Sydow G
Arch Geschwulstforsch. 1975;45(8):773-81.
Glycolysis is not of importance for the process of carcinogenesis. It is very likely, however, that certain molecular-biological and genetic changes are produced which enable the malignant cell to develop an intensive glycolysis, for instance, to form specialized glycolytic isoenzymes already during oncogenesis, and may possible become effective in the primary tumour. As soon as the capacity of the cancer cell to intensive aerobic and anaerobic glycolysis has become manifest, this process is an irreversible one. The extent of glycolysis of a malignoma is greatly dependent on the degree of its dedifferentiation and vascularization (glucose supply), although a direct correlation between growth and the amount of lactic acid formed does not seem to exist. However, a certain utilization of glucose is essential for cell proliferation (supply of basic substances). In many cases there is a correlation between the extent of glycolysis measurable under optimal conditions in vitro (glycolytic power) in a malignant tumour and its growth rate recognizable in vivo. The formation of a strong capacity for glucose degradation via the Embden-Meyerhof pathway that cannot be fully utilized by the whole tumour in vivo is first of all designed to ensure survival and proliferation of cells even at extremely low levels of glucose supply. This process can be regarded as an adaptation of cancer cells to a situation of unsufficient supply. This circumstance endows the cancer cell with an essential advantage over the normal cell which enables or even promotes its invasive and destructive growth and metastatic dissemination. In this respect they differ, for instance, from benignant neoplasms. The possibility is discussed to control neoplastic growth by adjusting an optimal pH difference between normal and tumour tissue by combined administration of detoxicated drugs which are converted to their toxic forms only in the tumour by means of strongly pH-dependent exogenous enzymes.
糖酵解对致癌过程并不重要。然而，很可能会产生某些分子生物学和基因变化，使恶性细胞能够进行强烈的糖酵解，例如在肿瘤发生过程中就形成专门的糖酵解同工酶，并且可能在原发性肿瘤中发挥作用。一旦癌细胞进行强烈有氧和无氧糖酵解的能力显现出来，这个过程就是不可逆的。恶性肿瘤的糖酵解程度在很大程度上取决于其去分化程度和血管形成（葡萄糖供应），尽管生长与所形成乳酸量之间似乎不存在直接关联。然而，一定量的葡萄糖利用对于细胞增殖（基本物质供应）至关重要。在许多情况下，恶性肿瘤在体外最佳条件下可测量的糖酵解程度（糖酵解能力）与其在体内可识别的生长速率之间存在关联。通过Embden-Meyerhof途径形成的强大葡萄糖降解能力，而这种能力在体内整个肿瘤中无法被充分利用，首先是为了确保即使在葡萄糖供应极低的水平下细胞也能存活和增殖。这个过程可被视为癌细胞对供应不足情况的一种适应。这种情况赋予癌细胞相对于正常细胞的一个重要优势，使其能够甚至促进其侵袭性和破坏性生长以及转移扩散。在这方面，例如它们与良性肿瘤不同。有人讨论了通过联合使用经解毒的药物来控制肿瘤生长的可能性，这些药物仅在肿瘤中借助强烈依赖pH的外源性酶转化为其有毒形式，从而调节正常组织与肿瘤组织之间的最佳pH差异。
