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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...
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...
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...
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...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...

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Updated: Jun 8, 2026

Spontaneous Murine Model of Anaplastic Thyroid Cancer
05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

[Familial thyroid carcinomas].

K W Schmid1, S Ting, S-Y Sheu

  • 1Institut für Pathologie und Neuropathologie, Universitätsklinikum Essen, Universität Duisburg-Essen, Hufelandstr. 55, 45122, Essen. kw.schmid@uk-essen.de

Der Pathologe
|September 21, 2010
PubMed
Summary
This summary is machine-generated.

Hereditary thyroid cancers, including papillary, follicular, and medullary types, often develop earlier and are multifocal. Prophylactic thyroidectomy is recommended for familial medullary thyroid carcinoma but not other hereditary thyroid cancers.

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An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
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Establishment and Characterization of Patient-Derived Xenograft Models of Anaplastic Thyroid Carcinoma and Head and Neck Squamous Cell Carcinoma
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Area of Science:

  • Oncology
  • Genetics
  • Endocrinology

Background:

  • Hereditary thyroid carcinomas account for a significant proportion of thyroid cancers, with varying prevalence across subtypes (papillary, follicular, medullary).
  • These hereditary forms often present earlier and exhibit multifocal growth compared to sporadic cases.
  • While neoplastic C cell hyperplasia precedes familial medullary thyroid carcinoma, precursor lesions for other hereditary thyroid cancers remain largely unknown.

Purpose of the Study:

  • To review the characteristics and management of hereditary thyroid carcinomas.
  • To differentiate hereditary thyroid cancer subtypes based on genetic predisposition and clinical presentation.
  • To evaluate the current recommendations for prophylactic thyroidectomy in hereditary thyroid cancer.

Main Methods:

  • Literature review of hereditary thyroid carcinoma.
  • Analysis of clinical presentation and genetic associations.
  • Evaluation of prophylactic surgical intervention guidelines.

Main Results:

  • Familial medullary thyroid carcinoma (MTC) is linked to RET protooncogene mutations and has a distinct clinical course.
  • Neoplastic C cell hyperplasia is a known precursor lesion for familial MTC.
  • Prophylactic thyroidectomy is currently not advised for hereditary papillary thyroid carcinoma (PTC) or follicular thyroid carcinoma (FTC).

Conclusions:

  • Hereditary thyroid carcinomas have distinct clinical features and genetic underpinnings.
  • Early detection and genetic counseling are crucial for managing hereditary thyroid cancer syndromes.
  • Management strategies, including prophylactic thyroidectomy, must be tailored to specific hereditary thyroid cancer subtypes, with current evidence supporting it primarily for familial MTC.