Abstract
Abstract Background: Mutations in the promoter region of the telomerase reverse transcriptase (TERT) gene have recently been described in thyroid cancer and have been linked with poor prognosis. The mutations result in cancer-specific telomerase reactivation. However, functional effects of TERT promoter mutations other than telomere maintenance remain elusive. Methods: We examined papillary thyroid cancer data from The Cancer Genome Atlas. Clinicopathologic characteristics were compared between patients with or without TERT promoter mutations. A control cohort was selected from patients without TERT promoter mutations by propensity score matching. Differentially expressed genes were generated by comparing transcriptome profiling between the two groups. Results: A total of 382 patients with papillary thyroid cancer were included for analysis. TERT promoter mutations were identified in 36 patients. TERT promoter mutations were associated with older age, larger tumor size, the presence of extrathyroidal extension, more advanced TNM stage, and high risk of recurrence. Following propensity score matching, pathway analysis of differentially expressed genes indicated that TERT promoter mutations were associated with upregulation of DNA damage response and downregulation of nitric oxide signaling and fatty acid β-oxidation. Conclusion: Our results confirmed that acquisition of TERT promoter mutations in papillary thyroid cancer leads to bypass of replicative senescence. Furthermore, the mutations may be associated with other signaling and metabolic alterations. Our findings can potentially identify extended therapeutic targets. Citation Format: Shih-Ping Cheng, Ming-Nan Chien, Chien-Liang Liu, Yi-Chiung Hsu, Po-Sheng Yang, Jie-Jen Lee. Transcriptome evaluation of papillary thyroid cancer with TERT promoter mutation [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2017 Oct 26-30; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2018;17(1 Suppl):Abstract nr A194.
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