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Mechanisms of disease: hydrogen peroxide, DNA damage and mutagenesis in the development of thyroid tumors.

机译:疾病机理:甲状腺肿瘤发展中的过氧化氢,DNA损伤和诱变。

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摘要

Somatic mutations can be identified in two-thirds of papillary and follicular thyroid carcinomas and 'hot' thyroid nodules, whereas equivalent mutations relevant for benign 'cold' thyroid nodules are unknown. This Review summarizes current knowledge about early molecular conditions for nodular and tumor transformation in the thyroid gland. We reconstruct a line of events that could explain the predominant neoplastic character (i.e. originating from a single mutated cell) of thyroid nodular lesions. This process might be triggered by the oxidative nature of thyroid hormone synthesis or additional oxidative stress caused by iodine deficiency or smoking. If the antioxidant defense is not effective, this oxidative stress can cause DNA damage followed by an increase in the spontaneous mutation rate, which is a platform for tumor genesis. The hallmark of thyroid physiology--H2O2 production during hormone synthesis--is therefore very likely to be the ultimate cause of frequent mutagenesis in the thyroid gland. DNA damage and mutagenesis could provide the basis for the frequent nodular transformation of endemic goiters.
机译:可以在三分之二的乳头状和滤泡性甲状腺癌和“热”甲状腺结节中识别出体细胞突变,而与良性“冷”甲状腺结节相关的等效突变是未知的。这篇综述总结了有关甲状腺中结节和肿瘤转化的早期分子条件的最新知识。我们重建了一系列事件,可以解释甲状腺结节性病变的主要肿瘤特征(即起源于单个突变细胞)。甲状腺激素合成的氧化性或碘缺乏或吸烟引起的额外氧化应激可能触发了这一过程。如果抗氧化防御措施无效,则这种氧化应激会导致DNA损伤,继而增加自发突变率,这是肿瘤发生的平台。因此,甲状腺生理学的标志(激素合成过程中产生的H2O2)很可能是导致甲状腺频繁诱变的最终原因。 DNA损伤和诱变可以为地方性甲状腺肿的频繁结节性转化提供基础。

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