## 4 Selenium in Thyroid Bland
### Selenium and Thyroid Cancer  
Thyroid cancer is the most common endocrine tumor, responsible for more than half a million new cases per year, ranking 9 th place in cancers prevalence worldwide [92; 93]. It remains rare in children and adolescent, the median age of diagnostic is 45 to 50 years old [94], it is diagnosed three times more often in women than in men [95]. Thyroid cancer includes three main types of tumors: medullary thyroid carcinoma, anaplastic thyroid carcinoma and differentiated thyroid carcinoma [96]. Differentiated carcinoma alone accounts for about 90% of thyroid cancers. It is derived from the follicular cells of the thyroid, which are responsible for the production of thyroid hormones [95]. The relationship between Se status and cancer has been debated for a long time. Observational studies and randomized controlled trials have shown conflicting results. In a meta-analysis and meta-regression conducted by [PERSON] et al. [97], the results were in favor of a significant association between Se and cancer. High Se exposure may reduce risk of cancer, especially those of: lung, breast, esophagus, stomach and prostate [97]. On the other hand, [PERSON] et al. [57] and [PERSON] and [PERSON] [98] published a review that reports the results of various trials suggesting dramatic effects of Se on cancer development. The Selenium and Vitamin E Cancer Prevention Trial (SELECT) is one of the largest intervention studies, launched in 2001 and involving more than 32,000 American males. The trial investigated the effect of vitamin E and/or L-selenomethionine supplementations, primarily against the development of prostate cancer and other type of cancers, that is, colorectal cancer, lung cancer and bladder cancer [14]. The results of SELECT showed an increase in prostate cancer risk for patients supplemented with the highest Se levels [13]. However, the results of this study should be interpreted taking into account certain limitations. The possibility that the supplements given to men exceeded the adequate doses to prevent prostate cancer and on the other hand, men selected were characterized by a relatively high baseline selenium status, which suggests that selenium only reduces the risk of prostate cancer in selenium-deficient men and not in the general population [14].This may explain why certain clinical trials have not shown any side effects in cancer patients after intravenous administration of sodium selenite [99]. In a review of [PERSON] et al., different information was collected to explain the divergence concerning the role of Se in the pathophysiology of cancer [100]. First: the effects of Se may be more effective against the progression of cancer, at advanced stages of the disease rather than at early stages. Its role could therefore be more important in preventing cancer progression than in its development. Second: the effects of Se are observed at concentrations lower or higher than the required concentrations to optimize selenoprotein activities especially GPx and SePP. The effects of selenium status on cancer show a U-shape curve. Third: genetic variability could also be of importance. Several single nucleotide polymorphisms (SNP) of certain selenoprotein genes have been linked to different types of cancer. A change in the status of Se has been demonstrated in the pathogenesis of thyroid cancer [101; 102]. Significantly lower levels of Se in thyroid cancer patients were found compared to the control group in several studies [10; 103; 104; 101]. In contrast, other studies do not provide evidence of a significant association between Se deficiency and thyroid cancer [105; 106]. Table 2 presents some studies and results conducted on Se and/or selenoproteins in serum, tissue, fingernail and urine of thyroid cancer subjects. In Table 2, we highlight that most studies indicate low Se levels in the patients with thyroid cancer. Se deficiency in various diseases, including cancer, could be related to a high level of free radicals caused by oxidative stress [95].