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

p53: regular or super?

Martine F Roussel1

  • 1Department of Genetics and Tumor Cell Biology, Danny Thomas Research Tower, 5006C, St Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA. martine.roussel@stjude.org

Cancer Cell
|December 25, 2002
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

Nuclear export as a therapeutic vulnerability in ZFTA-RELA ependymoma.

Neuro-oncology·2026
Same author

A Conserved Enhancer Locus in Extrachromosomal DNA and Homogeneously Staining Regions Activates MYC Transcription in Group 3 Medulloblastoma.

Cancer research·2026
Same author

Patient-derived pediatric brain tumor orthotopic xenografts and tumor organoids faithfully recapitulate primary tumors.

Science advances·2026
Same author

PHIP suppresses NuRD to enable the growth of SWI/SNF-mutant cancers.

Nature communications·2026
Same author

Targeting the p53 pathway to treat atypical teratoid rhabdoid tumors.

Neuro-oncology pediatrics·2026
Same author

Hidden-driver inference reveals synergistic brain-penetrant therapies for medulloblastoma.

bioRxiv : the preprint server for biology·2025
Same journal

Circadian Homeostasis of Liver Metabolism Suppresses Hepatocarcinogenesis.

Cancer cell·2026
Same journal

Vascular RhoJ Is an Effective and Selective Target for Tumor Angiogenesis and Vascular Disruption.

Cancer cell·2026
Same journal

Intratumoral B cells under stress.

Cancer cell·2026
Same journal

Chronic stress unleashes an intratumor phage-fibroblast-B cell circuit to promote tumor growth.

Cancer cell·2026
Same journal

Molecular phenotypes and spatial archetypes: A new framework for cancer-associated fibroblasts.

Cancer cell·2026
Same journal

OpenIO: An open framework for AI-native immunotherapy.

Cancer cell·2026
See all related articles

Super p53 mice with increased p53 expression are protected from tumor development. This protection occurs without causing premature aging side effects in the mice.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The p53 tumor suppressor protein plays a critical role in preventing cancer.
  • Modulating p53 levels is a key strategy in cancer research.
  • Previous attempts to enhance p53 function have sometimes led to adverse effects like premature aging.

Purpose of the Study:

  • To investigate the effects of increased p53 expression under its endogenous promoter in "super p53" mice.
  • To determine if elevated p53 levels can prevent tumorigenesis.
  • To assess whether this approach avoids the aging-related side effects seen with other p53 modulation methods.

Main Methods:

  • Generation of "super p53" transgenic mice with elevated p53 expression.
  • Monitoring tumor development and incidence in these mice.

Related Experiment Videos

  • Evaluation of aging phenotypes and lifespan.
  • Main Results:

    • "Super p53" mice exhibited significant protection against spontaneous and induced tumorigenesis.
    • Increased p53 expression did not result in premature aging phenotypes.
    • Lifespan analysis showed no detrimental effects associated with elevated p53.

    Conclusions:

    • Elevating p53 expression via its endogenous promoter is a viable strategy for cancer prevention.
    • This method effectively suppresses tumor formation without inducing deleterious aging effects.
    • The "super p53" mouse model offers a promising platform for studying p53-mediated tumor suppression and aging.