Khatami Fatemeh, Tavangar Seyed Mohammad
Chronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
Department of Pathology, Dr. Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Iran Biomed J. 2018 May 1;22(3):142-50. doi: 10.22034/ibj.22.3.142. Epub 2017 Nov 11.
Medullary thyroid carcinoma (MTC) is an infrequent, calcitonin producing neuroendocrine tumor and initiates from the parafollicular C cells of the thyroid gland. Several genetic and epigenetic alterations are collaterally responsible for medullary thyroid carcinogenesis. In this review article, we shed light on all the genetic and epigenetic hallmarks of MTC. From the genetic perspective, RET, HRAS, and KRAS are the most important genes that are characterized in MTC. From the epigenetic perspective, Ras-association domain family member 1A, telomerase reverse transcriptase promoter methylations, overexpression of histone methyltransferases, EZH2 and SMYD3, and wide ranging increase and decrease in non-coding RNAs can be responsible for medullary thyroid carcinogenesis.
甲状腺髓样癌（MTC）是一种罕见的、产生降钙素的神经内分泌肿瘤，起源于甲状腺的滤泡旁C细胞。多种遗传和表观遗传改变共同导致甲状腺髓样癌的发生。在这篇综述文章中，我们阐述了MTC的所有遗传和表观遗传特征。从遗传学角度来看，RET、HRAS和KRAS是MTC中最具特征的重要基因。从表观遗传学角度来看，Ras关联结构域家族成员1A、端粒酶逆转录酶启动子甲基化、组蛋白甲基转移酶EZH2和SMYD3的过表达以及非编码RNA的广泛增减可能导致甲状腺髓样癌的发生。
