So Young Rha

Predictive value of the preablation serum thyroglobulin level after thyroidectomy Is combined with postablation 131I whole body scintigraphy for successful ablation in patients with differentiated thyroid carcinoma

Objectives:To investigate the clinical importance of the combined use of serum thyroglobulin (Tg) levels measured just before ablation (ablation-Tg) and postablation 131I whole body scintigraphy (WBS) patterns for predicting ablation success in patients with differentiated thyroid carcinoma who received total thyroidectomy and 131I ablation therapy. Methods:We retrospectively studied the early clinical outcomes for 81 differentiated thyroid carcinoma patients treated with total thyroidectomy and high-dose 131I ablation therapy between June 2001 and July 2004. Results:Ablation success was achieved in 42 (97.7%) of the 43 patients with uptake in the thyroid bed only and ablation-Tg levels less than 10 ng/mL, whereas successful ablation was achieved in 9 (75.0%) of the 12 patients with uptake in the thyroid bed only and ablation-Tg levels equal to or greater than 10 ng/mL (P = 0.029). Among 15 patients with uptake including a lymph node and ablation-Tg levels less than 10 ng/mL, 14 patients (93.3%) showed ablation success, whereas successful ablation was achieved in only 2 (18.2%) of the 11 patients with uptake including a lymph node and ablation-Tg levels equal to or greater than 10 ng/mL (P < 0.001). Conclusions:These data indicate that the combined use of serum Tg levels measured just before ablation and the 131I WBS patterns after ablation may be an early predictor of ablation success in patients with differentiated thyroid carcinoma who received total thyroidectomy and high-dose 131I ablation therapy.

Significance of the expression of major histocompatibility complex class II antigen, HLA‐DR and ‐DQ, with recurrence of papillary thyroid cancer

Normal thyroid epithelial cells lack major histocompatibility complex (MHC) Class II antigen. Oncogenic kinases involved in papillary thyroid carcinoma (PTC) trigger the expression of Class II transactivator and MHC Class II complex. However, the relationship between MHC Class II antigen expression and clinical outcome in PTC is unknown. To investigate the frequency of MHC Class II antigen expression in PTC and to identify the effects of MHC Class II antigen expression on clinical outcomes in PTC patients, the expression of HLA‐DR/‐DQ antigen was analyzed in surgical specimens from 77 PTCs and 44 benign nodules (23 nodular hyperplasias, 21 follicular adenomas). Of the 77 PTC cases, 36 (46.8%) cases expressed HLA‐DR and 41 (53.2%) cases expressed HLA‐DQ. Next, we investigated clinicopathological characteristics and found that HLA‐DR(+) and/or HLA‐DQ(+) PTC tended to present without nodal metastasis. Multivariate analyses clearly showed that HLA‐DR(+) or HLA‐DQ(+) PTC has a low risk of recurrence (HLA‐DR OR = 0.22, CI, 0.06–0.9; p = 0.03, HLA‐DQ OR = 0.25, CI, 0.07–0.9, p = 0.03). The Kaplan–Meier estimate revealed a significantly lower recurrence‐free probability in patients with HLA‐DR(−) PTC and HLA‐DQ(−) PTC (Log‐rank test; χ2 = 4.59 and 6.07, p = 0.03 and 0.01, respectively). In conclusion, PTC frequently expresses MHC Class II antigen, and the expression of MHC Class II antigen correlated inversely with the risk of recurrence of PTC.

Regulation of inhibitors of differentiation family proteins by thyroid-stimulating hormone in FRTL-5 thyroid cells.

Members of the inhibitors of differentiation (Id) family of helix-loop-helix (HLH) proteins are known to play important roles in the proliferation and differentiation of many cell types. Thyroid-stimulating hormone (TSH) regulates proliferation and differentiation by activating TSH receptor (TSHR) in thyrocytes. In this study, we found that Id2, one of the Id family proteins, is a major target for regulation by TSH in FRTL-5 thyroid cells. TSH rapidly increases the Id2 mRNA level in FRTL-5 thyroid cells but the Id2 protein showed biphasic regulatory patterns, being transiently reduced and subsequently induced by TSH treatment. Transient reduction of Id2 protein was noted within 2 hr of TSH treatment and was mediated by proteasomal degradation. Moreover, reduced Id2 expression correlated with the activity of the phosphatidylinositol 3 kinase pathway, which is activated by TSH. Although TSH increases the activity of the Id2 promoter, TSH-induced activation of this promoter was independent of c-Myc. Id2 did not alter TTF-1- and Pax-8-mediated effects on the regulation of the Tg promoter. Thus, in summary, we found that TSH regulates Id2 expression, but that Id2 does not alter the expression of thyroid-specific genes, such as Tg, in FRTL-5 thyroid cells.