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Related Concept Videos

Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
The Thyroid Gland01:23

The Thyroid Gland

The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...

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Related Experiment Video

Updated: Jul 16, 2026

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

The IGF-I axis in thyroid carcinoma.

A Ciampolillo1, C De Tullio, E Perlino

  • 1Section of Internal Medicine, Endocrinology and Metabolic Disease, Department of Emergency and Organ Transplantation, University of Bari, Policlinico, Bari, Italy. a.ciampolillo@endo.uniba.it

Current Pharmaceutical Design
|March 10, 2007
PubMed
Summary

Insulin-like growth factor I (IGF-I) and its receptor (IGF-I R) are linked to thyroid cancer growth. Higher levels correlated with larger tumor size and spread, but not patient factors or metastasis.

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Spontaneous Murine Model of Anaplastic Thyroid Cancer
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Spontaneous Murine Model of Anaplastic Thyroid Cancer

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Last Updated: Jul 16, 2026

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
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An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

Spontaneous Murine Model of Anaplastic Thyroid Cancer
05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Insulin-like growth factor I (IGF-I) and its receptor (IGF-I R) play roles in cell growth and survival.
  • These factors are implicated in the development of various human cancers.
  • Previous studies suggest involvement in thyroid carcinomas.

Purpose of the Study:

  • To investigate the expression and correlation of IGF-I and IGF-I R in human thyroid carcinomas.
  • To determine if IGF-I and IGF-I R levels relate to tumor characteristics and clinical outcomes.

Main Methods:

  • Immunohistochemical analysis of IGF-I and IGF-I R expression in thyroid carcinoma tissues.
  • Correlation analysis between IGF-I/IGF-I R immunoreactivity and clinicopathological parameters such as tumor diameter, extension, patient age, gender, tumor stage, and lymph node metastasis.
  • Analysis of IGF-I messenger RNA (mRNA) levels.

Main Results:

  • Increased immunoreactivity for both IGF-I and IGF-I R was observed in human thyroid carcinomas.
  • Upregulation of IGF-I mRNA was also noted.
  • IGF-I and IGF-I R immunoreactivity positively correlated with tumor diameter and intrathyroidal extension.
  • No significant correlation was found with patient's gender, age, tumor stage, or lymph node metastases.
  • IGF-I effects are complex, depending on IGF-I R and binding proteins.

Conclusions:

  • IGF-I and IGF-I R are upregulated in thyroid carcinomas and associated with tumor progression.
  • These findings highlight the potential role of the IGF-I pathway in thyroid cancer pathogenesis.
  • Further research into IGF-I signaling may offer therapeutic targets for thyroid cancer.