Progress in Kidney Cancer Outcomes Through Collaboration, Innovation, and Discovery
Year: 2018
Type: article
Abstract: Over the last 3 years, investigators have leveraged a growing understanding of kidney cancer biology to target critical pathways and produce durable benefits, even rare remissions, for patients with advanced kidney cancer.2][3][4][5] In this Special Series issue of Journal of Clinical Oncology, kidney cancer experts describe how recent advances can be integrated into clinical management strategies and focus on important future priorities, including correlating genomic analyses with clinical outcomes to identify molecular predictive biomarkers, understanding the mechanisms by which kidney cancer develops and becomes resistant to standard therapies, and exploiting new discoveries to produce durable clinical benefits and maintain quality of life for patients with advanced disease.As editors for this issue, we summarize the contributions of the invited reviews and comment on the continued need for collaboration and resources to leverage the advances described.The comprehensive genetic analysis of clear-cell renal cell carcinoma (ccRCC) performed by the Cancer Genome Atlas Kidney Cancer Research Network (TCGA KCRN) investigators and others highlighted the importance of several pathways in kidney carcinogenesis, including von Hippel-Lindau (VHL)-hypoxia-inducible factor (HIF), chromatin remodeling/histone methylation, and tumor metabolism. 6,7These priority targets provided a roadmap for future translational research that is the focus of several of the articles in this special issue.The review by Hsieh et al 8 explore the consequences of the most common genetic alterations (eg, chromosome 3p loss, mutations in the VHL tumor suppressor gene and chromatin regulatory genes [eg, PBRM1, BAP1, and SETD2]) in ccRCCs. 91][12][13][14] Although drugs against one HIF-responsive gene product, vascular endothelial growth factor (VEGF), have contributed to significant progress over the past decade, the treatment of advanced kidney cancer remains inadequate. 15,16he authors explain how an improved understanding of the interrelationship between VHL inactivation and chromatin dysregulation may lead to improvements in risk stratification, treatment selection, and patient outcomes.Despite the fact that a master regulator of tumor metabolism, the mammalian target of rapamycin complex 1, is activated in most kidney cancer, only a subset
Source: Journal of Clinical Oncology
DOI: 10.1200/jco.18.01198
Authors: David F. McDermott, Michael Carducci
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2898804644