Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 369369
Title Iodide kinetics and experimental I-131 therapy in a xenotransplanted human sodium-iodide symporter-transfected human follicular thyroid carcinoma cell line
Author(s) Smit, J.W.A.; Elst, J.P. van der; Karperien, M.; Que, I.; Stokkel, M.; Heide, D. van der; Romijn, J.A.
Source Journal of Clinical Endocrinology and Metabolism 87 (2002)3. - ISSN 0021-972X - p. 1247 - 1253.
Department(s) Human and Animal Physiology
WIAS
Publication type Refereed Article in a scientific journal
Publication year 2002
Keyword(s) messenger-rna levels - sodium/iodide symporter - radioiodine therapy - prostate-cancer - retinoic acid - frtl-5 cells - expression - gene - hormone - cloning
Abstract 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
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