Increased glucose uptake and accumulation of lactate even under normoxic conditions, which is frequently termed "aerobic glycolysis" or the "Warburg Effect", are common features of cultured cancer cells. The metabolic properties of tumor cells in vitro are reflected in solid primary tumors in the clinic by a lactate accumulation, which can be markedly variable between individual cancers. This is even true when equal tumor stages and pathohistological grades are considered. The degree of lactate accumulation can predict for metastases, as well as overall and disease-free survival of patients, as shown by several clinical studies on different tumor entities (1). The link between lactate and metastasis is based on a lactate-mediated enhancement of random migration of single cancer cells and cancer cell clusters, and on a lactate-induced secretion of hyaluronan by tumor-associated fibroblasts that create a milieu favorable for migration. Furthermore, radioresistance has been positively correlated with lactate concentrations, suggesting an antioxidative capacity of lactate. Findings on interactions of tumor metabolites with immune cells indicate a contribution of lactate to the immune escape of tumors, e. g. by impeding migration and cytokine release of dendritic cells or cytotoxic T cells (1). Furthermore, lactate bridges the gap between high lactate levels in wound healing, chronic inflammation, and cancer development. Tumor cells ensure sufficient oxygen and nutrient supply for proliferation through lactate-induced secretion of VEGF, resulting in the formation of new vessels. In summary, accumulation of lactate in solid tumors is a pivotal and early event in the development of malignancies. Thereby, tissue levels of lactate in primary tumors are closely correlated with the prospective malignant behavior of the disease. The determination of lactate should enter further clinical trials to confirm its relevance in cancer biology. A summary of lactate biology in cancer has been published by (1).

(Supported by the DFG: PAK124; Mu576/14-1, /14-2, 15/-1, /15-2, /17-1; SA1749/3-1)

(1) Hirschhaeuser, F., Sattler, U. G. A. and Mueller_Klieser: Invited review; Cancer Res. 71(22): 6921–6925 (2011).