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Related Concept Videos

Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
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...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

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Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...
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.
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Related Experiment Video

Updated: Jun 2, 2026

Spontaneous Murine Model of Anaplastic Thyroid Cancer
05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

Multiple endocrine neoplasia type 2: an overview.

Jessica Moline1, Charis Eng

  • 1Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.

Genetics in Medicine : Official Journal of the American College of Medical Genetics
|May 10, 2011
PubMed
Summary

Multiple endocrine neoplasia type 2 (MEN2) involves RET gene mutations, leading to high risks of medullary thyroid carcinoma and other tumors. Early diagnosis and management are crucial for preventing life-threatening conditions.

Related Experiment Videos

Last Updated: Jun 2, 2026

Spontaneous Murine Model of Anaplastic Thyroid Cancer
05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

Area of Science:

  • Endocrinology
  • Genetics
  • Oncology

Background:

  • Multiple endocrine neoplasia type 2 (MEN2) comprises three subtypes linked to germline RET proto-oncogene mutations.
  • MEN2 subtypes carry a significant risk of medullary thyroid carcinoma (MTC), pheochromocytomas, and primary hyperparathyroidism.

Purpose of the Study:

  • To provide a comprehensive overview of MEN2, including clinical presentations, diagnostic strategies, and management guidelines.
  • To emphasize the critical role of early clinical recognition and genetic testing for RET mutations in managing MEN2-associated neoplasms.

Main Methods:

  • Review of clinical descriptions of MEN2 subtypes.
  • Summary of diagnostic and testing strategies for germline RET mutations.
  • Outline of management, surveillance, and differential diagnosis for MEN2.

Main Results:

  • MEN2 subtypes share a high lifetime risk for MTC (70-100%) and pheochromocytomas (50%).
  • MEN2A has a 20-30% risk of primary hyperparathyroidism; MEN2B presents with distinct physical features and gastrointestinal issues.
  • Germline RET mutations are the underlying cause across all MEN2 subtypes.

Conclusions:

  • Clinical recognition of MEN2 subtypes and timely RET mutation testing are essential for effective prevention and management.
  • Proactive surveillance and management strategies are critical for individuals and families at risk of MEN2-related neoplasms.