[Molecular pathogenesis of thyroid tumors].
[Molecular pathogenesis of thyroid tumors].
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【甲状腺肿瘤的分子发病机制】
DOI：
10.1055/s-0041-101491
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发表时间：
2015
影响因子：
0.6
通讯作者：
Führer D
中科院分区：
文献类型：
--
作者：
Tiedje V;Zwanziger D;Ting S;Schmid KW;Führer D
甲状腺肿瘤的分子发病机制在过去的几年里一直是一个不断发展的领域。细胞内酪氨酸激酶的结构性激活已被认为是甲状腺癌的一个标志。通过体细胞基因突变或基因重排激活MAPK和PI3K通路似乎在滤泡细胞源性肿瘤的发病机制中起着关键作用。在低分化肿瘤和间变性肿瘤中，分化型甲状腺癌的基因改变通常是累积的，但也可以观察到新的基因突变。C细胞来源的髓样甲状腺癌通过RET激酶的结构性激活而进化，要么是种系RET突变，要么是体细胞RET和Ras突变。对分子发病机制的更好了解使甲状腺癌患者靶向治疗的发展成为可能。确定酪氨酸激酶抑制剂治疗的分子反应标记物是可取的。
The molecular pathogenesis of thyroid tumors has been an evolving field in the past years. The constitutive activation of intracellular tyrosine kinases has been identified as a hallmark of thyroid cancer. The activation of MAPK and PI3K pathways through somatic gene mutations or gene rearrangements seem to play a pivotal role in the pathogenesis of follicular-cell-derived tumors. In poorly differentiated tumors and anaplastic tumors often an accumulation of genetic alterations from differentiated thyroid cancer but also novel gene mutations can be observed. The C-cell-derived medullary thyroid cancer evolves through the constitutive activation of the RET kinase, either through germline RET mutations or somatic RET and RAS mutations. The better knowledge of the molecular pathogenesis allowed the development of targeted therapies in thyroid cancer patients. The identification of molecular response markers to tyrosine kinase inhibitor therapy is desirable.