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首页> 外文期刊>Molecular cytogenetics >Understanding aneuploidy in cancer through the lens of system inheritance, fuzzy inheritance and emergence of new genome systems
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Understanding aneuploidy in cancer through the lens of system inheritance, fuzzy inheritance and emergence of new genome systems

机译：通过系统遗传的镜片，模糊遗传和新基因组系统的出现，了解癌症中的一种单倍性

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In the past 15?years, impressive progress has been made to understand the molecular mechanism behind aneuploidy, largely due to the effort of using various -omics approaches to study model systems (e.g. yeast and mouse models) and patient samples, as well as the new realization that chromosome alteration-mediated genome instability plays the key role in cancer. As the molecular characterization of the causes and effects of aneuploidy progresses, the search for the general mechanism of how aneuploidy contributes to cancer becomes increasingly challenging: since aneuploidy can be linked to diverse molecular pathways (in regards to both cause and effect), the chances of it being cancerous is highly context-dependent, making it more difficult to study than individual molecular mechanisms. When so many genomic and environmental factors can be linked to aneuploidy, and most of them not commonly shared among patients, the practical value of characterizing additional genetic/epigenetic factors contributing to aneuploidy decreases. Based on the fact that cancer typically represents a complex adaptive system, where there is no linear relationship between lower-level agents (such as each individual gene mutation) and emergent properties (such as cancer phenotypes), we call for a new strategy based on the evolutionary mechanism of aneuploidy in cancer, rather than continuous analysis of various individual molecular mechanisms. To illustrate our viewpoint, we have briefly reviewed both the progress and challenges in this field, suggesting the incorporation of an evolutionary-based mechanism to unify diverse molecular mechanisms. To further clarify this rationale, we will discuss some key concepts of the genome theory of cancer evolution, including system inheritance, fuzzy inheritance, and cancer as a newly emergent cellular system. Illustrating how aneuploidy impacts system inheritance, fuzzy inheritance and the emergence of new systems is of great importance. Such synthesis encourages efforts to apply the principles/approaches of complex adaptive systems to ultimately understand aneuploidy in cancer.
机译：在过去的15年里，已经提出了令人印象深刻的进步，以了解非整倍性背后的分子机制，主要是由于使用各种 - 学习方法来研究模型系统（例如酵母和小鼠模型）和患者样品以及患者样品以及染色体改变介导的基因组不稳定性的新实现起着癌症的关键作用。随着动脉倍差的原因和效果的分子表征进展，对非整倍性有助于癌症的一般机制变得越来越具有挑战性：由于非倍性可以与不同的分子途径（关于既有原因和效应）相关联，因此机会它是癌性的高度上下文依赖性，使得研究比单个分子机制更难以研究。当如此多的基因组和环境因素可以与非整倍性相关，而且大多数未在患者中共享的大部分内容时，表征额外的遗传/表观遗传因素的实际价值是有助于非整倍性的影响。基于癌症通常代表复杂的自适应系统的事实，其中下水平试剂（例如每个单独的基因突变）和紧急性质（例如癌症表型）没有线性关系，我们要求基于的新战略癌症中共倍性的进化机制，而不是持续分析各个单独的分子机制。为了说明我们的观点，我们简要介绍了这一领域的进步和挑战，表明纳入基于进化的机制，以统一不同的分子机制。为了进一步澄清这一理由，我们将讨论癌症进化基因组理论的一些关键概念，包括系统遗传，模糊遗传和癌症作为一种新的突出细胞系统。说明非洲行为影响系统继承，模糊遗传和新系统的出现都具有重要意义。这种综合促使努力应用复杂的自适应系统的原理/方法，最终了解癌症中的一种单倍性。

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