Kulsh Jay
Independent Scientist, Los Angeles, CA, USA.
Oncol Ther. 2023 Jun;11(2):153-169. doi: 10.1007/s40487-023-00221-y. Epub 2023 Feb 13.
The presence of mutated genes strongly correlates with the incidence of cancer. Decades of research, however, has not yielded any specific causative gene or set of genes for the vast majority of cancers. The Cancer Genome Atlas program was supposed to provide clarity, but it only gave much more data without any accompanying insight into how the disease begins and progresses. It may be time to notice that epidemiological studies consistently show that the environment, not genes, has the principal role in causing cancer. Since carcinogenic chemicals in our food, drink, air, and water are the primary culprits, we need to look at the biochemistry of cancer, with a focus on enzymes that invariably facilitate transformations in a cell. In particular, attention should be paid to the rate-limiting enzyme in DNA synthesis, ribonucleotide reductase (RnR), whose activity is tightly linked to tumor growth. Besides circumstantial evidence that cancer is induced at this enzyme's vulnerable free-radical-containing active site by various carcinogens, its role in initiating retinoblastoma and human papillomavirus (HPV)-related cervical cancers has been well documented in recent years. Blocking the activity of malignant RnR is a certain way to arrest cancer.
突变基因的存在与癌症发病率密切相关。然而,数十年的研究并未为绝大多数癌症找出任何特定的致病基因或基因组合。癌症基因组图谱计划本应带来清晰的结果,但它只是提供了更多数据,却没有对该疾病如何发生和发展给出任何相关见解。或许是时候注意到,流行病学研究一直表明,环境而非基因在引发癌症方面起主要作用。由于我们食物、饮料、空气和水中的致癌化学物质是主要元凶,我们需要研究癌症的生物化学,重点关注那些总是促进细胞内转化的酶。尤其应当关注DNA合成中的限速酶——核糖核苷酸还原酶(RnR),其活性与肿瘤生长紧密相关。除了各种致癌物在该酶易受自由基攻击的活性位点诱导癌症的间接证据外,近年来其在引发视网膜母细胞瘤和人乳头瘤病毒(HPV)相关宫颈癌中的作用也有充分记载。阻断恶性RnR的活性无疑是阻止癌症的一种方法。