Libenson L, Jena M
Med Hypotheses. 1979 Jan;5(1):67-82. doi: 10.1016/0306-9877(79)90062-8.
Since the inception of experimental cancer research, all theories concerning the mechanism of transformation of normal cells into neoplastic cells were constructed on the basis of the postulate that interaction of an agent and cell constituents is a condition indispensable for the occurrence of the neoplastic transformation. In the course of the past three decades, however, all attempts to uncover agents responsible for the transformations induced by chemically inert films implanted in living tissues or for the "spontaneous" transformations in vitro in cell cultures devoid of added neoplastogens, yielded consistently negative results. In regard to the neoplastogenic effect of imbedded inert films, the present article takes into consideration that films implanted in living tissues hinder the circulation of interstitial fluid in their vicinity and as a result elicit anoxia and protracted low pH gradients in the environment of the cells adjacent to the films. The effects of such protracted low pH on the metabolic activities of the surviving cells are examined and a working hypothesis is offered concerning the role of protracted environmental low pH in the mechanism of film neoplastogenesis.
自实验性癌症研究开展以来,所有关于正常细胞转变为肿瘤细胞机制的理论都是基于这样一个假设构建的:即某种因子与细胞成分的相互作用是肿瘤转变发生不可或缺的条件。然而,在过去三十年里,所有试图找出导致植入活组织的化学惰性薄膜所引发的转变或在未添加致癌物的细胞培养物中“自发”转变的因子的尝试,始终都得到了阴性结果。关于植入的惰性薄膜的致瘤作用,本文考虑到植入活组织的薄膜会阻碍其周围组织液的循环,从而在与薄膜相邻的细胞环境中引发缺氧和持久的低pH梯度。本文研究了这种持久的低pH对存活细胞代谢活动的影响,并就持久的环境低pH在薄膜致瘤机制中的作用提出了一个可行的假设。