Why the study?
To provide an overview of the molecular mechanisms contributing to thyroid tumorigenesis associated with inactivation of the PRKAR1A gene in the context of Carney Complex and mouse models.
This review summarizes the molecular mechanisms by which PRKAR1A gene inactivation and subsequent PKA activation contribute to thyroid tumorigenesis.
Answers are grounded in this paper and cite their sources.
Provides mechanistic insights into PRKAR1A-driven thyroid tumorigenesis; extends molecular understanding but leaves clinical translation open.
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.
No takes yet. Share an insight, caveat, or question.
Pitsava et al. (2021) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: