The prognosis and treatment outcome of patients with advanced renal cell carcinoma have substantially improved with the multitude of currently available molecularly targeted therapies. The rapid addition of novel therapeutic options has made the treatment algorithm complex and has created a significant challenge for the community oncologist, who is faced with selecting a drug for a given patient from a growing list of agents. The optimal treatment sequence remains to be determined, and effective management of side effects and toxicities is currently the key. These targeted therapies are associated with toxicity profiles that are classically distinct from those associated with conventional chemotherapy agents. In order to help community oncologists optimize patient outcomes, this review summarizes clinical issues associated with specific therapies and the background pivotal data.
Biology of Renal Cell Carcinoma The past several decades have witnessed a significant increase in the understanding of the biology of RCC, leading to development of many new therapeutic targets and a greater availability of newer drugs for RCC management. A majority of kidney cancers are believed to be related to changes in a gene called von Hippel–Lindau (VHL). A loss of functional VHL gene results in an increased amount of a protein known as hypoxia-inducible factor, which thereafter leads to highly vascular tumors. Overexpression of hypoxia-inducible factor in kidney cancer is also related to stimulation of a receptor called the mammalian target of rapamycin (mTOR). Both the vascular endothelial growth factor (VEGF) and the mTOR pathways clearly provide opportunities for the development of molecularly targeted drugs in RCC (Figure).
Reprinted with permission from Courtney et al. Curr Oncol Rep. 2009;11(3):218-226.
GF indicates growth factor; GFR, growth factor receptor; HIF, hypoxia-inducible factor; mTORC1, mTORC2, mammalian target of rapamycin complexes 1 and 2; PDK1, phosphoinositide-dependent kinase-1; PI3K, phosphatidylinositol 3-kinase; SDF, stromal cell-derived factor; VEGF, vascular endothelial growth factor; VHL, von Hippel-Lindau.
|Title||Expiration Date||CME Credits|
|Oncology Briefings™: Current Perspectives on Preventing and Managing Tumor Lysis Syndrome||Jun 30, 2019||1.0|
|Community Practice Connections™: 2nd Annual International Congress on Oncology Pathology™||Aug 31, 2019||1.5|