ST6GAL1 and pancreatic ductal adenocarcinoma: Hsieh et al showed that fructose feeding of human pancreatic ductal adenocarcinoma (PDAC) cells resulted in upregulation of β-galactoside α2,6-sialyltransferase 1 (ST6Gal1) and increased levels of cell surface α2,6-sialylation, likely due to increase substrate availability as excess fructose is converted into hexosamine and sialic acid pathway metabolites (32).