Firminger H I
Natl Cancer Inst Monogr. 1976 Nov;44:15-8.
We are all subjected to varying amounts of mutating, potential cancer-inducing events, which are cumulative. In most instances, the accumulations are repaired or are lethal. If a viable clone survives, it must proliferate in order to become manifest and eventually to overpower the host's normal regulatory and defense mechanisms. The proliferation may be incited and sustained by cocarcinogens, hormone excess, chronic infections such as schistosomiasis, and in the case of lymphoid cells, by immune incompetence. On the other side are the protective reparing enzymes, which serve to cut out the damaged segments of DNA and repair them as fast as they can. The normal homeostatic mechanisms tend to keep cell proliferation and activity within the beneficial bounds of need. The controlling forces that cause cells to stop reproducing themselves and differentiate to perform a useful function also tend to slow or even stop the useless proliferation if all the cells can undergo maturation to a postmitotic state. There are also the protective mechanisms of immunity: Sensitized B lymphocytes tag the antigenic sites of tumor cells and activate the T-cell macrophages to destroy the tagged cells.
我们都受到不同程度的、具有潜在致癌性的突变事件影响，这些事件是累积性的。在大多数情况下，这些累积的突变会被修复或具有致死性。如果一个存活的克隆体幸存下来，它必须增殖才能显现出来，并最终战胜宿主的正常调节和防御机制。增殖可能由促癌物、激素过量、慢性感染（如血吸虫病）引发并持续，对于淋巴细胞而言，免疫功能不全也会导致其增殖。另一方面是保护性修复酶，它们会切除受损的DNA片段并尽快进行修复。正常的稳态机制倾向于将细胞增殖和活性维持在有益的需求范围内。如果所有细胞都能成熟到有丝分裂后状态，那么促使细胞停止自我复制并分化以执行有用功能的控制力量，也往往会减缓甚至停止无用的增殖。此外还有免疫保护机制：致敏的B淋巴细胞标记肿瘤细胞的抗原位点，并激活T细胞巨噬细胞来破坏被标记的细胞。
