The metabolism of renal cell carcinomas and liver cancer

Tu Nguyen, Anne Le

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Different oncogenic mutations lead to different metabolic phenotypes in renal cell carcinomas (RCC).Loss of the von Hippel-Lindau (VHL) tumor suppressor gene results in metabolic alterations including aerobic glycolysis in RCC.Fumarate hydratase mutations result in an increase in aerobic glycolysis in RCC.Different oncogenic mutations lead to different metabolic phenotypes in primary liver cancer.MYC and MET mutations regulate glucose and glutamine differently in primary liver cancer.Glucose metabolism increased by acetylated phosphoglycerate kinase 1 (PGK1) leads to the promotion of cancer cell proliferation and tumorigenesis in the liver.

Original languageEnglish (US)
Title of host publicationAdvances in Experimental Medicine and Biology
PublisherSpringer New York LLC
Pages107-118
Number of pages12
DOIs
StatePublished - 2018

Publication series

NameAdvances in Experimental Medicine and Biology
Volume1063
ISSN (Print)0065-2598
ISSN (Electronic)2214-8019

Keywords

  • Glucose metabolism
  • Glutamine metabolism
  • Metabolic phenotypes
  • Oncogenic heterogeneity
  • Primary liver cancer
  • Renal cell carcinoma

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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