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首页> 外文期刊>Cell biology international. >Reappraisal of the Hansemann-Boveri hypothesis on the origin of tumors.
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Reappraisal of the Hansemann-Boveri hypothesis on the origin of tumors.

机译：重新评估关于肿瘤起源的Hansemann-Boveri假说。

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Cancer is now known to be a genetic disease. In tumor development, cell nuclei undergo mutations, which can result in cytologically visible chromosome aberrations. The aneuploid errors may involve amplification or deletion of whole chromosomes or segments thereof. David Hansemann [1858-1920] and Theodor Boveri [1862-1915] were major contributors to early debates on the relationship between chromosomal defects, tumorigenesis and malignancies. In 1890, Hansemann observed asymmetrical nuclear divisions in human epithelial cancers. In these abnormal, but bipolar, divisions, a fraction of the chromosomes fails to segregate properly. Hansemann carefully documented the occurrence of asymmetric divisions in a wide variety of tumors. However, he remained a lifelong skeptic with regard to whether such events could be considered the underlying cause of tumors. Almost a quarter of a century after Hansemann's initial observations, Boveri considered the origin of tumors based on his earlier recognition of the functional specificity of each chromosome. He also explicitly drew on Hansemann's observations in proposing a model for tumorigenesis. Its central tenet was that a tumor typically originates from a single cell that has inherited a defined, but incorrectly combined, set of chromosomes. The rare occurrence of a pluripolar spindle represented Boveri's paradigm for a type of abnormal mitosis that can produce a host of random chromosomal combinations. He suggested that some of these combinations will induce tumorous transformation, and will inevitably arise occasionally. Since pluripolar and unbalanced bipolar divisions fail to distribute the hereditary chromatic material correctly, both of these mechanisms can give rise to tumor progenitors.
机译：现在已知癌症是一种遗传疾病。在肿瘤发展过程中，细胞核发生突变，这可能导致细胞学上可见的染色体畸变。非整倍体错误可能涉及整个染色体或其片段的扩增或缺失。 David Hansemann [1858-1920]和Theodor Boveri [1862-1915]是有关染色体缺陷，肿瘤发生和恶性肿瘤之间关系的早期辩论的主要贡献者。 1890年，汉斯曼（Hansemann）在人类上皮癌中观察到不对称核分裂。在这些异常但双极性的分裂中，一部分染色体无法正确分离。 Hansemann仔细记录了多种肿瘤中不对称分裂的发生。但是，对于这些事件是否可以被认为是肿瘤的根本原因，他始终持怀疑态度。在汉斯曼（Hansemann）的最初观察之后大约四分之一世纪，布韦里（Boveri）根据他对每个染色体功能特异性的早期认识，考虑了肿瘤的起源。在提出肿瘤发生模型时，他还明确借鉴了汉斯曼的观察。它的中心宗旨是，肿瘤通常起源于单个细胞，该单个细胞继承了一组已定义但错误组合的染色体。多极纺锤体的罕见出现代表了Boveri对于一种异常有丝分裂的范例，这种异常有丝分裂可以产生许多随机的染色体组合。他建议这些组合中的一些会诱导肿瘤转化，并且不可避免地会偶尔出现。由于多极和不平衡的双极分裂不能正确地分布遗传性有色物质，所以这两种机制都可以引起肿瘤祖细胞。

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