Jove
Visualize
Contact Us

Related Experiment Videos

Multiple myeloma/hypercalcemia.

Babatunde O Oyajobi1

  • 1University of Texas Health Science Center at San Antonio, Department of Cellular and Structural Biology (MSC 7762), San Antonio, Texas 78229-3900, USA. oyajobi@uthscsa.edu

Arthritis Research & Therapy
|July 20, 2007
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Oxidatively modified low-density lipoproteins are potential mediators of proteasome inhibitor resistance in multiple myeloma.

International journal of cancer·2021
Same author

A niche-dependent myeloid transcriptome signature defines dormant myeloma cells.

Blood·2019
Same author

Synthesis of a Bone-Targeted Bortezomib with In Vivo Anti-Myeloma Effects in Mice.

Pharmaceutics·2018
Same author

Inhibiting the osteocyte-specific protein sclerostin increases bone mass and fracture resistance in multiple myeloma.

Blood·2017
Same author

Combined treatment with a transforming growth factor beta inhibitor (1D11) and bortezomib improves bone architecture in a mouse model of myeloma-induced bone disease.

Bone·2016
Same author

A dominant-negative F-box deleted mutant of E3 ubiquitin ligase, β-TrCP1/FWD1, markedly reduces myeloma cell growth and survival in mice.

Oncotarget·2015
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Multiple myeloma causes bone destruction and hypercalcemia through osteoclast activity. Targeting receptor activator of nuclear factor-kappaB ligand (RANKL) offers a promising treatment strategy for myeloma bone disease.

Area of Science:

  • Oncology
  • Bone Biology
  • Metabolic Complications

Background:

  • Multiple myeloma is characterized by excessive osteoclast-mediated bone destruction.
  • Hypercalcemia is a frequent and potentially life-threatening metabolic complication of myeloma, driven by osteolysis.
  • Recent advances have identified key mediators of myeloma bone disease, including RANKL, MIP-1alpha, and Dickkopf 1.

Purpose of the Study:

  • To review the roles of key mediators in myeloma-induced osteolysis.
  • To discuss the potential of targeting RANKL as a therapeutic strategy for myeloma bone disease and associated hypercalcemia.

Main Methods:

  • Literature review of recent developments in myeloma bone disease pathogenesis.
  • Analysis of the roles of receptor activator of nuclear factor-kappaB ligand (RANKL), macrophage inflammatory protein-1alpha, and Dickkopf 1.

Related Experiment Videos

  • Discussion of therapeutic targeting of RANKL.

    • Main Results:

    • Receptor activator of nuclear factor-kappaB ligand (RANKL) is identified as a final common mediator of osteoclastic bone resorption in myeloma.
    • Dickkopf 1 is shown to be over-expressed and stimulates osteoclast formation and activity.
    • RANKL plays a crucial role in mediating osteolysis and hypercalcemia in multiple myeloma.

    Conclusions:

    • Understanding the molecular mediators of myeloma bone disease has advanced significantly.
    • Targeting RANKL presents a potential novel therapeutic approach for managing myeloma bone disease and hypercalcemia.