Nonradiation Risk Factors for Thyroid Cancer in the US Radiologic Technologists Study

Meinhold, Cari L.; Ron, Elaine; Schonfeld, Sara J.; Alexander, Bruce H.; Freedman, D. Michal; Linet, Martha S.; González, Amy Berrington de

doi:10.1093/aje/kwp354

Cited by 171 publications

(214 citation statements)

References 50 publications

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“…Epidemiological studies have consistently reported that individuals who are either overweight or obese are at an increased risk of thyroid cancer (23)(24)(25)(26)(27). The increasing trend of obesity might be another factor that accounts for some of the observed increasing incidence of thyroid cancer, although the degree of its contribution is unclear.…”

Section: Thyroid Cancer Epidemic 477mentioning

confidence: 99%

The Epidemic of Thyroid Cancer in the United States: The Role of Endocrinologists and Ultrasounds

Udelsman

Zhang

2014

Thyroid

204

128

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Background: The incidence of thyroid cancer has increased at an alarming rate in both men and women in the United States. The etiology of this epidemic is unclear. We tested the hypothesis that a significant component of this epidemic is due to increased detection of occult disease. We examined whether the density of endocrinologists and general surgeons as well as employment of cervical ultrasonography were factors associated with this epidemic. Methods: Thyroid cancer incidence rates by states were obtained from the United States Cancer Statistics 1999-2009 reported by the National Program of Cancer Registries. The densities of endocrinologists and general surgeons and the employment of cervical ultrasonography were calculated on a statewide basis and correlated with the incidence of thyroid cancer. Results: Age-standardized incidence rates of thyroid cancer have increased in every state in the United States. Significant regional variations were noted, with the highest incidence rates in the northeast and the lowest in the south. The incidence rates were significantly correlated with the density of endocrinologists (r = 0.58, p < 0.0001 for males; r = 0.44, p = 0.0031 for females) and the employment of cervical ultrasonography (r = 0.40, p = 0.0091 for males; r = 0.36, p = 0.0197 for females). Both the density of endocrinologists and general surgeons and employment of cervical ultrasonography could explain 57% of the variability in state-level incidence for males and 49% for females. Conclusions: These data offer evidence to suggest that the epidemic of thyroid cancer is due to increased detection of a reservoir of previously occult disease. The increased detection of thyroid cancer results in therapeutic interventions including surgery and radioactive thyroid treatment that may be of limited benefit.

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Section: Thyroid Cancer Epidemic 477mentioning

confidence: 99%

The Epidemic of Thyroid Cancer in the United States: The Role of Endocrinologists and Ultrasounds

Udelsman

Zhang

2014

Thyroid

204

128

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“…A reduced risk of thyroid gland cancer due to cigarette smoking status has been found in several studies [1][2][3]45]. Mack et al performed an international pooled analysis of 14 case-control studies and found 40% reduction in risk of papillary and follicular thyroid cancers among current smokers compared to never smokers.…”

