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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...
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...
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...
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...

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Related Experiment Video

Updated: May 16, 2026

Four-color Fluorescence Immunohistochemistry of T-cell Subpopulations in Archival Formalin-fixed, Paraffin-embedded Human Oropharyngeal Squamous Cell Carcinoma Samples
07:43

Four-color Fluorescence Immunohistochemistry of T-cell Subpopulations in Archival Formalin-fixed, Paraffin-embedded Human Oropharyngeal Squamous Cell Carcinoma Samples

Published on: July 29, 2017

PDCD4 expression in thyroid neoplasia.

Gianmaria Pennelli1, Matteo Fassan, Caterina Mian

  • 1Department of Medicine (DIMED), Surgical Pathology and Cytopathology Unit, University of Padua, Padua, Italy.

Virchows Archiv : an International Journal of Pathology
|December 6, 2012
PubMed
Summary
This summary is machine-generated.

Programmed cell death 4 (PDCD4) is downregulated in thyroid tumors, while miR-21 is upregulated. This suggests PDCD4 plays a role in thyroid cancer development and progression.

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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: May 16, 2026

Four-color Fluorescence Immunohistochemistry of T-cell Subpopulations in Archival Formalin-fixed, Paraffin-embedded Human Oropharyngeal Squamous Cell Carcinoma Samples
07:43

Four-color Fluorescence Immunohistochemistry of T-cell Subpopulations in Archival Formalin-fixed, Paraffin-embedded Human Oropharyngeal Squamous Cell Carcinoma Samples

Published on: July 29, 2017

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
  • Genetics

Background:

  • Thyroid cancer development involves complex morphogenesis and molecular pathways.
  • Programmed cell death 4 (PDCD4) is a known tumor suppressor gene.
  • PDCD4 expression is regulated by microRNA-21 (miR-21).

Purpose of the Study:

  • To investigate the expression of PDCD4 in human follicular-cell-derived thyroid neoplastic lesions.
  • To explore the relationship between PDCD4 expression and miR-21 levels in thyroid tumors.
  • To assess the association of PDCD4 downregulation with clinicopathological features of thyroid cancer.

Main Methods:

  • Immunohistochemistry was used to assess PDCD4 protein expression in 100 thyroid tumors and 25 controls.
  • Quantitative real-time PCR (qRT-PCR) and in situ hybridization were employed to measure miR-21 expression in 75 cases.
  • Thyroid tumors included follicular adenomas, follicular carcinomas, papillary carcinomas, and poorly-differentiated/anaplastic cancers.

Main Results:

  • Nonneoplastic thyroid cells exhibited strong nuclear PDCD4 expression.
  • PDCD4 protein expression was significantly downregulated in all types of thyroid neoplastic lesions compared to controls.
  • PDCD4 downregulation correlated significantly with less differentiated cancer phenotypes and advanced tumor stages.
  • miR-21 expression was consistently upregulated in neoplastic thyroid tissues relative to nonneoplastic tissues.

Conclusions:

  • PDCD4 exhibits a significant role in thyroid carcinogenesis.
  • Downregulation of PDCD4 and upregulation of miR-21 are associated with thyroid neoplasia.
  • Further research is warranted to evaluate the diagnostic and prognostic potential of PDCD4 in thyroid cancer.