Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Graves Disease II: Pathophysiology

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: Introduction

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 II: Pathophysiology

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...

Hyperthyroidism I: Introduction

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...

Inflammatory Bowel Disease III: Crohn's Disease

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...

Synthesis and Regulation of Thyroid Hormones

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Cannabinoid receptors orchestrate distinct anti-tumour pathways in gastric cancer via and beyond specialized pro-resolving mediators.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2026

Same author

Tumor suppressor function of formyl peptide receptor 1 in gastrointestinal cancers: a focus on the underlying signaling.

Frontiers in cell and developmental biology·2025

Same author

Tailoring the formulation of wholemeal wheat flour: the selection and recombination of milling fractions to control acrylamide and deoxynivalenol contamination.

Food chemistry: X·2025

Same author

SHP2 is a multifunctional target in anaplastic thyroid carcinoma: Cell intrinsic and immune-dependent anti-tumor effects.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2025

Same author

Formyl peptide receptor 1 signaling strength orchestrates the switch from pro-inflammatory to pro-resolving responses: The way to exert its anti-angiogenic and tumor suppressor functions.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2025

Same author

Improving functional capacity in haemophilia through adapted physical activity: a pilot study protocol.

BMJ open sport & exercise medicine·2025

Search research articles

Related Experiment Video

Updated: Jun 19, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Thyroid cancer and inflammation.

Valentina Guarino¹, Maria Domenica Castellone, Elvira Avilla

¹Dipartimento di Biologia e Patologia Cellulare e Molecolare/Istituto di Endocrinologia ed Oncologia Sperimentale del CNR G. Salvatore, Italy.

Molecular and Cellular Endocrinology

|October 20, 2009

Summary

Inflammation plays a key role in thyroid cancer development, particularly papillary thyroid carcinomas (PTCs). Targeting inflammatory molecules offers a promising therapeutic strategy for thyroid cancer.

Related Experiment Videos

Last Updated: Jun 19, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Area of Science:

Oncology
Immunology
Endocrinology

Background:

Inflammation is linked to various cancers, including thyroid cancer.
Autoimmune thyroid diseases, like Hashimoto's thyroiditis, are associated with increased thyroid cancer incidence.
Papillary thyroid carcinomas (PTCs) frequently exhibit inflammatory cell infiltrates.

Purpose of the Study:

To review the multifaceted relationship between thyroid cancer and inflammation.
To explore the role of inflammatory cells and molecules in thyroid cancer progression.
To discuss the potential of targeting inflammation for thyroid cancer treatment.

Main Methods:

Review of existing literature on thyroid cancer and inflammation.
Analysis of the protumorigenic functions of inflammatory cells in thyroid cancer.
Examination of the pro-inflammatory signaling pathways activated by thyroid cancer oncoproteins.

Main Results:

Inflammatory cells, including lymphocytes and macrophages, are present in thyroid tumors and may promote tumor growth.
Thyroid cancer oncoproteins (RET/PTC, RAS, BRAF) induce inflammatory responses in thyroid cells.
A strong association exists between autoimmune thyroiditis and increased PTC incidence.

Conclusions:

Inflammation is an integral component of thyroid cancer pathogenesis.
Inflammatory molecules represent potential therapeutic targets for thyroid cancer.
Targeting inflammation may offer novel treatment strategies for patients with thyroid cancer.