甲状腺癌是女性第7位常见的恶性肿瘤，乳头状甲状腺癌占其中的90%以上。近期研究发现，在甲状腺结节患者中，血清促甲状腺激素（TSH）升高是乳头状甲状腺癌的危险因素，但TSH通路如何诱导甲状腺滤泡细胞恶变的分子机制并不清楚。我们前期的研究发现，PPARG的共激活因子PRDM16的功能变化可导致乳头状甲状腺癌发生， 其可能信号通路是由PAX8-PPARG融合基因功能上调，引起下游Wnt/beta-catenin通路信号增强，最终引起受TSH通路信号持续增强。我们将进一步分析PRDM16基因的功能变化在不同分化阶段的甲状腺滤泡细胞中的动态表达情况及其对于甲状腺滤泡细胞、甲状腺肿瘤细胞生物学行为的影响，并深入研究PRDM16在甲状腺滤泡细胞及肿瘤细胞中对下游基因的调控，最终揭示TSH通路诱发乳头状甲状腺癌过程中的分子机制，为临床乳头状甲状腺癌的诊断和治疗提供理论依据。

Thyoid cancer is the most popular endocrine malignant, which is the 7th cancer in women, and about 90% thyoid cancer is papillary thyroid cancer (PTC). Recently reasearches show high level thyroid stimulating hormone（TSH）causes higher risk of thyroid cancer. In our research, we confirm this phenomenon in Chinese patients. Unfortunately, the molecular mechanism of how TSH-cAMP pathway casused thyroid cancer was unclear,we find PRDM16,the co-activator of PPARGgene could casue PTC.The signal might be conducted in the pathway of PAX8-PPARG to Wnt/beta-catenin to TSH-G protein. In future study, we will analysis the change of function in these pathways because of the loss of PRDM16. Finally，our research will elucidate the mechanism of TSH-G protein pathway in the PTC and provide the expanlation for the clinical diagnose and treatment of PTC.