Nutritional and physiological consequences of tumour glycolysis

A frequent characteristic of many malignant tumours is an increase in anaerobic glycolysis, that is the conversion of glucose to lactate, when compared to normal tissues. The causes of this intensification involve changes in enzyme and glucose transporter levels, shifts of the isoenzyme patterns in the cancer cells to those similar to foetal tissues and a breakdown in the normal control mechanisms, most notably the Pasteur effect. The host must adapt, with a corresponding increase in gluconeogenesis. This change, along with other adaptations made by the host, eventually results in the syndrome known as cancer cachexia, which is characterized by anorexia and depletion and redistribution of the host energy stores. In some ways many malignant tumours behave much like parasites, drawing upon the host for nutrients such as glucose and returning waste products such as lactate to the host for recycling or disposal. This cycling of glucose and lactate between host and tumour has been the target for a number of proposed and tested treatments, with regard to the possible inhibition of tumour growth and/or possible prevention of some or all of the cachectic effects. Some of these suggested treatments have reached the point of clinical testing and show promise for continued research.