Jove
Visualize
Contact Us
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

Related Experiment Videos

BCR gene expression blocks Bcr-Abl induced pathogenicity in a mouse model.

F Lin1, G Monaco, T Sun

  • 1Department of Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, TX 77030, USA.

Oncogene
|April 21, 2001
PubMed
Summary

Increased BCR gene expression significantly inhibits the oncogenic effects of Bcr-Abl in chronic myelogenous leukemia (CML) models. This finding suggests BCR gene therapy could be a potential treatment for CML.

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

Towards real-time pork breed and boar taint classification using rapid evaporative ionisation mass spectrometry.

NPJ science of food·2026
Same author

The Response and Recovery of Carbon and Water Fluxes in Australian Ecosystems Exposed to Severe Drought.

Global change biology·2025
Same author

Erratum: Lymphopenia-induced lymphoproliferation drives activation of naive T cells and expansion of regulatory populations.

iScience·2025
Same author

BDA Library and Museum.

British dental journal·2024
Same author

Editorial: Muscles at the expense of liver injury. Is it worth it?

Alimentary pharmacology & therapeutics·2024
Same author

Effect of different durations of using a standing frame on the rate of hip migration in children with moderate to severe cerebral palsy: a feasibility study for a randomised controlled trial.

Physiotherapy·2022

Area of Science:

  • Molecular Biology
  • Oncology
  • Hematology

Background:

  • The Bcr-Abl oncoprotein, encoded by the Philadelphia chromosome, is the primary driver of chronic myelogenous leukemia (CML).
  • Previous studies indicated that Bcr expression can interfere with the oncogenic functions of Bcr-Abl.
  • Understanding the physiological impact of Bcr expression on Bcr-Abl oncogenesis is crucial for CML therapeutic development.

Purpose of the Study:

  • To investigate the effects of inducible BCR gene expression on the leukemogenic potential of Bcr-Abl in a murine model.
  • To assess the impact of Bcr protein activity on Bcr-Abl-induced CML pathogenesis.
  • To evaluate the therapeutic potential of modulating BCR expression in CML.

Main Methods:

  • Utilized a K562 cell clone (K6 K562) with a tetracycline (Tet)-repressible CMV promoter controlling exogenous BCR gene expression.

Related Experiment Videos

  • Injected K6 K562 cells into NOD/scid mice under conditions of suppressed or induced BCR expression.
  • Monitored mouse survival, disease progression, and characterized hematopoiesis and neoplastic lesions.

    • Main Results:

    • Suppressed BCR expression led to rapid death (within 35 days) in 100% of mice, characterized by wasting syndrome, bone marrow aplasia, and neoplasia.
    • Induced BCR expression at the time of injection resulted in 80% survival with no detectable lesions in hematopoietic organs (P<0.0001).
    • Reversing BCR suppression after disease initiation significantly improved survival, with 30% of mice surviving beyond 50 days.

    Conclusions:

    • BCR gene expression strongly inhibits the oncogenic effects of Bcr-Abl in a physiological mouse model of CML.
    • Inducible BCR expression can prevent or reverse CML-like disease progression in mice.
    • These findings highlight the potential of BCR gene therapy as a novel strategy for treating chronic myelogenous leukemia.