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Iodide kinetics and experimental (131)I therapy in a xenotransplanted human sodium-iodide symporter-transfected human follicular thyroid carcinoma cell line

机译:异种移植的人碘化钠同向转运蛋白转染的人滤泡性甲状腺癌细胞系中的碘化物动力学和实验性(131)I治疗

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摘要

Uptake of iodide is a prerequisite for radioiodide therapy in thyroid cancer. However, loss of iodide uptake is frequently observed in metastasized thyroid cancer, which may be explained by diminished expression of the human sodium-iodide symporter (hNIS). We studied whether transfection of hNIS into the hNIS-deficient follicular thyroid carcinoma cell line FTC133 restores the in vivo iodide accumulation in xenografted tumors and their susceptibility to radioiodide therapy. In addition, the effects of low-iodide diets and thyroid ablation on iodide kinetics were investigated. Tumors were established in nude mice injected with the hNIS-transfected cell line FTC133-NIS30 and the empty vector transfected cell line FTC133-V4 as a control. Tumors derived from FTC133-NIS30 in mice on a normal diet revealed a high peak iodide accumulation (17.4% of administered activity, measured with an external probe) as compared with FTC133-V4 (4.6%). Half-life in FTC133-NIS30 tumors was 3.8 h. In mice kept on a low-iodide diet, peak activity in FTC133-NIS30 tumors was diminished (8.1%), whereas thyroid iodide accumulation was increased. In thyroid-ablated mice kept on a low-iodide diet, half-life of radioiodide was increased considerably (26.3 h), leading to a much higher area under the time-radioactivity curve than in FTC133-NIS30 tumors in mice on a normal diet without thyroid ablation. Experimental radioiodide therapy with 2 mCi (74 MBq) in thyroid-ablated nude mice, kept on a low-iodide diet, postponed tumor development (4 wk after therapy, one of seven animals revealed tumor vs. five of six animals without therapy). However, 9 wk after therapy, tumors had developed in four of the seven animals. The calculated tumor dose was 32.2 Gy. We conclude that hNIS transfection into a hNIS-defective thyroid carcinoma cell line restores the in vivo iodide accumulation. The unfavorable iodide kinetic characteristics (short half-life) can be partially improved by conventional conditioning with thyroid ablation and low-iodide diet, leading to postponed tumor development after radioiodide therapy. However, to achieve sufficient radioiodide tumor doses for therapy, further strategies are necessary, aiming at the mechanisms of iodide efflux in particular
机译:摄取碘是甲状腺癌放射碘治疗的先决条件。然而,在转移性甲状腺癌中经常观察到碘摄取的损失,这可以通过人类碘化钠共转运体(hNIS)的表达减少来解释。我们研究了将hNIS转染到hNIS缺陷型滤泡性甲状腺癌细胞FTC133中是否能恢复异种移植肿瘤中体内碘的积累及其对放射性碘治疗的敏感性。此外,还研究了低碘饮食和甲状腺消融对碘动力学的影响。在注射了hNIS转染的细胞系FTC133-NIS30和空载体转染的细胞系FTC133-V4作为对照的裸鼠中建立了肿瘤。与FTC133-V4(4.6%)相比,在正常饮食下的小鼠中源自FTC133-NIS30的肿瘤显示出高的碘化物累积峰(17.4%的给药活性,使用外部探针测量)。 FTC133-NIS30肿瘤的半衰期为3.8小时。在低碘饮食下的小鼠中,FTC133-NIS30肿瘤的峰值活性降低了(8.1%),而甲状腺碘化物的积累却增加了。在低碘饮食的甲状腺消融小鼠中,放射性碘的半衰期显着增加(26.3小时),导致时间放射性曲线下的面积比正常饮食的FTC133-NIS30肿瘤高得多无甲状腺消融。在低碘饮食下,对甲状腺消融的裸鼠进行2 mCi(74 MBq)的实验性放射性碘疗法,延缓了肿瘤的发展(治疗后4周,七只动物中的一只显示出肿瘤,而六只动物中的五只则未治疗)。但是,治疗后9周,七只动物中有四只已经出现肿瘤。计算的肿瘤剂量为32.2 Gy。我们得出的结论是,将hNIS转染到hNIS缺陷的甲状腺癌细胞系中可恢复体内碘化物的积累。常规的甲状腺消融和低碘饮食可以改善不良的碘动力学特性(半衰期短),从而导致放射性碘治疗后肿瘤的发生延迟。但是,为了获得足够的放射性碘治疗肿瘤剂量,有必要采取进一步的策略,尤其是针对碘流出的机制。

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