甲状腺癌
甲状腺
人口
癌症研究
癌症
致癌物
医学
祖细胞
生理学
内科学
内分泌学
化学
生物
干细胞
细胞生物学
生物化学
环境卫生
作者
Fiorenza Gianì,Roberta Masto,Maria Antonietta Trovato,Pasqualino Malandrino,Marco Russo,Gabriella Pellegriti,Paolo Vigneri,Riccardo Vigneri
出处
期刊:Cancers
[MDPI AG]
日期:2021-08-12
卷期号:13 (16): 4052-4052
被引量:28
标识
DOI:10.3390/cancers13164052
摘要
In recent decades, the incidence of thyroid cancer has increased more than most other cancers, paralleling the generalized worldwide increase in metal pollution. This review provides an overview of the evidence supporting a possible causative link between the increase in heavy metals in the environment and thyroid cancer. The major novelty is that human thyroid stem/progenitor cells (thyrospheres) chronically exposed to different metals at slightly increased environmentally relevant concentrations show a biphasic increase in proliferation typical of hormesis. The molecular mechanisms include, for all metals investigated, the activation of the extracellular signal-regulated kinase (ERK1/2) pathway. A metal mixture, at the same concentration of individual metals, was more effective. Under the same conditions, mature thyrocytes were unaffected. Preliminary data with tungsten indicate that, after chronic exposure, additional abnormalities may occur and persist in thyrocytes derived from exposed thyrospheres, leading to a progeny population of transformation-prone thyroid cells. In a rat model predisposed to develop thyroid cancer, long-term exposure to low levels of metals accelerated and worsened histological signs of malignancy in the thyroid. These studies provide new insight on metal toxicity and carcinogenicity occurring in thyroid cells at a low stage of differentiation when chronically exposed to metal concentrations that are slightly increased, albeit still in the "normal" range.
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