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Brand and colleagues show that increased tumour lactate dehydrogenase A (LDHA)-mediated lactic acid production dampens activation and cytokine production of infiltrating T and natural killer (NK) cells allowing tumours to escape immune detection and promoting tumour growth.
Mayers, Torrenceet al. show that lung tumours driven by oncogenic KRAS and loss of p53 depend on branched-chain amino acid metabolism, whereas pancreatic tumours driven by the same genetic defects do not.
Three studies demonstrate the preclinical potential of a novel class of hypoxia-inducible factor 2α (HIF2α) antagonists in the treatment of von Hippel–Lindau (pVHL)-deficient clear cell renal cell carcinoma.
This Foreword introduces the nine Review articles in our Focus on Tumour Metabolism and discusses the main areas of tumour metabolism for further research.
Acidosis reprograms the metabolism of cancer cells toward fatty acid oxidation by downregulating acetyl-CoA carboxylase ACC2 through histone deacetylation
Sousaet al. demonstrate a reciprocal metabolic cross-talk between pancreatic stellate cells (PSCs) and pancreatic tumour cells whereby secreted autophagic alanine from PSCs is taken up by tumour cells and used as an alternative carbon source to support tumour growth.
Chaeet al. show that mitochondrially-localized AKT phosphorylates pyruvate dehydrogenase kinase 1 (PDK1) to promote tumour cell growth and survival in hypoxic conditions.
Two papers show that specific diets or pharmacological agents that mimic fasting inhibit tumour growth in combination with chemotherapy through effects on the immune system.
