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10.1158/1078-0432.CCR-13-2993

http://scihub22266oqcxt.onion/10.1158/1078-0432.CCR-13-2993
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C4795462!4795462!25564569
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suck abstract from ncbi


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pmid25564569      Clin+Cancer+Res 2015 ; 21 (1): 10-7
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  • New Strategies in Renal Cell Carcinoma: Targeting the Genetic and Metabolic Basis of Disease #MMPMID25564569
  • Srinivasan R; Ricketts CJ; Sourbier C; Linehan WM
  • Clin Cancer Res 2015[Jan]; 21 (1): 10-7 PMID25564569show ga
  • The development of new forms of treatment of advanced renal cell carcinoma over the past two decades has been primarily focused on targeting the VHL/HIF pathway. The recent identification of mutations of chromatin remodeling genes in clear cell renal carcinoma (RCC), of genomic heterogeneity and of a Warburg-like metabolic phenotype in advanced disease has had a profound effect on our understanding of the evolution of clear cell RCC and on potential approaches to personalized therapy. Early approaches to therapy for patients with advanced type 1 papillary renal cell carcinoma that have centered around the MET/HGF pathway will expand as more genomic information becomes available. Sporadic and familial Type 2 papillary renal cell carcinoma are characterized by enhanced aerobic glycolysis and share an antioxidant response phenotype. In fumarate hydratase-deficient RCC, fumarate-induced succination of KEAP1 activates Nrf2 signaling. CUL3 and Nrf2 mutations as well as an Nrf2 activation phenotype are found in sporadic type 2 papillary RCC. Therapeutic approaches designed to target the Nrf2 pathway as well as to impair blood flow and glucose delivery in these cancers that are highly dependent on a robust tumor vasculature and on ready availability of glucose for energy production and glycolysis are in development.
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