Ricci Sante Basso, Cerchiari Ugo
Department of Radiotherapy, Fondazione IRCCS Istituto Nazionale per lo Studio e la Cura dei Tumori, Milan, Italy.
Oncol Lett. 2010 Nov;1(6):941-945. doi: 10.3892/ol.2010.176. Epub 2010 Sep 23.
It has been established that malignant tumors as well as metastases, of almost all histological types, can regress spontaneously although certain histological types regress more frequently than others. Various causes thereof include apoptosis, the immune system and particular conditions of the tumor microenvironment. The action of the genome in the regression of tumors is not clear, but some data, apart from those of apoptosis, support its involvement. The hypothesis that the immune system exhibits variations in efficacy, even to a marked extent, in determining partial or total regression of tumors appears to be plausible. Such variable efficacy may be supported by blockage of growth and the proliferation of cancer cells at the level of the tumor microenvironment, the intervention of various factors such as inhibitors of metalloproteinases and angiogenesis, and the absence or scarcity of particular proteins. The consequence of such a blockage would be a relative increase in the number of natural killer cells and other elements involved in the immune system in relation to the number of circulating cancer cells in the blood. A relative increase in the number of elements of the immune system is more effective than an absolute increase, since an absolute increase is able to stimulate, as frequently occurs for feedback in biological equilibria, inhibitor receptors that reduce the efficacy of the same elements (mainly natural killer and CD8(+) T cells). Such an increase in the efficacy of the immune system can lead, at least in certain cases, to the so-called spontaneous regression of malignant tumors. Clinical practice has demonstrated that metastases are less frequent in patients with renal carcinoma undergoing hemodialysis compared with patients with renal carcinoma not on hemodialysis. This finding can be interpreted, in correlation with the blockage of cancer cells in tissues, as a consequence of a partial blockage of metastatic cancer cells at the level of the dialytic membrane, with a subsequent increase in the relative efficacy of the immune system.
已经确定，几乎所有组织学类型的恶性肿瘤以及转移瘤都可以自发消退，尽管某些组织学类型比其他类型更频繁地消退。其各种原因包括细胞凋亡、免疫系统和肿瘤微环境的特定条件。基因组在肿瘤消退中的作用尚不清楚，但除了细胞凋亡的数据外，一些数据支持其参与其中。免疫系统在决定肿瘤部分或完全消退时表现出效力变化，甚至在很大程度上变化的假说似乎是合理的。这种可变的效力可能受到肿瘤微环境水平上癌细胞生长和增殖的阻断、各种因素如金属蛋白酶和血管生成抑制剂的干预以及特定蛋白质的缺乏或稀少的支持。这种阻断的结果将是自然杀伤细胞和免疫系统中其他相关元素的数量相对于血液中循环癌细胞数量的相对增加。免疫系统元素数量的相对增加比绝对增加更有效，因为绝对增加能够像生物平衡中的反馈经常发生的那样，刺激降低相同元素（主要是自然杀伤细胞和CD8(+) T细胞）效力的抑制性受体。免疫系统效力的这种增加至少在某些情况下可以导致所谓的恶性肿瘤自发消退。临床实践表明，与未进行血液透析的肾癌患者相比，接受血液透析的肾癌患者转移较少。这一发现与癌细胞在组织中的阻断相关，可以解释为透析膜水平上转移癌细胞部分阻断的结果，随后免疫系统的相对效力增加。
