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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...
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...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
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...
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...

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Related Experiment Video

Updated: May 21, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Inflammation in thyroid oncogenesis.

Federica Liotti, Carla Visciano, Rosa Marina Melillo

    American Journal of Cancer Research
    |June 9, 2012
    PubMed
    Summary

    Inflammation significantly impacts cancer development, influencing everything from cell growth to metastasis. Understanding thyroid cancer and inflammation pathways can reveal new diagnostic and therapeutic targets.

    Area of Science:

    • Oncology
    • Immunology

    Background:

    • Cancer development is strongly linked to inflammation.
    • Inflammation can influence genomic stability, gene expression, cell proliferation, apoptosis, and metastasis.
    • Inflammation also impacts immune surveillance and treatment responses.

    Purpose of the Study:

    • To review the relationship between thyroid cancer and inflammation.
    • To explore the role of immune infiltrates in papillary thyroid carcinoma (PTC).
    • To identify potential therapeutic targets by characterizing cancer-related inflammation (CRI) pathways.

    Main Methods:

    • Review of existing literature on thyroid cancer and inflammation.
    • Analysis of studies linking Hashimoto's thyroiditis (HT) to increased PTC risk.
    • Examination of the role of immune infiltrates in PTC progression.
    Keywords:
    Cancer-related inflammationchemokineinflammatory cellthyroid cancer

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    Main Results:

    • Hashimoto's thyroiditis (HT) is associated with an increased risk of papillary thyroid carcinoma (PTC).
    • Intense immune infiltrates are frequently observed in PTC.
    • Immune infiltrates may play a crucial role in thyroid cancer carcinogenesis and progression.

    Conclusions:

    • Inflammation is a key factor in thyroid cancer development and progression.
    • Characterizing CRI pathways is essential for discovering novel diagnostic and therapeutic strategies for thyroid cancer.