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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 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...
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...
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: May 25, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

RET TKI: potential role in thyroid cancers.

Alessandro Antonelli1, Poupak Fallahi, Silvia Martina Ferrari

  • 1Department of Internal Medicine, University of Pisa, School of Medicine, Via Roma 67, 56100 Pisa, Italy. alessandro.antonelli@med.unipi.it

Current Oncology Reports
|January 31, 2012
PubMed
Summary

Targeted therapies show promise in stabilizing advanced thyroid cancer by inhibiting key molecular pathways like RET and VEGFR. Further research is needed to optimize these treatments for extended survival and improved quality of life.

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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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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
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Published on: August 23, 2019

Spontaneous Murine Model of Anaplastic Thyroid Cancer
05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Thyroid cancer incidence is rising, often presenting as advanced disease with loss of differentiation and metastasis.
  • Understanding molecular pathways like RET/PTC and VEGFR has enabled targeted drug development.
  • Existing targeted therapies aim to inhibit oncogenic kinases involved in cancer growth and proliferation.

Purpose of the Study:

  • To evaluate the role of targeted therapies in managing advanced thyroid cancer.
  • To assess the efficacy of drugs inhibiting RET and VEGFR in disease stabilization.
  • To explore the potential of targeted therapies in improving patient survival and quality of life.

Main Methods:

  • Clinical trials were conducted to assess targeted therapies.
  • Drugs evaluated included those inhibiting RET (sorafenib, imatinib, vandetanib).
  • The study focused on disease course stabilization as a primary outcome.

Main Results:

  • Targeted therapies inhibiting RET demonstrated an ability to stabilize the course of thyroid cancer.
  • These treatments offer a potential strategy for managing advanced disease.
  • Initial findings suggest a role in disease management, but further investigation is required.

Conclusions:

  • Targeted therapies targeting oncogenic kinases show potential in stabilizing advanced thyroid cancer.
  • The introduction of these therapies aims to prolong life and maintain quality of life.
  • Additional studies are necessary to fully realize the benefits and long-term outcomes of these treatments.