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生命密码:统一人类生命周期和人类肿瘤起源的理论。

The "life code": A theory that unifies the human life cycle and the origin of human tumors.

机构信息

Department of Anatomic Pathology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX, 77030, United States.

出版信息

Semin Cancer Biol. 2020 Feb;60:380-397. doi: 10.1016/j.semcancer.2019.09.005. Epub 2019 Sep 12.

DOI:10.1016/j.semcancer.2019.09.005
PMID:31521747
Abstract

Tumors arise from the transformation of normal stem cells or mature somatic cells. Intriguingly, two types of tumors have been observed by pathologists for centuries: well-differentiated tumors and undifferentiated tumors. Well-differentiated tumors are architecturally similar to the tissues from which they originate, whereas undifferentiated tumors exhibit high nuclear atypia and do not resemble their tissue of origin. The relationship between these two tumor types and the human life cycle has not been clear. Here I propose a unifying theory that explains the processes of transformation of both tumor types with our life cycle. Human life starts with fertilization of an egg by a sperm to form a zygote. The zygote undergoes successive rounds of cleavage division to form blastomeres within the zona pellucida, with progressive decreases in cell size, and the cleaved blastomeres then compact to form a 32-cell or a "64n" morula [n = 1 full set of chromosomes]. Thus early embryogenesis can be interpreted as a progressive increase in ploidy, and if the zona pellucida is considered a cell membrane and cleavage is interpreted as endomitosis, then the 32-cell morula can be considered a multinucleated giant cell (or 64n syncytium). The decrease in cell size is accompanied by an increase in the nuclear-to-cytoplasmic (N/C) ratio, which then selectively activates a combined set of embryonic transcription factors that dedifferentiate the parental genome to a zygotic genome. This process is associated with a morphologic transition from a morula to a blastocyst and formation of an inner cell mass that gives rise to a new embryonic life. If the subsequent differentiation proceeds to complete maturation, then a normal life results. However, if differentiation is blocked at any point along the continuum of primordial germ cell to embryonic maturation to fetal organ maturation, a well-differentiated tumor will develop. Depending on the level of developmental hierarchy at which the stem cell differentiation is blocked, the resulting tumor can range from highly malignant to benign. Undifferentiated tumors are derived from mature somatic cells through dedifferentiation via a recently described reprogramming mechanism named the giant cell life cycle or the giant cell cycle. This mechanism can initiate "somatic embryogenesis" via an increase in ploidy ranging from 4n to 64n or more, similar to that in normal embryogenesis. This dedifferentiation mechanism is initiated through an endocycle and is followed by endomitosis, which leads to the formation of mononucleated or multinucleated polyploid giant cancer cells (PGCCs), that is, cancer stem-like cells that mimic the blastomere-stage embryo. The giant cell life cycle leads to progressive increases in the N/C ratio and awakens the suppressed embryonic reprogram, resulting in mature somatic transformation into undifferentiated tumors. Thus, the increase in ploidy explains not only normal embryogenesis for well-differentiated tumors but also "somatic embryogenesis" for undifferentiated tumors. I refer to this ploidy increase as the 'life code". The concept of the "life code" may provide a simple theoretical framework to guide our immense efforts to understand cancer and fight this disease.

摘要

肿瘤起源于正常干细胞或成熟体细胞的转化。有趣的是,病理学家几个世纪以来一直观察到两种类型的肿瘤:分化良好的肿瘤和未分化的肿瘤。分化良好的肿瘤在结构上与起源组织相似,而未分化的肿瘤表现出高度核异型性,与起源组织不相似。这两种肿瘤类型与人类生命周期之间的关系尚不清楚。在这里,我提出了一个统一的理论,用我们的生命周期来解释这两种肿瘤类型的转化过程。人类的生命始于卵子被精子受精形成受精卵。受精卵经过连续的卵裂分裂,在透明带内形成卵裂球,细胞体积逐渐减小,然后分裂的卵裂球紧密形成 32 细胞或“64n”桑葚胚[n=1 套完整的染色体]。因此,早期胚胎发生可以被解释为倍性的逐渐增加,如果透明带被认为是细胞膜,而卵裂被解释为核内有丝分裂,那么 32 细胞桑葚胚可以被认为是多核巨细胞(或 64n 合胞体)。细胞体积的减小伴随着核质比(N/C 比)的增加,这会选择性地激活一组组合的胚胎转录因子,使亲本基因组去分化为合子基因组。这个过程伴随着从桑葚胚到囊胚的形态转变,以及形成一个内细胞团,它产生一个新的胚胎生命。如果随后的分化继续完全成熟,那么就会产生正常的生命。然而,如果分化在原始生殖细胞到胚胎成熟到胎儿器官成熟的连续体中的任何一点被阻断,就会发展出分化良好的肿瘤。根据干细胞分化被阻断的发育层次水平,所产生的肿瘤可以从高度恶性到良性不等。未分化的肿瘤是由成熟的体细胞通过去分化产生的,去分化是通过最近描述的一种称为巨细胞生命周期或巨细胞周期的重编程机制。这种机制可以通过从 4n 到 64n 或更高的倍数增加来启动“体胚胎发生”,类似于正常胚胎发生。这种去分化机制是通过内周期启动的,随后是核内有丝分裂,导致单核或多核多倍体巨癌细胞(PGCCs)的形成,即类似于桑椹胚期胚胎的癌症干细胞样细胞。巨细胞生命周期导致 N/C 比的逐渐增加,并唤醒被抑制的胚胎重编程,导致成熟体细胞转化为未分化肿瘤。因此,倍性的增加不仅解释了分化良好的肿瘤的正常胚胎发生,也解释了未分化肿瘤的“体胚胎发生”。我将这种倍性增加称为“生命密码”。“生命密码”的概念可能为理解癌症和对抗这种疾病提供一个简单的理论框架。

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