Microbes, macrophages, and melanin: a unifying theory of disease as exemplified by cancer.

IF 5.9 2区 医学 Q1 IMMUNOLOGY Frontiers in Immunology Pub Date : 2025-02-06 eCollection Date: 2024-01-01 DOI:10.3389/fimmu.2024.1493978
Stacie Z Berg, Jonathan Berg
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Abstract

It is widely accepted that cancer mostly arises from random spontaneous mutations triggered by environmental factors. Our theory challenges the idea of the random somatic mutation theory (SMT). The SMT does not fit well with Charles Darwin's theory of evolution in that the same relatively few mutations would occur so frequently and that these mutations would lead to death rather than survival of the fittest. However, it would fit well under the theory of evolution, if we were to look at it from the vantage point of pathogens and their supporting microbial communities colonizing humans and mutating host cells for their own benefit, as it does give them an evolutionary advantage and they are capable of selecting genes to mutate and of inserting their own DNA or RNA into hosts. In this article, we provide evidence that tumors are actually complex microbial communities composed of various microorganisms living within biofilms encapsulated by a hard matrix; that these microorganisms are what cause the genetic mutations seen in cancer and control angiogenesis; that these pathogens spread by hiding in tumor cells and M2 or M2-like macrophages and other phagocytic immune cells and traveling inside them to distant sites camouflaged by platelets, which they also reprogram, and prepare the distant site for metastasis; that risk factors for cancer are sources of energy that pathogens are able to utilize; and that, in accordance with our previous unifying theory of disease, pathogens utilize melanin for energy for building and sustaining tumors and metastasis. We propose a paradigm shift in our understanding of what cancer is, and, thereby, a different trajectory for avenues of treatment and prevention.

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微生物、巨噬细胞和黑色素:以癌症为例的疾病统一理论。
人们普遍认为,癌症大多是由环境因素引发的随机自发突变引起的。我们的理论挑战了随机体细胞突变理论(SMT)的观点。SMT与查尔斯·达尔文的进化论不太相符,因为相同的相对较少的突变会如此频繁地发生,而这些突变会导致死亡,而不是适者生存。然而,如果我们从病原体及其支持微生物群落在人类中定居并为自己的利益而使宿主细胞发生突变的有利角度来看,这与进化论是吻合的,因为这确实给了它们进化上的优势,它们能够选择基因突变并将自己的DNA或RNA插入宿主。在本文中,我们提供的证据表明,肿瘤实际上是由生活在硬基质包裹的生物膜内的各种微生物组成的复杂微生物群落;这些微生物是导致癌症基因突变和控制血管生成的原因;这些病原体通过隐藏在肿瘤细胞、M2或M2样巨噬细胞和其他吞噬性免疫细胞中传播,并在它们内部移动到被血小板伪装的远处部位,它们也对血小板进行重新编程,并为远处部位转移做准备;癌症的危险因素是病原体能够利用的能量来源;而且,根据我们之前的疾病统一理论,病原体利用黑色素作为能量来形成和维持肿瘤和转移。我们提出了一个范式转变,在我们的理解癌症是什么,因此,治疗和预防途径的不同轨迹。
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来源期刊
CiteScore
9.80
自引率
11.00%
发文量
7153
审稿时长
14 weeks
期刊介绍: Frontiers in Immunology is a leading journal in its field, publishing rigorously peer-reviewed research across basic, translational and clinical immunology. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide. Frontiers in Immunology is the official Journal of the International Union of Immunological Societies (IUIS). Encompassing the entire field of Immunology, this journal welcomes papers that investigate basic mechanisms of immune system development and function, with a particular emphasis given to the description of the clinical and immunological phenotype of human immune disorders, and on the definition of their molecular basis.
期刊最新文献
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