Kondo Tetsuo, Asa Sylvia L, Ezzat Shereen
Department of Pathology, University of Yamanashi, Japan.
Endocrinol Metab Clin North Am. 2008 Jun;37(2):389-400, ix. doi: 10.1016/j.ecl.2007.12.002.
Gain-of-function mutations in oncogenes have aided our understanding of the molecular mechanisms of thyroid carcinogenesis. Mutations or deletions cause inactivation of tumor suppressor genes in thyroid carcinomas. However, recent advances have disclosed the significance of epigenetic events in the development and progression of human tumorigenesis. Indeed, various tumor-suppressor genes and thyroid hormone-related genes are epigenetically silenced in thyroid tumors. This article reviews the evidence for epigenetic gene dysregulation in follicular cell-derived thyroid carcinomas including papillary thyroid carcinoma, follicular thyroid carcinoma, and undifferentiated thyroid carcinoma. The authors also discuss future applications of epigenetics as ancillary diagnostic tools and in the design of targeted therapies for thyroid cancer.
癌基因的功能获得性突变有助于我们理解甲状腺癌发生的分子机制。突变或缺失导致甲状腺癌中肿瘤抑制基因失活。然而，最近的进展揭示了表观遗传事件在人类肿瘤发生发展过程中的重要性。事实上，各种肿瘤抑制基因和甲状腺激素相关基因在甲状腺肿瘤中发生表观遗传沉默。本文综述了滤泡细胞源性甲状腺癌（包括乳头状甲状腺癌、滤泡状甲状腺癌和未分化甲状腺癌）中表观遗传基因失调的证据。作者还讨论了表观遗传学作为辅助诊断工具以及在甲状腺癌靶向治疗设计中的未来应用。
