Dipartimento di Scienze del Farmaco, Università di Padova, Padova, Italy.
Medical Biochemistry Department, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.
Biochem Pharmacol. 2014 May 15;89(2):162-70. doi: 10.1016/j.bcp.2014.02.018. Epub 2014 Mar 4.
Antiangiogenic therapy has become a mainstay of cancer therapeutics, but clinical responses are generally short-term owing to the development of secondary resistance. Tumor starvation by antiangiogenic drugs is largely attributed to increased hypoxia and impaired nutrients supply, suggesting that angiogenesis inhibition causes remarkable metabolic perturbations in the tumor microenvironment. We review here recent acquisitions concerning metabolic effects of angiogenesis blockade in tumors and discuss the possibility that some metabolic features of tumor cells - i.e. their dependency from glucose as primary energy substrate - might affect tumor responses to anti-vascular endothelial growth factor treatment. Moreover, we discuss the hypothesis that anti-angiogenic therapy might foster metabolic evolution of tumors. The therapeutic implications of this hypothesis will be discussed further here.
抗血管生成治疗已成为癌症治疗的主要手段，但由于继发性耐药的发展，临床反应通常是短期的。抗血管生成药物引起的肿瘤饥饿主要归因于缺氧增加和营养供应受损，表明血管生成抑制会导致肿瘤微环境中显著的代谢紊乱。在这里，我们回顾了最近关于肿瘤血管生成阻断的代谢效应的研究成果，并讨论了肿瘤细胞的一些代谢特征（即它们对葡萄糖作为主要能量底物的依赖性）是否可能影响肿瘤对血管内皮生长因子治疗的反应的可能性。此外，我们还讨论了抗血管生成治疗可能促进肿瘤代谢进化的假说。本文将进一步讨论这一假说的治疗意义。
