旅客8
医学
甲状腺癌
粘液瘤
癌变
甲状腺
甲状腺乳突癌
生物
癌症
甲状腺癌
伦瓦提尼
内科学
内分泌学
病理
癌症研究
基因
遗传学
转录因子
作者
Georgia Pitsava,Constantine A. Stratakis,Fabio R. Faucz
出处
期刊:Cancers
[MDPI AG]
日期:2021-07-30
卷期号:13 (15): 3834-3834
被引量:3
标识
DOI:10.3390/cancers13153834
摘要
Thyroid cancer is the most common type of endocrine malignancy and the incidence is rapidly increasing. Follicular (FTC) and papillary thyroid (PTC) carcinomas comprise the well-differentiated subtype and they are the two most common thyroid carcinomas. Multiple molecular genetic and epigenetic alterations have been identified in various types of thyroid tumors over the years. Point mutations in BRAF, RAS as well as RET/PTC and PAX8/PPARγ chromosomal rearrangements are common. Thyroid cancer, including both FTC and PTC, has been observed in patients with Carney Complex (CNC), a syndrome that is inherited in an autosomal dominant manner and predisposes to various tumors. CNC is caused by inactivating mutations in the tumor-suppressor gene encoding the cyclic AMP (cAMP)-dependent protein kinase A (PKA) type 1α regulatory subunit (PRKAR1A) mapped in chromosome 17 (17q22–24). Growth of the thyroid is driven by the TSH/cAMP/PKA signaling pathway and it has been shown in mouse models that PKA activation through genetic ablation of the regulatory subunit Prkar1a can cause FTC. In this review, we provide an overview of the molecular mechanisms contributing to thyroid tumorigenesis associated with inactivation of the RRKAR1A gene.
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