Thyroid growth factors and oncogenes

Clark, Orlo H.; Duh, Quan‐Yang

doi:10.1007/978-1-4615-3088-6_4

Cited by 4 publications

(2 citation statements)

References 83 publications

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“…The merits of treatment with thyroid hormone to suppress serum TSH levels and the growth of thyroid nodules is controversial [2]. Some studies have documented regression of benign thyroid nodes [1,[3][4][5][6], whereas others have shown no significant effect [7,8]. Articles document that patients with differentiated thyroid cancer of follicular cell origin (papillary, follicular, Hurthle cell) should be treated with enough thyroid hormone to keep serum TSH levels in the low-normal or suppressed range [1,6,9].…”

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confidence: 99%

Desensitization in Normal and Neoplastic Human Thyroid Cell Lines

et al. 1998

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Abstract. Because some papillary thyroid cancers continue to grow when thyroid-stimulating hormone (TSH) levels are suppressed, we questioned whether desensitization (i.e., a decreased cAMP response to repeat stimulation with TSH) occurs in normal and neoplastic thyroid tissue. If desensitization does occur, is it similar or different in these human thyroid cells? Normal and papillary thyroid cancer cells from the same patient were cultured as we have previously described. Normal and neoplastic thyroid tissues responded to TSH (0.01-10.0 mU/ml) by increasing cAMP production and growth in a dose-dependent manner. In normal cells there was an 11-fold mean increase in cAMP production at 4 hours, and all thyroid cultures responded. In neoplastic cells cAMP production increased from 1.5-fold to 3.0-fold with a mean 2.0-fold increase at 4 hours. In normal thyroid cells the cAMP response to a second TSH stimulus (desensitization) decreased up to 75% (range 25-75%), and desensitization occurred in all normal thyroid cell cultures. In neoplastic thyroid cells, however, the cAMP response to a second TSH stimulus decreased up to 17% (range 0 -17%); and desensitization occurred in only two of the five neoplastic thyroid cell cultures. Thus when normal thyroid and neoplastic cells from the same patients were studied, greater desensitization occurred in the normal cells (75% vs. 17%). These studies document that there is greater desensitization in normal tissue than in neoplastic thyroid tissue, which may account for the increased growth of thyroid neoplasms in the presence of ever-changing low levels of TSH.

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Desensitization in Normal and Neoplastic Human Thyroid Cell Lines

et al. 1998

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“…Although thyroid volume does not increase after adolescence, the thyroid gland has the capacity to hypertrophy and proliferate in response to stimuli [32]. Thyroid growth is regulated by intrinsic systemic and locally produced factors including thyroid stimulating hormone (TSH), epidermal growth factor (EGF), transforming growth factors alpha and beta (TGF α and β), insulin-like growth factors 1 and 2 (IGF-1 and 2), fibroblast growth factor (FGF), hepatocyte growth factor (HGF), platelet-derived growth factor (PDGF), and insulin [33,34].…”

Section: Growth Factors Thyroid Proliferation and Thyroid Cancermentioning

confidence: 99%

Impaired Glucose Metabolism, Anti-Diabetes Medications, and Risk of Thyroid Cancer

Kushchayeva

Kushchayev

Jensen

et al. 2022

Cancers

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The prevalence of obesity is progressively increasing along with the potential high risk for insulin resistance and development of type 2 diabetes mellitus. Obesity is associated with increased risk of many malignancies, and hyperinsulinemia has been proposed to be a link between obesity and cancer development. The incidence of thyroid cancer is also increasing, making this cancer the most common endocrine malignancy. There is some evidence of associations between obesity, insulin resistance and/or diabetes with thyroid proliferative disorders, including thyroid cancer. However, the etiology of such an association has not been fully elucidated. The goal of the present work is to review the current knowledge on crosstalk between thyroid and glucose metabolic pathways and the effects of obesity, insulin resistance, diabetes, and anti-hyperglycemic medications on the risk of thyroid cancer development.

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Actions of epidermal growth factor and its receptor in the thyroid

Nilsson

1995

Trends in Endocrinology & Metabolism

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Thyroid growth factors and oncogenes

Cited by 4 publications

References 83 publications

Desensitization in Normal and Neoplastic Human Thyroid Cell Lines

Desensitization in Normal and Neoplastic Human Thyroid Cell Lines

Impaired Glucose Metabolism, Anti-Diabetes Medications, and Risk of Thyroid Cancer

Actions of epidermal growth factor and its receptor in the thyroid

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