hotte ◽  
Anil K. Kapoor
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Cell Cancer ◽  
Interleukin 2 ◽  
Standard Of Care ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Until recently, patients with advanced, unresectable or metastatic renal cell cancer (RCC) had very few therapeutic options. Cytokine therapy, consistingmainly of interferon-a and interleukin-2, was considered the mainstay of therapy. A better understanding of the biology of RCC has led to the development of novel therapeutic agents that target angiogenesis. Inactivation of thevon Hippel-Lindau tumour-suppressor gene VHL, which is present in the vast majority of clear-cell RCC tumours, leads to overexpression of the vascular endothelial growth factor, which in turn promotes angiogenesis. Recent observationsfrom a number of positive studies with agents such as sunitinib malate, sorafenib, temsirolimus and bevacizumab have led to a rapid and exciting change in the standard of care for patients with advanced renal cell carcinoma. This article reviews these agents in the context of their use in clinical practiceand provides suggestions about the appropriateness of various agents inspecific clinical situations.

Perioperative Therapy in Renal Cell Carcinoma: What Do We Know, What Have We Learned, What's Next?

2018 ◽  
Vol 36 (36) ◽  
pp. 3608-3614 ◽  
Author(s):  
Naomi B. Haas ◽  
Robert G. Uzzo
Keyword(s):  
Renal Cell Carcinoma ◽  
High Risk ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Kinase Inhibitor ◽  
Cell Cancer ◽  
Disease Free Survival ◽  
Vascular Endothelial ◽  
Perioperative Therapy ◽  
Endothelial Growth Factor

Recent adjuvant vascular endothelial growth factor tyrosine kinase inhibitor trials in resected high-risk renal cell carcinoma that compared sunitinib, sorafenib, pazopanib, and axitinib with placebo controls have demonstrated mixed impact on disease-free survival, no improvement in overall survival, and, thus, controversy. Here, we discuss the results and conduct of these trials to provide new insight into the goals and strategies of treating resected renal cell cancer that is at high risk for recurrence. The potential for leveraging what we have learned from these trials to conduct successful contemporary adjuvant and perioperative immune checkpoint inhibition trials and future adjuvant trial design is discussed.

scholarly journals Is It Safe to Restart Antivascular Endothelial Growth Factor Therapy in Patients with Renal Cell Carcinoma after Cardiac Ischemia?

2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Bo Zhao ◽  
Laura S. Wood ◽  
Karen James ◽  
Brian I. Rini
Keyword(s):  
Renal Cell Carcinoma ◽  
Growth Factor ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Cardiac Ischemia ◽  
Vascular Endothelial ◽  
Cardiac Events ◽  
Factor Therapy ◽  
Growth Factor Therapy ◽  
Endothelial Growth Factor

Agents targeting vascular endothelial growth factor (VEGF) represent active drugs in treating patients with advanced renal cell carcinoma (RCC). Studies have shown that sunitinib and axitinib can be associated with cardiac toxicity. Whether these agents should be restarted in patients who experience cardiac ischemia remains uncertain. Here, we present three patients with metastatic RCC who restarted sunitinib or axitinib after intervention of active ischemic cardiac disease without causing subsequent relevant cardiac events. This experience suggests that these agents can be continued after management of cardiac ischemia.

DNA damage repair (DDR) pathway alteration in advanced renal cell carcinoma (RCC) is association with good progression-free survival with tyrosine kinase inhibitor (TKI) therapy.

2021 ◽  
Vol 39 (6_suppl) ◽  
pp. 346-346
Author(s):  
Wei Zhai ◽  
Junyun Wang ◽  
Ning He ◽  
Jiale Zhou ◽  
Jianfei Wang ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Kinase Inhibitor ◽  
Progression Free Survival ◽  
Vascular Endothelial ◽  
Damage Repair ◽  
Endothelial Growth Factor

346 Background: Alterations in DNA damage repair (DDR) genes are associated with human tumorigenesis and may be as potential biomarkers for vascular endothelial growth factor (VEGF) tyrosine kinase inhibitor (TKI) therapy in renal cell carcinoma. However, biologic significance and relevance to TKI targeted therapy in metastatic RCC are unknown. Methods: Genomic data and treatment outcomes were retrospectively collected for patients with metastatic RCC. Tumor and germline DNA were subject to targeted next generation sequencing across 642 genes of interest, including 60 DDR genes. Patients were dichotomized according to underlying DDR gene alteration into (1) DDR gene alterations present (Mut DDR); (2) wildtype (WT) DDR gene alterations present (WT DDR). Association between DDR status and therapeutic benefit was investigated separately for and vascular endothelial growth factor (VEGF) tyrosine kinase inhibitor (TKI) therapy. Results: Mut DDR were detected in 17/40 patients (42.5%). The most frequently DDR altered genes were TP53. For patients with TKI treatment, Mut DDR status was associated with superior progression free survival (log-rank p = 0.048), but not with superior overall survival (log-rank p = 0.39); after adjusting for International Metastatic Renal Cell Carcinoma Database Consortium risks and extent of prior therapy, the HR for Mut DDR was 2.68 (95% CI: 0.96–7.46; p = 0.059). Conclusions: DDR alterations are recurrent genomic events in patients with advanced RCC and were mostly clonal in this cohort. Dysfunction events in these genes may affect outcome with TKI therapy in adanced RCC, and these hypothesis-generating results deserve further study.

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