Albert de la Chapelle1, Krystian Jazdzewski. 1. Human Cancer Genetics Program, Comprehensive Cancer Center, The Ohio State University, 804 Biomedical Research Tower, 460 West 12th Avenue, Columbus, Ohio 43210, USA. albert.delachapelle@osumc.edu
Abstract
CONTEXT: Traditionally, factors predisposing to diseases are either genetic ("nature") or environmental, also known as lifestyle-related ("nurture"). Papillary thyroid cancer is an example of a disease where the respective roles of these factors are surprisingly unclear. EVIDENCE ACQUISITION: Original articles and reviews summarizing our current understanding of the role of microRNA in thyroid tumorigenesis are reviewed and evaluated. CONCLUSION: The genetic predisposition to papillary thyroid cancer appears to consist of a variety of gene mutations that are mostly either of low penetrance and common or of high penetrance but rare. Moreover, they likely interact with each other and with environmental factors. The culpable genes may not be of the traditional, protein-coding type. A limited number of noncoding candidate genes have indeed been described, and we propose here that the failure to find mutations in traditional protein-coding genes is not coincidental. Instead, a more likely hypothesis is that changes in the expression of multiple regulatory RNA genes, e.g. microRNAs, may be a major mechanism. Our review of the literature strongly supports this notion in that a polymorphism in one microRNAs (miR-146a) predisposes to thyroid carcinoma, whereas numerous other microRNAs are involved in signaling (mainly PTEN/PI3K/AKT and T3/THRB) that is central to thyroid carcinogenesis.
CONTEXT: Traditionally, factors predisposing to diseases are either genetic ("nature") or environmental, also known as lifestyle-related ("nurture"). Papillary thyroid cancer is an example of a disease where the respective roles of these factors are surprisingly unclear. EVIDENCE ACQUISITION: Original articles and reviews summarizing our current understanding of the role of microRNA in thyroid tumorigenesis are reviewed and evaluated. CONCLUSION: The genetic predisposition to papillary thyroid cancer appears to consist of a variety of gene mutations that are mostly either of low penetrance and common or of high penetrance but rare. Moreover, they likely interact with each other and with environmental factors. The culpable genes may not be of the traditional, protein-coding type. A limited number of noncoding candidate genes have indeed been described, and we propose here that the failure to find mutations in traditional protein-coding genes is not coincidental. Instead, a more likely hypothesis is that changes in the expression of multiple regulatory RNA genes, e.g. microRNAs, may be a major mechanism. Our review of the literature strongly supports this notion in that a polymorphism in one microRNAs (miR-146a) predisposes to thyroid carcinoma, whereas numerous other microRNAs are involved in signaling (mainly PTEN/PI3K/AKT and T3/THRB) that is central to thyroid carcinogenesis.
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Authors: Sylwia E Wojcik; Simona Rossi; Masayoshi Shimizu; Milena S Nicoloso; Amelia Cimmino; Hansjuerg Alder; Vlad Herlea; Laura Z Rassenti; Kanti R Rai; Thomas J Kipps; Michael J Keating; Carlo M Croce; George A Calin Journal: Carcinogenesis Date: 2009-11-19 Impact factor: 4.944
Authors: Sandya Liyanarachchi; Anna Wojcicka; Wei Li; Malgorzata Czetwertynska; Elzbieta Stachlewska; Rebecca Nagy; Kevin Hoag; Bernard Wen; Rafal Ploski; Matthew D Ringel; Izabella Kozłowicz-Gudzinska; Wojciech Gierlikowski; Krystian Jazdzewski; Huiling He; Albert de la Chapelle Journal: Thyroid Date: 2013-08-29 Impact factor: 6.568
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