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疾病机制:儿童甲状腺癌的分子遗传学

Mechanisms of Disease: molecular genetics of childhood thyroid cancers.

作者信息

Yamashita Shunichi, Saenko Vladimir

机构信息

Department of Molecular Medicine, Atomic Bomb Disease Institute, Nagasaki University, Graduate School of Biomedical Sciences, Japan.

出版信息

Nat Clin Pract Endocrinol Metab. 2007 May;3(5):422-9. doi: 10.1038/ncpendmet0499.

DOI:10.1038/ncpendmet0499
PMID:17452969
Abstract

Childhood thyroid cancers are uncommon and have a fairly good prognosis. Papillary adenocarcinoma is the most prevalent malignant tumor of the thyroid in children and adults with radiation-induced or sporadic cancer. The incidence of thyroid cancer in children increased dramatically in the territories affected by the Chernobyl nuclear accident; this increase is probably attributable to (131)I and other short-lived isotopes of iodine released into the environment. There was a broad range of latency periods in children who developed thyroid cancer; some periods were less than 5 years. The mutational spectrum of childhood thyroid cancers demonstrates that gene rearrangements that lead to the activation of mitogen-activated protein kinase signaling seem to have a pivotal role; point mutations are rare. So far none of the cancer genes or tumor suppressors, or a peculiar gene expression pattern, has been specifically implicated in radiation-induced thyroid carcinogenesis. The frequency of certain oncogenes does, however, vary in tumors that develop after different periods of latency. Such differences in the distribution of gene abnormalities in radiation-related cancers implies that they associate with patients' age at exposure and diagnosis, clinicopathological manifestations of disease and depend on an individual's genetic characteristics. Here we review results of pathological and molecular studies in childhood thyroid cancer.

摘要

儿童甲状腺癌并不常见,预后相当良好。乳头状腺癌是儿童和成人中最常见的甲状腺恶性肿瘤,包括辐射诱发的和散发性的癌症。在切尔诺贝利核事故影响的地区,儿童甲状腺癌的发病率急剧上升;这种增加可能归因于释放到环境中的碘-131和其他短寿命碘同位素。患甲状腺癌的儿童潜伏期差异很大;有些不到5年。儿童甲状腺癌的突变谱表明,导致丝裂原活化蛋白激酶信号激活的基因重排似乎起关键作用;点突变很少见。到目前为止,尚未发现任何癌症基因或肿瘤抑制基因,或特殊的基因表达模式与辐射诱发的甲状腺癌发生有特定关联。然而,某些癌基因的频率在不同潜伏期后发生的肿瘤中有所不同。辐射相关癌症中基因异常分布的这种差异意味着它们与患者暴露和诊断时的年龄、疾病的临床病理表现有关,并取决于个体的遗传特征。在此,我们综述儿童甲状腺癌的病理和分子研究结果。

相似文献

1
Mechanisms of Disease: molecular genetics of childhood thyroid cancers.疾病机制:儿童甲状腺癌的分子遗传学
Nat Clin Pract Endocrinol Metab. 2007 May;3(5):422-9. doi: 10.1038/ncpendmet0499.
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[Study of HRas1 minisatellite frequencies in children with thyroid papillary cancer].[甲状腺乳头状癌患儿中HRas1微卫星频率的研究]
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Thyroid cancer incidence among people living in areas contaminated by radiation from the Chernobyl accident.切尔诺贝利事故辐射污染地区居民的甲状腺癌发病率。
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Genetic aberrations in Chernobyl-related thyroid cancers: implications for possible future nuclear accidents or nuclear attacks.切尔诺贝利相关甲状腺癌中的基因畸变:对未来可能发生的核事故或核攻击的启示。
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Chernobyl and thyroid cancer.切尔诺贝利与甲状腺癌。
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[Gene expression profiling in human thyroid tumors].[人类甲状腺肿瘤中的基因表达谱分析]
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