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Studies have shown that radioactive iodine therapy (RAIT) affects the development of second cancer in thyroid cancer patients. The impact of other factors, such as dyslipidemia are not clear. A retrospective analysis of thyroid cancer patients with a 1,251,913 person-year follow-up was conducted using data from the Health Insurance Review and Assessment database in South Korea from January 2008 to December 2018. We investigated factors related to second cancer development using a nested case-control analysis to avoid length bias. The overall risk of developing second cancer was higher in thyroid cancer patients than in the general population [standardized incidence ratio, 3.34; 95% confidence interval (CI) 3.30–3.39]. Second cancer incidence was higher in patients who received RAIT than in those who did not [odds ratio (OR) 1.130; 95% CI 1.094–1.169]. Moreover, the risk of second cancer was higher in patients with dyslipidemia than in those without dyslipidemia (OR 1.265; 95% CI 1.223–1.309). After adjustment for RAIT, the incidence of a second cancer was higher in patients with dyslipidemia than in those without dyslipidemia (OR 1.262; 95% CI 1.221–1.306). The risk of second cancer development in patients with thyroid cancer appears to be high. Dyslipidemia may be associated with an increased risk of several types of second cancers.

GITR (glucocorticoid-induced TNF receptor) is a recently identified member of the TNF receptor superfamily. The receptor is preferentially expressed on CD4(+)CD25(+) regulatory T cells and GITR signals break the suppressive activity of the subset. In this study, we wanted to reveal the in vivo function of GITR in herpes simplex virus type 1 (HSV-1) infection. A single injection of anti-GITR mAb (DTA-1) immediately after viral infection significantly increased the number of CD4(+) and CD8(+) T cells expressing CD25, an activation surface marker, and secreting IFN-gamma. We confirmed these in vivo observations by showing ex vivo that re-stimulation of CD4(+) or CD8(+) T cells with a CD4(+) or CD8(+) T-cell-specific HSV-1 peptide, respectively, induced a significant elevation in cell proliferation and in IFN-gamma secretion. Our results indicate that GITR signals play a critical role in the T-cell immunity to HSV-1.