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癌症克隆性与场论

Cancer clonality and field theory.

作者信息

Matioli G T

机构信息

USC Medical School, Los Angeles 90033.

出版信息

Med Hypotheses. 1988 Oct;27(2):149-51. doi: 10.1016/0306-9877(88)90162-4.

Abstract

We discuss a "genomic" mechanism capable of yielding clonal malignancies (e.g. hemopoietic leukemias) without the prerequisite of multiple or single mutations. This hypothetical mechanism is based upon the anachronistic (illegal) expression of a special gene P, where P stands for "potential". P. is a stimulus promoting renewal of stem and most immature cells of hemopoietic tissues. In normal conditions, these cells renew themselves only after receiving P from special microenvironmental cells or field "sources". When illegally expressed by a previously dependent cell, the autocatalyzed potential competes with differentiating factors and slows down terminal differentiation. This sets the cell on a temporary (or extended) "limit cycle" between competing attractors viz: renewal and extinction, whereby both progenitor and clonal progeny are locked between continuous proliferation and terminal differentiation for a time longer than their normal, absolutely source dependent counterparts.

摘要

我们讨论了一种“基因组”机制,该机制能够产生克隆性恶性肿瘤(如造血系统白血病),而无需多个或单个突变这一前提条件。这种假设的机制基于一个特殊基因P的过时(非法)表达,其中P代表“潜能”。P是一种促进造血组织干细胞和大多数未成熟细胞更新的刺激因子。在正常情况下,这些细胞只有在从特殊的微环境细胞或局部“源”接收P后才会自我更新。当先前依赖的细胞非法表达时,自我催化的潜能会与分化因子竞争并减缓终末分化。这使细胞处于竞争吸引子(即更新和消亡)之间的临时(或延长的)“极限环”上,由此祖细胞和克隆后代在持续增殖和终末分化之间被锁定的时间比它们正常的、完全依赖源的对应细胞更长。

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