Moderate doses of iodide in vivo inhibit cell proliferation and the expression of thyroperoxidase and Na+/I− symporter mRNAs in dog thyroid

Uyttersprot, Nathalie; Pelgrims, N; Carrasco, Nancy; Gervy, Christine; Maenhaut, Carine; Dumont, Jacques Emile; Miot, Françoise

doi:10.1016/s0303-7207(97)00108-1

Cited by 155 publications

(121 citation statements)

References 49 publications

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“…Indeed, iodide intake in Japan is known to be high and it has been shown that iodide exerts down-regulatory actions on NIS expression. 29,30 This remark might also be applied to the immunohistochemical study of Dohan and colleagues 14 who reported an overexpression of hNIS in 70% of thyroid cancer (as compared to adjacent NT) and no expression in the 30% remaining cases. The authors did not give information on the thyroid status of the patients.…”

Section: Discussionmentioning

confidence: 93%

Evidence for Transcriptional and Posttranscriptional Alterations of the Sodium/Iodide Symporter Expression in Hypofunctioning Benign and Malignant Thyroid Tumors

Trouttet-Masson

Selmi-Ruby

Bernier-Valentin

et al. 2004

The American Journal of Pathology

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Section: Discussionmentioning

confidence: 93%

Evidence for Transcriptional and Posttranscriptional Alterations of the Sodium/Iodide Symporter Expression in Hypofunctioning Benign and Malignant Thyroid Tumors

Trouttet-Masson

Selmi-Ruby

Bernier-Valentin

et al. 2004

The American Journal of Pathology

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“…NIS expression was also increased by TSH in RasC40 cells, albeit to slightly reduced levels compared to parental cells. Di erential e ects on Tg and NIS expression were also observed following treatment with low doses of iodide (Uyttersprot et al, 1997), suggesting that the expression of these proteins is regulated through distinct mechanisms. Interestingly, a recent report indicates that Pax-8, one of three thyroid-speci®c transcription factors , plays a prominent role in the regulation of NIS expression (Ohno et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Ras signaling through PI3K confers hormone-independent proliferation that is compatible with differentiation

Cass

Meinkoth

2000

Oncogene

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Hormones are specialized mitogens that stimulate proliferation in their di erentiated target cells. Thyrotropin (TSH), the physiologic regulator of thyroid cells, stimulates cAMP-mediated proliferation and thyroidspeci®c gene expression. The mitogenic e ects of TSH require Ras, therefore Ras activation should be compatible with the maintenance of thyroid di erentiation. However, expression of activated Ras extinguishes the di erentiated phenotype of thyroid cells. One explanation for this apparent paradox is the selective utilization of Ras e ector pathways. We tested the hypothesis that Ras signaling through PI3K mediates the mitogenic e ects of TSH in cells which retain their di erentiated character. Expression of a Ras e ector mutant (RasV12S35) that signals preferentially through Raf-1, although su cient to confer TSH-independent proliferation, abolished hormone-regulated expression of thyroglobulin and the sodium/iodide symporter. In contrast, expression of a Ras mutant (RasV12C40) that binds selectively to PI3K conferred TSH-independent proliferation without marked e ects on thyroid-speci®c gene expression. Unlike the inhibitory e ects of TSH on the proliferation of RasV12S35-expressing cells, TSH enhanced RasV12C40-stimulated proliferation by further increasing the activity of p70s6k, an important mediator of the mitogenic e ects of TSH and RasV12C40. These results demonstrate that channeling Ras-dependent signals to PI3K confers TSH with the ability to stimulate proliferation in di erentiated cells. Oncogene (2000) 19, 924 ± 932.

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“…Such a diet reduces the endogenous pool of iodine, thereby contributing to the increased uptake and half-life of 131 I in the thyroid remnant. This enhanced uptake might result from increased NIS gene expression, a higher specific activity of 131 I or the increased sensitivity of the remaining thyroid tissue to TSH (19,20). Despite the controversy regarding the appropriate degree and duration of a LID (26,27), the general recommendation is that patients should consume a LID, generally consisting of less than 50 μg iodine/day, for 1 to 4 weeks (18,22).…”

Section: Discussionmentioning

confidence: 99%

“…A LID reduces plasma iodine levels, leading to increased expression of sodium-iodide symporter (NIS), thereby increasing 131 I uptake (19,20). Although this practice has been widely accepted for the management of differentiated thyroid cancer (DTC), its use in evaluating and treating benign thyroid diseases, particularly GD, has not been demonstrated.…”

Section: Introductionmentioning

confidence: 99%

Low iodine diet does not improve the efficacy of radioiodine for the treatment of Graves’ disease

Santarosa

Orlandi

Fiorin

et al. 2015

Arch. Endocrinol. Metab.

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Objective: Consuming a low-iodine diet (LID) is a widely accepted practice before administering radioiodine ( 131 I) to evaluate and to treat thyroid disease. Although this procedure is well established for the management of patients with differentiated thyroid cancer, its use in patients with benign disease is unclear. So, we aimed to evaluate the influence of a LID on the outcome in patients with Graves' disease (GD) treated with 131 I. Subjects and methods: We evaluated 67 patients with GD who were divided into 2 groups: one group (n = 31) consumed a LID for 1-2 weeks, and the second group (n = 36) was instructed to maintain a regular diet (RD). Results: The LID group experienced a 23% decrease in urinary iodine after 1 week on the diet and a significant 42% decrease after 2 weeks on the diet. The majority (53%) of the patients in the LID group had urinary iodine levels that were consistent with deficient iodine intake. However, there was no difference in the rate of hyperthyroidism's cure between the LID and the RD groups 6 months after 131 I therapy. Furthermore, the therapeutic efficacy did not differ in patients with varying degrees of sufficient iodine intake (corresponding urinary iodine levels: < 10 μg/dL is deficient; 10-29.9 μg/dL is sufficient; and > 30 μg/dL is excessive). Conclusion:In the present study, we demonstrated that although a LID decreased urinary iodine levels, those levels corresponding with sufficient or a mild excess in iodine intake did not compromise the therapeutic efficacy of 131 I for the treatment of GD. Arch Endocrinol Metab. 2015;59(6):501-6

show abstract

Moderate doses of iodide in vivo inhibit cell proliferation and the expression of thyroperoxidase and Na+/I− symporter mRNAs in dog thyroid

Cited by 155 publications

References 49 publications

Evidence for Transcriptional and Posttranscriptional Alterations of the Sodium/Iodide Symporter Expression in Hypofunctioning Benign and Malignant Thyroid Tumors

Evidence for Transcriptional and Posttranscriptional Alterations of the Sodium/Iodide Symporter Expression in Hypofunctioning Benign and Malignant Thyroid Tumors

Ras signaling through PI3K confers hormone-independent proliferation that is compatible with differentiation

Low iodine diet does not improve the efficacy of radioiodine for the treatment of Graves’ disease

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