Transgenic models for proliferative and hyperfunctional thyroid diseases

Ledent, Catherine; Coppée, Frédérique; Dumont, Jacques Emile; Vassart, Gilbert; Parmentier, Marc

doi:10.1055/s-0029-1211683

Cited by 14 publications

(3 citation statements)

References 14 publications

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“…46 Mice were profoundly hypothyroid and required T4 supplementation in order to survive to an age where they could reproduce. By the age of 4-6 weeks and as early as 9 days of age, most mice developed solid, anaplastic carcinomas with hemorrhage, necrosis, and few, if any, residual thyroid follicles.…”

Section: Mouse Models Of Anaplastic Thyroid Carcinomamentioning

confidence: 99%

“…Tg-SV40 LT Anaplastic thyroid carcinomas developed in transgenic mice expressing thyroid-targeted Simian virus 40 large T antigen on a C57B/6J 3 DBA/2J background, which is the only published transgenic mouse model of this type of thyroid cancer. 46 Mice were profoundly hypothyroid and required T4 supplementation in order to survive to an age where they could reproduce. By the age of 4-6 weeks and as early as 9 days of age, most mice developed solid, anaplastic carcinomas with hemorrhage, necrosis, and few, if any, residual thyroid follicles.…”

Section: Mouse Models Of Anaplastic Thyroid Carcinomamentioning

confidence: 99%

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Genetic Alterations in Thyroid Cancer: The Role of Mouse Models

2007

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Abstract. Thyroid carcinomas are the most common endocrine neoplasms in humans, with a globally increasing incidence. Thyroid follicular cells and neuroendocrine (parafollicular) C cells are each susceptible to neoplastic transformation, resulting in thyroid cancers of differing phenotypes with unique associated genetic mutations and clinical outcomes. Over the past 15 years, several sophisticated genetically engineered mouse models of thyroid cancer have been created to further our understanding of the genetic events leading to thyroid carcinogenesis in vivo. The most significant mouse models of papillary, follicular, anaplastic, and medullary thyroid carcinoma are highlighted, with particular emphasis on the relationship between the relevant oncogenes in these models and genetic events in the naturally occurring human disease. Limitations of each model are presented, and the need for additional models to better recapitulate certain aspects of the human disease is discussed.

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Section: Mouse Models Of Anaplastic Thyroid Carcinomamentioning

confidence: 99%

Section: Mouse Models Of Anaplastic Thyroid Carcinomamentioning

confidence: 99%

Genetic Alterations in Thyroid Cancer: The Role of Mouse Models

2007

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“…Indeed, similar effects result from constitutive activation of G s in AAs (51), in the McCune-Albright syndrome, and in mice thyroid expressing the G s -specific adenosine A2 receptor (52). Moreover, the growth effects of TSH on human thyroid cells in culture are fully reproduced by forskolin, a specific activator of adenylate cyclase (53).…”

Section: Comparative Biology Of Fnah Scnah and Aamentioning

confidence: 89%

Genetic hyperthyroidism: hyperthyroidism due to activating TSHR mutations

Hebrant¹,

Staveren²,

Maenhaut³

et al. 2011

European Journal of Endocrinology

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Three syndromes affecting the thyroid gland are described in the literature separately: familial nonautoimmune hyperthyroidism, sporadic congenital nonautoimmune hyperthyroidism, and autonomous adenomas. Recent studies have shown that these three syndromes are caused by similar activating mutations of the TSH receptor gene (TSHR), and that the consequences of these mutations on the physiology and gene expression of the thyroid are qualitatively, but not quantitatively, similar. The three syndromes and two suggested unrecognized variants are in fact facets of the same disease, genetic hyperthyroidism due to TSHR mutations, the expression of which depends on the intensity of activation, its timing, and on the number of affected cells.

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Growth Regulation of Thyroid and Thyroid Tumors in Humans

et al. 2000

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In a study of growth regulation of the human thyroid gland and thyroid tumors we investigated the impact of iodine and that of the thyroid-specific growth-stimulating hormone TSH. Further studies included locally active growth factors such as the epidermal growth factor, insulin-like growth factor, and tissue transforming growth factors alpha and beta. In addition to studies of growth regulation by the various growth factors in mostly normal thyrocytes, the impact of tumor-specific mutations in oncogenes and tumor-suppressor genes was investigated. The results demonstrated distinct changes in tissue specificity and sensitivity to external stimuli. This rather complex view on thyrocyte growth regulation may be confusing, but it describes the biologic reality more precisely. Increased knowledge of the regulatory processes may lead to the development of new tumor- and patient-specific therapeutic approaches, especially for preventing benign goiter recurrence and for treating follicular and papillary thyroid cancers.

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Transgenic models for proliferative and hyperfunctional thyroid diseases

Cited by 14 publications

References 14 publications

Genetic Alterations in Thyroid Cancer: The Role of Mouse Models

Genetic Alterations in Thyroid Cancer: The Role of Mouse Models

Genetic hyperthyroidism: hyperthyroidism due to activating TSHR mutations

Growth Regulation of Thyroid and Thyroid Tumors in Humans

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