A new hypothesis for the cancer mechanism.
A new hypothesis for the cancer mechanism.
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DOI：
10.1007/s10555-011-9342-8
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发表时间：
2012-06
影响因子：
9.2
通讯作者：
Gonzalez-Angulo, Ana M.
中科院分区：
文献类型：
--
作者：
Meng, Xiaolong;Zhong, Jie;Liu, Shuying;Murray, Mollianne;Gonzalez-Angulo, Ana M.
几个观察结果使我们对癌症机制提出了一个新的假设。首先，癌症只出现在那些具有复杂伤口愈合能力的多细胞生物体上。第二，在临床上，可以在所有癌症中确定被视为风险因素的伤口。最后，癌基因激活不仅出现在癌症中，而且出现在正常生理和非癌症病理过程中。我们提出的假设是，癌症是一个自然的伤口愈合相关的过程，其中包括癌基因激活，细胞因子分泌，干细胞募集分化和组织重塑。伤口激活一些细胞的癌基因，后者分泌细胞因子以招募干细胞来愈合伤口。然而，如果伤口的原因或如果伤口持续存在，例如在持续的紫外线和致癌物暴露下，持续的伤口愈合过程将导致临床癌症肿块。当伤口存在时，自然界中没有系统在中间阶段停止或逆转伤口愈合过程。癌症机制的结果是愈合伤口或耗尽整个系统（死亡）。这种癌症机制的逻辑与身体中其他生理代谢的基本原理是一致的-为了生存。这一假说有助于理解许多来自突变理论的癌症之谜，例如为什么癌症只存在于一小部分多细胞生物中，尽管它们在DNA复制过程中都有潜在的突变风险。该假说可用于解释和指导癌症预防、复发、转移、体外和体内研究以及个性化治疗。
Several observations have led us to a new hypothesis for cancer mechanism. First, that cancer appears only on those multicellular organisms with complicated wound-healing capacities. Second, that wounds considered as risk factors can be identified in all cancers in clinics. And finally, that oncogene activation appears not only in cancer, but also in normal physiology and noncancer pathology processes. Our proposed hypothesis is that cancer is a natural wound healing-related process, which includes oncogene activations, cytokine secretions, stem cell recruitment differentiation, and tissue remodeling. Wounds activate oncogenes of some cells and the latter secrete cytokines to recruit stem cells to heal the wounds. However, if the cause of the wound or if the wound persists, such as under the persistent UV and carcinogen exposures, the continuous wound healing process will lead to a clinical cancer mass. There is no system in nature to stop or reverse the wound healing process in the middle stage when the wound exists. The outcome of the cancer mechanism is either healing the wound or exhausting the whole system (death). The logic of this cancer mechanism is consistent with the rationales of the other physiological metabolisms in the body—for survival. This hypothesis helps to understand many cancer mysteries derived from the mutation theory, such as why cancer only exists in a small proportion of multicellular organisms, although they are all under potential mutation risks during DNA replications. The hypothesis can be used to interpret and guide cancer prevention, recurrence, metastasis, in vitro and in vivo studies, and personalized treatments.
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影响因子：
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作者：
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通讯作者：
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