Tumour growth activation by the central nervous system--An integrative theory of cancer.

Alberto Recio
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引用次数: 2

Abstract

The currently recognised mechanisms of the biology of cancer are not yet enough to explain the high incidence of the disease in industrialised countries. Survival and proliferation of cancer cells demand a well orchestrated combination of functional capabilities, or hallmarks, which requires complex signalling networks that often exceed the tumour boundaries. Based on latest research on environmental health, and aiming to provide cancer with a coherent set of organizing principles, we propose an integrative model of carcinogenesis founded on tumour growth activation by the central nervous system as an adaptive, allostatic response to both environmental and emotional challenges. In this way, chronicity of physical as well as psychological stressors may be directly involved in cancer genesis and progression, after an early inflammatory stage. The model also contemplates accidental activation of the tumour growth programme following direct DNA damage, but as a rare event that does not account for most cancers in humans. Bodily and cellular mechanisms designed to facilitate tumorigenesis may include exacerbation of the sympathetic activity, overexpression of membrane ion channels, promotion of selected mutations and methylations, degradation of the mitochondria, and reprogramming of adult stem cells.
中枢神经系统激活肿瘤生长——肿瘤的综合理论。
目前公认的癌症生物学机制还不足以解释这种疾病在工业化国家的高发病率。癌细胞的生存和增殖需要功能能力或特征的良好协调组合,这需要复杂的信号网络,这些信号网络通常超出肿瘤边界。基于对环境健康的最新研究,并旨在为癌症提供一套连贯的组织原则,我们提出了一个基于中枢神经系统对环境和情绪挑战的适应性,非稳态反应的肿瘤生长激活的综合致癌模型。通过这种方式,生理和心理压力源的慢性性可能在早期炎症期后直接参与癌症的发生和发展。该模型还考虑了直接DNA损伤后肿瘤生长程序的意外激活,但这是一个罕见的事件,不能解释大多数人类癌症的原因。促进肿瘤发生的身体和细胞机制可能包括交感神经活动的加剧、膜离子通道的过度表达、选择性突变和甲基化的促进、线粒体的降解和成体干细胞的重编程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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