Hepatocellular carcinoma (HCC) is the third leading cause of cancer death worldwide yet has limited therapeutic options. We recently demonstrated that inhibition of de novo nicotinamide adenine dinucleotide (NAD(+)) synthesis is responsible for DNA damage, thereby initiating hepatocarcinogenesis. We propose that boosting NAD(+) levels might be used as a prophylactic or therapeutic approach in HCC.
Keywords: Aryl hydrocarbon receptor (AhR); DNA damage; Estrogen receptor (ER); GEMMs; HCC; NAD+; URI; nicotinamide riboside; pancreatic tumor; prevention; therapy.