Metabolism of Neoplastic Tissue

sis, an outstanding characteristic of neoplastic cells, remains unexplained. This phenomenon has been variously attributed to disturbances of res piration, to deficiencies of electron transport en zymes or co-factors, and to a lack of the citric acid cycle (2, 4, 14, 23). However, none of these hy potheses has decisive experimental support, and against them can be cited the observations that tumors as a class possess the same electron trans port components and consume oxygen about as rapidly as do moderately active normal tissues, and oxidize fatty acid and carbohydrate interme diates via the citric acid cycle (10, 24). In a search for other explanations for the high glycolysis of tumor cells, the possibility that this type of tissue differs from the non-neoplastic in its capacities for synthesis and breakdown of phos phate bonds deserves consideration. The participa tion of phosphorylated intermediates as well as nucleotides, such as adenosine diand triphos phate (ADP and ATP), in many steps of glucose catabolism implies that the balance between phos phorylative and dephosphorylative rates might strongly influence the rate of glycolysis. The rapid growth of tumors undoubtedly depends on a varie ty of synthetic processes which require the utiliza tion of phosphate bond energy. Thus, the high synthetic activity associated with neoplasia may be a primary factor affecting the balance between phosphate uptake and release, affecting, in turn, the rate of glucose catabolism. The hypothesis of an altered phosphate metabo lism in neoplasia has been advanced by Potter and