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The epigenetics of cancer etiology.

机译：癌症病因学的表观遗传学。

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摘要

Epigenetic dysregulation is central to cancer development and progression. This dysregulation includes hypomethylation leading to oncogene activation and chromosomal instability, hypermethylation and tumor suppressor gene silencing, and chromatin modification acting directly, and cooperatively with methylation changes, to modify gene expression. In addition, disrupted genomic imprinting appears to contribute to colorectal cancer risk, and serves as a gatekeeper in Wilms tumor. A cancer predisposing disorder, Beckwith-Wiedemann syndrome, usually arises from epigenetic errors, solidifying the causal role of epigenetics in cancer. While cancer epigenetics has been reviewed extensively elsewhere, the main focus of this review will be to present the view that epigenetics and genetics are complementary in the area of cancer etiology, the focus of this volume. I propose a hypothesis in which epigenetic alterations contribute to tumor progression, but they also increase the probability that genetic changes, when they occur, will lead to cancer initiation. This hypothesis could contribute to a new understanding of the role of environmental carcinogens that may not be fully explained through a purely genetic view or by tests, such as bacterial mutation frequency, that ignore epigenetic factors.
机译：表观遗传失调是癌症发展和进展的关键。这种失调包括导致致癌基因激活和染色体不稳定性的甲基化不足，甲基化过度和肿瘤抑制基因沉默，以及直接和与甲基化改变协同作用的染色质修饰，从而修饰基因表达。另外，破坏的基因组印迹似乎增加了结直肠癌的风险，并充当了威尔姆斯肿瘤的看门人。 Beckwith-Wiedemann综合征是易患癌症的疾病，通常由表观遗传学错误引起，巩固了表观遗传学在癌症中的因果作用。虽然癌症表观遗传学已在其他地方进行了广泛的综述，但本综述的主要重点将是提出表观遗传学和遗传学在癌症病因学领域是本卷的重点互补的观点。我提出了一种假说，其中表观遗传学改变有助于肿瘤进展，但它们也增加了遗传学改变（一旦发生）将导致癌症发作的可能性。该假设可能有助于人们对环境致癌物的作用有了新的认识，而单纯的遗传学观点或忽略表观遗传因素的测试（例如细菌突变频率）可能无法完全解释环境致癌物的作用。

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