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Related Concept Videos

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
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...
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.
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Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
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Related Experiment Video

Updated: Jun 22, 2026

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform
06:21

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform

Published on: May 10, 2024

Vitamin D receptor polymorphisms in differentiated thyroid carcinoma.

Marissa Penna-Martinez1, Elizabeth Ramos-Lopez, Julienne Stern

  • 1Department of Internal Medicine I, Division of Endocrinology, Diabetes, and Metabolism, University Hospital Frankfurt, Frankfurt am Main, Germany.

Thyroid : Official Journal of the American Thyroid Association
|June 9, 2009
PubMed
Summary

Vitamin D receptor (VDR) gene polymorphisms are linked to differentiated thyroid cancer risk. Lower 1,25(OH)(2)D(3) levels were observed in patients, suggesting a role in thyroid carcinoma development.

Related Experiment Videos

Last Updated: Jun 22, 2026

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform
06:21

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform

Published on: May 10, 2024

Area of Science:

  • Endocrinology
  • Genetics
  • Oncology

Background:

  • Vitamin D receptor (VDR) expression is upregulated in various tumors, potentially indicating an endogenous response to tumor progression.
  • The role of VDR gene polymorphisms in thyroid carcinoma and their association with vitamin D metabolite levels require investigation.

Purpose of the Study:

  • To investigate the association between VDR gene polymorphisms and thyroid carcinoma.
  • To analyze the influence of VDR gene polymorphisms on plasma levels of 25(OH)D(3) and 1,25(OH)(2)D(3) in thyroid carcinoma patients.

Main Methods:

  • Genotyping of four VDR polymorphisms (ApaI, TaqI, BsmI, FokI) in 172 thyroid carcinoma patients (132 papillary, 40 follicular) and 321 healthy controls.
  • Correlation analysis of VDR genotypes and haplotypes with plasma levels of 25(OH)D(3) and 1,25(OH)(2)D(3).

Main Results:

  • Specific VDR genotypes (AA of ApaI, FF of FokI) and haplotypes (Ta, af, Tab, Tabf) were significantly associated with follicular thyroid cancer (FTC) risk.
  • Lower circulating 1,25(OH)(2)D(3) levels were observed in both papillary and follicular thyroid cancer patients compared to controls.
  • No significant differences in genotype or haplotype frequencies were found between papillary thyroid cancer patients and controls. VDR polymorphisms were not associated with plasma vitamin D metabolite levels.

Conclusions:

  • Lower circulating 1,25(OH)(2)D(3) levels are associated with differentiated thyroid carcinoma.
  • Certain VDR polymorphisms and haplotypes may confer protection against or increase the risk of follicular thyroid carcinoma.
  • Further studies with larger patient cohorts are needed to confirm these findings.