HIF1A and neoplasm: MUC1-CT interacts with p53 to attenuate the p53-dependent tumor growth suppression and stabilizes HIF-1α to increase a number of effects: glucose uptake and glycolysis, nucleotide and fatty acid biosynthesis, direct regulation of tumor cell metabolic programming, and also allows the increased demand of nutrients and biosynthetic intermediates for fast dividing and metabolizing tumor cells [69].