Section: Thyroid Gland Cancermentioning

confidence: 99%

Wpływ palenia papierosów na tarczycę — aktualizacja

Sawicka‐Gutaj¹,

Gutaj²,

Sowiński³

et al. 2014

Endokrynologia Polska

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Many studies have shown that cigarette smoking exerts multiple effects on the thyroid gland. Smoking seems to induce changes in thyroid function tests, like decrease in TSH and increase in thyroid hormones. However, these alterations are usually mild. In addition, tobacco smoking may also play a role in thyroid autoimmunity. Many studies have confirmed a significant influence of smoking on Graves' hyperthyroidism and particularly on Graves' orbitopathy. Here, smoking may increase the risk of disease development, may reduce the effectiveness of treatment, and eventually induce relapse. The role of smoking in Hashimoto's thyroiditis is not as well established as in Graves' disease. Nonetheless, lower prevalence of thyroglobulin antibodies, thyroperoxidase antibiodies and hypothyroidism were found in smokers. These findings contrast with a study that reported increased risk of hypothyroidism in smokers with Hashimoto's thyroiditis. Moreover, cigarette smoking increases the incidence of multinodular goitre, especially in iodine-deficient areas. Some studies have examined cigarette smoking in relation to the risk of thyroid cancer. Interestingly, many of them have shown that smoking may reduce the risk of differentiated thyroid cancer. Furthermore, both active and passive smoking during pregnancy might modify maternal and foetal thyroid function. This review evaluates the current data concerning the influence of cigarette smoking on thyroid gland, including hormonal changes, autoimmunity and selected diseases. These findings, however, in our opinion, should be carefully evaluated and some of them are not totally evidence-based. Further studies are required to explain the effects of smoking upon thyroid pathophysiology. StreszczenieWyniki wielu badań dowodzą, że palenie papierosów wywiera istotny wpływ na gruczoł tarczowy. Wykazano, że nikotynizm modyfikuje parametry hormonalne tarczycy, w szczególności prowadzi do obniżenia stężenia TSH. Sugeruje się, że może również powodować nieznaczny wzrost stężenia wolnych hormonów tarczycy. Ponadto, palenie papierosów odgrywa istotną rolę w procesach autoimmunologicznych związanych z gruczołem tarczowym. Dowiedziono, że nikotynizm wywiera negatywny wpływ na przebieg choroby Gravesa i Basedowa oraz orbitopatii Gravesa i Basedowa. Palenie papierosów nie tylko zwiększa ryzyko rozwoju powyższych schorzeń, ale zmniejsza również skuteczność terapii i zwiększa ryzyko nawrotu. Wpływ palenia papierosów na chorobę Hashimoto nie jest tak jednoznacznie dowiedziony, jak w chorobie Gravesa i Basedowa. Sugeruje się, że palenie papierosów może negatywnie korelować z mianem przeciwciał przeciwko tyreoglobulinie oraz tyreoperoksydazie, zmniejszając w konsekwencji ryzyko rozwoju hipotyreozy. Palenie papierosów zwiększa ryzyko wystąpienia wola guzkowego szczególnie na obszarach niedoboru jodu. Interesująco przedstawiają się również wyniki badań nad wpływem palenia papierosów na ryzyko wystąpienia raka tarczycy. Wiele z nich dowodzi, że u palaczy ryzyko raka zróżnicowanego tarczycy jest mn...

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“…Recent studies showed that the risk of thyroid cancer was significantly increased by excess body weight, either overweight or obesity (Meinhold et al 2010, Aschebrookcancer (PTC), Kim et al (2013a) found that a higher BMI was correlated with a more aggressive PTC phenotype, such as increased tumor size, extrathyroidal invasion, and advanced disease stage, independent of age, sex, and other confounding factors. While compelling epidemiological data support the positive correlation of obesity with increased risk thyroid cancer, the molecular mechanisms by which obesity increase the risk of thyroid cancer progression are poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of STAT3 activity delays obesity-induced thyroid carcinogenesis in a mouse model

Park

Han

Zhao

et al. 2015

Endocrine-Related Cancer

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Compelling epidemiologic studies indicate that obesity is a risk factor for many human cancers, including thyroid cancer. In recent decades, the incidence of thyroid cancer has dramatically increased along with a marked rise in obesity prevalence. We previously demonstrated that a high fat diet (HFD) effectively induced the obese phenotype in a mouse model of thyroid cancer (Thrb PV/PV Pten C/K mice). Moreover, HFD activates the STAT3 signal pathway to promote more aggressive tumor phenotypes. The aim of the present study was to evaluate the effect of S3I-201, a specific inhibitor of STAT3 activity, on HFD-induced aggressive cancer progression in the mouse model of thyroid cancer. WT and Thrb PV/PV Pten C/K mice were treated with HFD together with S3I-201 or vehicle-only as controls. We assessed the effects of S3I-201 on HFD-induced thyroid cancer progression, the leptin-JAK2-STAT3 signaling pathway, and key regulators of epithelial-mesenchymal transition (EMT). S3I-201 effectively inhibited HFD-induced aberrant activation of STAT3 and its downstream targets to markedly inhibit thyroid tumor growth and to prolong survival. Decreased protein levels of cyclins D1 and B1, cyclin dependent kinase 4 (CDK4), CDK6, and phosphorylated retinoblastoma protein led to the inhibition of tumor cell proliferation in S3I-201-treated Thrb PV/PV Pten C/K mice. Reduced occurrence of vascular invasion and blocking of anaplasia and lung metastasis in thyroid tumors of S3I-201-treated Thrb PV/PV Pten C/K mice were mediated via decreased expression of vimentin and matrix metalloproteinases, two key effectors of EMT. The present findings suggest that inhibition of the STAT3 activity would be a novel treatment strategy for obesity-induced thyroid cancer.

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Nonradiation Risk Factors for Thyroid Cancer in the US Radiologic Technologists Study

Cited by 171 publications

References 50 publications

The Epidemic of Thyroid Cancer in the United States: The Role of Endocrinologists and Ultrasounds

The Epidemic of Thyroid Cancer in the United States: The Role of Endocrinologists and Ultrasounds

Wpływ palenia papierosów na tarczycę — aktualizacja

Inhibition of STAT3 activity delays obesity-induced thyroid carcinogenesis in a mouse model

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