Related Experiment Video

Updated: Oct 2, 2026

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

Expression of TAp73 and DeltaNp73 isoform transcripts in thyroid tumours

A Ferru1, S Denis, J Guilhot

  • 1Laboratoire d'Oncologie Moléculaire EA3805, PBS, Cité Hospitalière de la Milétrie, Avenue du Recteur Pineau, 86021 Poitiers Cedex, France.

European Journal of Surgical Oncology : the Journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
|November 18, 2005
PubMed
Abstract

Insights

p73 gene expression is significantly reduced in thyroid tumors, including adenomas and differentiated carcinomas, compared to normal tissue. These changes disrupt normal correlations with other tumor suppressor genes like p53.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The p73 gene plays a crucial role in tumor suppression.
  • Understanding p73 expression patterns in thyroid malignancies is vital for cancer research.

Purpose of the Study:

  • To investigate the expression status of p73 transcripts (TAp73 and DeltaNp73) in various thyroid tumors.
  • To analyze the correlation between p73 expression and other key genes (p53, p14ARF, p16INK4a) in thyroid cancer.

Main Methods:

  • Quantitative reverse transcription-polymerase chain reaction (RT-PCR) was employed to measure transcript levels.
  • The study analyzed a panel of 60 thyroid malignancies and compared them to adjacent normal thyroid tissue.

Main Results:

  • Significant downregulation of TP73 transcripts was observed in thyroid adenomas and differentiated carcinomas relative to normal thyroid tissue.
  • In normal thyroid tissue, TAp73 and DeltaNp73 expression correlated with p53, p14ARF, and p16INK4a.
  • These correlations were notably absent in papillary (PTC) and follicular (FTC) carcinomas.

Conclusions:

  • Thyroid tumors exhibit significant alterations in TAp73 and DeltaNp73 expression.
  • The study highlights disrupted correlations between p73, p53, p14ARF, and p16INK4a in thyroid cancer, suggesting a role in tumorigenesis.

More Related Videos

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Spontaneous Murine Model of Anaplastic Thyroid Cancer05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

Related Concept Videos

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...
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...
Goiter01:27

Goiter

Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...