致癌机制中的突变学说,基于化学致癌剂与细胞DNA 作用而破坏其结构,导致细胞癌变这一事实,得到一定的证实。突变学说似乎解释了癌变最根本的原因以及癌细胞的各种表型变化。在此基础上,设计并合成了一系列传统的抗癌药,其中多为细胞毒药物。它们在抗肿瘤的同时,伴有破坏或抑制增殖旺盛的正常细胞的作用。后来又发现,有些抗癌药物用其治疗一种癌,但却诱发了另一种癌。加之耐药性的不断出现,使癌症化学治疗的临床效果受到影响。因此,开辟一些新的途径,寻找疗效显著而毒性更小的抗癌新药,成为当前迫切需要解决的重大课题。寻找低毒性抗癌药物,最初是建立在致癌机制的基因调控学说基础上的,认为细胞逆分化或者失控分化而致癌,癌细胞是失掉生长调节机能的细胞,是遗传信息表达异常的结果。既然癌是基因表达失调的结果,那么癌细胞恢复正常的可能性是存在的,从而产生了癌细胞可 The mutation theory in the carcinogenic mechanism is confirmed by the fact that the chemical carcinogen and cell DNA damage its structure and lead to cell canceration. The mutation theory seems to explain the most fundamental cause of canceration and the various phenotypic changes of cancer cells. On this basis, a series of traditional anticancer drugs were designed and synthesized, most of which are cytotoxic drugs. They are anti-tumor and have the effect of destroying or inhibiting the proliferation of normal cells. Later, it was discovered that some anti-cancer drugs use it to treat a cancer, but they have induced another type of cancer. In addition, the emergence of drug resistance has affected the clinical effects of cancer chemotherapy. Therefore, opening up some new ways to find new anti-cancer drugs with significant efficacy and less toxicity have become major issues that urgently need to be resolved. The search for low-toxicity anti-cancer drugs was originally based on the gene regulation theory of carcinogenesis, and it is believed that the cells are carcinogenic when differentiated or out of control, and that cancer cells are cells that have lost the function of growth regulation and are the result of abnormal expression of genetic information. Since cancer is the result of an imbalance in gene expression, there is a possibility that the cancer cells return to normal and cancer cells can be produced.