Related Experiment Video

Updated: Jul 10, 2026

Spontaneous Murine Model of Anaplastic Thyroid Cancer
05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

[Gene abnormalities in thyroid cancer]

Hiroyuki Namba1, Shunichi Yamashita

  • 1Department of Molecular Medicine, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Science.

Nihon Rinsho. Japanese Journal of Clinical Medicine
|November 21, 2007
PubMed

Insights

Genetic alterations in oncogenes and tumor suppressors drive thyroid cancer. Understanding these mutations, like BRAF and RAS, aids in developing targeted therapies and genetic diagnostics for thyroid cancer.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Thyroid cancer development involves genetic abnormalities in oncogenes and tumor suppressor genes.
  • Key oncogenes like RAS, RET/PTC, and BRAF mutations are frequently observed in papillary thyroid cancer, activating the MAP kinase pathway.
  • TP53 mutations are associated with the progression of differentiated thyroid cancers to anaplastic thyroid cancer.

Purpose of the Study:

  • To review genetic diagnostic methods for human thyroid cancers.
  • To explore the relationship between the phenotype and genotype of thyroid cancers.
  • To understand the fundamental mechanisms of oncogenesis and inform clinical applications.

Main Methods:

  • Review of existing literature on genetic alterations in thyroid carcinogenesis.
  • Analysis of genotype-phenotype correlations in thyroid cancer.
  • Discussion of current and emerging genetic diagnostic techniques.

Main Results:

  • Specific gene mutations (RAS, RET/PTC, BRAF, TP53) are strongly linked to thyroid cancer subtypes and progression.
  • These genetic alterations provide insights into the molecular pathways driving thyroid tumorigenesis.
  • Genetic profiling is crucial for understanding thyroid cancer heterogeneity.

Conclusions:

  • Genetic alterations are fundamental to thyroid carcinogenesis and cancer progression.
  • Knowledge of these genetic changes is essential for advancing genetic diagnosis and molecular targeted therapies for thyroid cancer.
  • Further research into genotype-phenotype relationships will refine clinical management strategies.

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

Establishment and Characterization of Patient-Derived Xenograft Models of Anaplastic Thyroid Carcinoma and Head and Neck Squamous Cell Carcinoma06:08

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

Published on: June 2, 2023

Related Concept Videos

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...
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...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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...
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...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...