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Mouse Models of Cancer Study02:43

Mouse Models of Cancer Study

Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
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In-vitro Mutagenesis

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Genetic Screens

Genetic screens are tools used to identify genes and mutations responsible for phenotypes of interest. Genetic screens help identify individuals or a group of people at risk of developing  genetic diseases and help them with early intervention, targeted therapy, and reproductive options.
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Dosage Compensation02:50

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Pharmacogenomics: Identification of New Drug Targets

Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...

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Pharmacologic Induction of Epidermal Melanin and Protection Against Sunburn in a Humanized Mouse Model
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Vitamin D action : Lessons learned from genetic mouse models.

David Goltzman1

  • 1Department of Medicine, McGill University Health Centre and McGill University, Montreal QC, Canada. david.goltzman@mcgill.ca

Annals of the New York Academy of Sciences
|April 16, 2010
PubMed
Summary
This summary is machine-generated.

Mouse models reveal how vitamin D regulates calcium and bone health. Vitamin D influences parathyroid function and bone formation, and also impacts cardiovascular health.

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Area of Science:

  • Endocrinology
  • Mineral Metabolism
  • Skeletal Physiology

Background:

  • The roles of 1,25-dihydroxyvitamin D [1,25(OH)(2)D] in mineral and skeletal physiology are extensively studied.
  • Mouse models with targeted gene deletions for 25-hydroxyvitamin D 1alpha-hydroxylase [1alpha(OH)ase] and the vitamin D receptor (VDR) offer insights into vitamin D's functions.

Purpose of the Study:

  • To investigate the regulatory roles of the 1,25(OH)(2)D/VDR system in mineral homeostasis, skeletal physiology, and extraskeletal actions.
  • To utilize genetically modified mouse models to dissect the specific contributions of 1alpha(OH)ase and VDR to various physiological processes.

Main Methods:

  • Generation and analysis of mouse models with targeted deletion of 1alpha(OH)ase and VDR genes.
  • Dietary manipulation to assess phenotypic changes and physiological responses.
  • Examination of parathyroid gland function, bone mineralization, calcium absorption, and osteoblastogenesis.
  • Evaluation of extraskeletal effects, including blood pressure, renin-angiotensin system activation, and cardiac function.

Main Results:

  • Parathyroid gland function is regulated by calcium and 1,25(OH)(2)D.
  • Bone mineralization is primarily influenced by ambient calcium and phosphorus levels, not directly by the 1,25(OH)(2)D/VDR system.
  • The 1,25(OH)(2)D/VDR system modulates calcium absorption, osteoblastogenesis, and bone formation.
  • 1alpha(OH)ase(-/-) mice exhibit increased blood pressure, renin-angiotensin system activation, myocardial hypertrophy, and cardiac dysfunction, which are preventable with 1,25(OH)(2)D(3) administration.

Conclusions:

  • The 1,25(OH)(2)D/VDR system plays a crucial role in calcium absorption and bone formation.
  • Vitamin D deficiency, modeled by genetic alterations, leads to significant extraskeletal pathologies, particularly cardiovascular dysfunction.
  • These mouse models are valuable tools for studying vitamin D deficiency pathophysiology and developing therapeutic interventions.