Primo N. Lara, Jr. Eric Jonasch (Editors). kidney cancer (2 ed). Springer International Publishing (2015) → Русский

An estimated 63,920 cases of kidney cancer were diagnosed in 2014 leading to 13,860 deaths from the disease [1]. Renal cell carcinoma represents approximately 95% of neoplasms arising from the kidney and is composed of a diverse group of malignancies with distinct genetic and molecular alterations, disparate histologic features, and unique clinical characteristics (Fig. 6.1). Despite this heterogeneity, targeted therapies for metastatic disease have centered on alterations in the von Hippel– Lindau (VHL)–hypoxia-inducible factor (HIF)– vascular endothelial growth factor (VEGF) pathway. While this approach is effective in clear cell Renal Cell Carcinoma (ccRCC), it has predictably met with limited success in patients with non-clear cell variants. The study of familial kidney cancer syndromes including von Hippel–Lindau (VHL) syndrome, hereditary papillary renal cell carcinoma (HPRC), hereditary leiomyomatosis and renal cell carcinoma (HLRCC), Birt–Hogg–Dubé syndrome (BHD), tuberous sclerosis complex (TSC), Cowden’s disease, and succinate dehydrogenase renal cell carcinoma (SDH-RCC) has identified a number of genes involved in nutrient, oxygen, and energy-sensing mechanisms that allow for metabolic adaptation in the tumor microenvironment [2] (Fig. 6.2). As our understanding of cancer biology has evolved, so has our insight into divergent metabolic processes that appear to be critical for tumor proliferation and survival [3, 4]. Comprehending the roles of these altered metabolic pathways and exploiting the metabolic differences between normal and cancer cells will potentially aid in developing novel therapeutic and disease-specific targets.