Hepatocytes promote liver metastasis of pancreatic cancer by providing serine

Pancreatic ductal adenocarcinoma (PDAC) cells that have lost the enzymatic machinery for serine synthesis survive and grow in the liver by reprogramming neighbouring hepatocytes into serine factories that feed the tumour. This metabolic cross-talk explains why the liver is such a permissive site for PDAC metastasis even when the cancer cells themselves are serine-auxotrophic. The work identifies host-cell serine supply, rather than tumour-intrinsic metabolism, as a potential therapeutic target, for example through dietary serine restriction or blockade of hepatocyte reprogramming. The findings come from preclinical models and require validation in patients before any clinical application.