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Related Concept Videos

Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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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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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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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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Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

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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...
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Loss of Tumor Suppressor Gene Functions01:12

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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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The Retinoblastoma Gene01:20

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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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Updated: Sep 13, 2025

Establishment and Characterization of Patient-Derived Xenograft Models of Anaplastic Thyroid Carcinoma and Head and Neck Squamous Cell Carcinoma
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Familial Thyroid Cancers Syndromes.

Reza Pishdad1, Giuseppe Barbesino2, Lori J Wirth3

  • 1Division of Endocrinology, Diabetes & Metabolism, Endocrine Associates, Massachusetts General Hospital, Harvard Medical School, WACC 730A, 55 Fruit Street, Boston, MA 02411, USA.

Endocrinology and Metabolism Clinics of North America
|July 27, 2025
PubMed
Summary
This summary is machine-generated.

This review details advances in hereditary thyroid cancer, focusing on genetic mutations like RET and personalized treatments. It emphasizes genetic testing and risk-based management for better patient outcomes.

Keywords:
DICER1 syndromeFamilial thyroid cancerMENMedullary thyroid cancerPTEN hamartoma (Cowden syndrome)PheochromocytomaPrimary hyperparathyroidismRET

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Area of Science:

  • Endocrinology
  • Oncology
  • Genetics

Background:

  • Hereditary thyroid cancer syndromes require updated understanding.
  • Familial medullary and nonmedullary thyroid cancers have distinct genetic bases.
  • Advances in molecular genetics offer new insights.

Purpose of the Study:

  • To review critical advances in hereditary thyroid cancer syndromes.
  • To explore genetic underpinnings and genotype-phenotype correlations.
  • To discuss personalized management strategies for these conditions.

Main Methods:

  • Comprehensive literature review.
  • Synthesis of current evidence on genetic mutations (e.g., RET).
  • Analysis of genotype-phenotype correlations and treatment outcomes.

Main Results:

  • Key genetic drivers, including RET mutations, identified.
  • Genotype-phenotype correlations elucidated for familial thyroid cancers.
  • Personalized management strategies, including prophylactic surgery and systemic therapies, are highlighted.

Conclusions:

  • Genetic testing is crucial for diagnosing hereditary thyroid cancer.
  • Targeted surveillance and risk-based treatment are essential.
  • Optimizing outcomes requires integrating genetic insights into clinical practice.