Cancer: Tumor Iron Metabolism, Mitochondrial Dysfunction and Tumor Immunosuppression;“A Tight Partnership—Was Warburg Correct?”

Over the last 30 years there have been numerous worldwide investigators involved in cancer research. Billions of dollars have been spent on drug development and cancer research;however, with all of the new agents and modalities of treatment, we have honestly not significantly improved the overall survival of the Stage IV cancer patient. There is and will not be a magic bullet treatment, thus the extensive title of this paper. We are convinced that unless we use multiple innovative therapies in combination with conventional treatment, we will never truly defeat this disease. We have attempted to address this problem by presenting in detail some of these complex mechanisms involved in tumorigenesis, progression, escape, and metastasis. Most investigators have their own special area of interest, but if we are to conquer this scourge, we must develop an extensive, multifaceted, comprehensive approach. Hopefully this article will contribute to awareness and further insight into this very serious and complicated problem, so we can improve quality of life and improve the survival of the Stage IV cancer patient.

假性缺氧驱动“衰老-癌变”的脾肾亏虚病机探讨

脾肾亏虚是"衰老-癌变"进程主要的脏腑病机。衰老过程中衰老代谢物烟酰胺腺嘌呤二核苷酸(NAD+)的降低,肿瘤代谢物(R)-2羟戊二酸[(R)-2HG]、延胡索酸和琥珀酸的累积,体现肾不藏精,脾失健运。缺氧诱导因子1α(HIF-1α)在正常组织升高,诱导假性缺氧状态,是衰老代谢物与肿瘤代谢物的整合性枢纽,驱动氧化磷酸化向瓦博格样有氧糖酵解的转变。假性缺氧通过表观遗传修饰如组蛋白甲基化、组蛋白乙酰化和DNA甲基化,诱导循序渐进的代谢重编程导致脾肾相互滋生化源不足,产生易于肿瘤发生的微环境,产生肿瘤样状态。健脾补肾可能通过"卡路里限制样效应",改善能量代谢障碍,延缓或逆转衰老-癌变进程。

三羧酸循环在嗜铬细胞瘤和副神经节瘤中的相关研究进展

在嗜铬细胞瘤和副神经节瘤（统称为PPGL）中，与三羧酸循环相关的基因发生突变，会导致三羧酸循环中间代谢产物水平紊乱，通过激活缺氧诱导因子（HIF）可引发假性缺氧应答，还会导致表观遗传变异、阻碍细胞分化和凋亡，共同促进PPGL发生和发展。本文综述了目前三羧酸循环在PPGL发生机制中的基础研究进展以及相关检测方法的应用。