Thyroid cancer is the most common sort of endocrine-related cancer with more prevalent in women and elderly individuals which has quickly widespread expansion in worldwide over the recent decades. Common features of malignant thyroid cells are to have accelerated metabolism and increased glucose uptake to optimize their energy supply which provides a fundamental advantage for growth. In tumor cells the retaining of required energy charge for cell survival is imperative, indeed glucose transporters are enable of promoting of this task. According to this relation it has been reported the upregulation of glucose transporters in various types of cancers. Human studies indicated that poor survival can be occurred following the high levels of GLUT1 expression in tumors. GLUT-1 and GLUT3 are the glucose transporters which seems to be mainly engaged with the oncogenesis of thyroid cancer and their expression in malignant tissues is much more than in the normal one. They are promising targets for the advancement of anticancer strategies. The lack of oncosuppressors have dominant effect on the membrane expression of GLUT1 and glucose uptake. Overexpression of hypoxia inducible factors have been additionally connected with distant metastasis in thyroid cancers which mediates transcriptional regulation of glycolytic genes including GLUT1 and GLUT3. Though the physiological role of the thyroid gland is well illustrated, but the metabolic regulations in thyroid cancer remain evasive. In this study we discuss proliferation pathways of the key regulators and signaling molecules such as PI3K-Akt, HIF-1, MicroRNA, PTEN, AMPK, BRAF, c-Myc, TSH, Iodide and p53 which includes in the regulation of GLUTs in thyroid cancer cells. Incidence of deregulations in cellular energetics and metabolism are the most serious signs of cancers. In conclusion, understanding the mechanisms of glucose transportation in normal and pathologic thyroid tissues is critically important and could provide significant insights in science of diagnosis and treatment of thyroid disease.

Background: Autoimmune thyroid diseases are among the most common autoimmune diseases in the world. They are usually accompanied by the presence of anti-thyroid antibodies as the early predictive marker. Genetic determinants of the susceptibility to develop thyroid antibodies are still poorly understood. This study aimed to investigate the relation between thyroid peroxidase (TPO) gene variants (53 SNPs) and positive TPOAb and also to evaluate the effect of some environmental factors on changes from negative to positive TPOAb (Seroconversion). Methods: Participants from the Tehran Thyroid Study (TTS) in phases 1 and 2 (N=5317, ≥ 20 years) were evaluated for the positive TPOAb and its relationship with 53 SNPs from TPO gene (a cross-sectional approach). At the second stage of the study (a longitudinal approach), negative TPOAb participants (control group, N= 4815) were followed up for about 5.5 (5.54±1.62) years until they have had positive results for TPOAb (“TPOAb seroconversion”). The association between TPO gene polymorphisms and TPOAb seroconversion was evaluated using logistic regression analysis and SKAT package (sequence kernel association test). Results: In cross-sectional analyses, 17 SNPs were associated with TPOAb positivity (521 positive TPOAb participants) after the adjustment for age, sex, body mass index (BMI), smoking, the number of parity and oral contraceptive consumption (P <0.05). In longitudinal analyses, there was an association between TPOAb seroconversion and four SNPs before, and three SNPs after adjustment (P <0.05). Conclusions: TPOAb seroconversion could be affected by some thyroid peroxidase gene variants.

Background: Autoimmune thyroid diseases (AITD) are among the most common autoimmune diseases in the world. They are usually accompanied by the presence of anti-thyroid antibodies as the early predictive marker. Genetic determinants of the susceptibility to develop thyroid antibodies are still poorly understood. This study aimed to investigate the relation between thyroid peroxidase (TPO) gene variants (53 SNPs) and positive TPOAb and also to evaluate the effect of some environmental factors on changes from negative to positive TPOAb (Seroconversion). Methods: Participants from the Tehran Thyroid Study (TTS) in phases 1 and 2 (N=5317, ≥ 20 years) were evaluated for the positive TPOAb and its relationship with 53 SNPs from TPO gene (a cross-sectional approach). At the second stage of the study (a longitudinal approach), negative TPOAb participants (control group, N= 4815) were followed up for about 5.5 (5.54±1.62) years until they have had positive results for TPOAb (“TPOAb seroconversion”). The association between TPO gene polymorphisms and TPOAb seroconversion was evaluated using logistic regression analysis and SKAT (sequence kernel association test) package. Results: In cross-sectional analyses, 17 SNPs were associated with TPOAb positivity (521 positive TPOAb participants) after the adjustment for age, sex, body mass index (BMI), smoking, the number of parity and oral contraceptive consumption (P <0.05). In longitudinal analyses, there was an association between TPOAb seroconversion and four SNPs before, and three SNPs after adjustment (P <0.05). Conclusions: TPOAb seroconversion could be affected by some thyroid peroxidase gene variants.