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

The mdm2 proto-oncogene

D S Haines1

  • 1Division of Hematology/Oncology, Allegheny University of the Health Sciences, Philadelphia, PA 19102, USA.

Leukemia & Lymphoma
|July 1, 1997
PubMed
Summary
This summary is machine-generated.

The mouse double minute 2 (mdm2) oncogene, when overexpressed, drives cancer by inhibiting the p53 tumor suppressor. This review explores mdm2

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

A deficiency in Mdm2 binding protein inhibits Myc-induced B-cell proliferation and lymphomagenesis.

Oncogene·2010
Same author

Retraction for D. R. Zweitzig, N. Shcherbik, and D. S. Haines: AAA ATPase P97 and adaptor UBXD1 suppress MDM2 ubiquitination and degradation and promote constitutive P53 turnover.

Molecular biology of the cell·2008
Same author

Assignment of the MDM2 binding protein gene (MTBP) to human chromosome band 8q24 by in situ hybridization.

Cytogenetics and cell genetics·2000
Same author

MDM2 interacts with the C-terminus of the catalytic subunit of DNA polymerase epsilon.

Nucleic acids research·2000
Same author

A novel cellular protein (MTBP) binds to MDM2 and induces a G1 arrest that is suppressed by MDM2.

The Journal of biological chemistry·2000
Same author

Identification of a tumor-derived p53 mutant with novel transactivating selectivity.

Oncogene·2000
Same journal

CPX‑351 vs. FLAG‑ida in patients with high-risk AML/MDS and MDS-related gene mutations: a subgroup analysis of the UK NCRI AML19 trial.

Leukemia & lymphoma·2026
Same journal

Specialist palliative care access and end-of-life hospitalizations in acute leukemia: a nationwide register study.

Leukemia & lymphoma·2026
Same journal

D-VRD vs. D-KRD induction in transplant-eligible multiple myeloma: a real-world comparison.

Leukemia & lymphoma·2026
Same journal

T-box factor EOMES is part of an aberrant network in Hodgkin lymphoma.

Leukemia & lymphoma·2026
Same journal

Overall survival of patients with chronic lymphocytic leukemia treated with venetoclax-obinutuzumab compared to age- and sex-matched general population.

Leukemia & lymphoma·2026
Same journal

Hypertension and time to treatment failure with acalabrutinib and ibrutinib in treatment-naïve CLL/SLL.

Leukemia & lymphoma·2026
See all related articles

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The mouse double minute 2 (mdm2) proto-oncogene was identified in amplified genes within a tumorigenic cell line.
  • Overexpression of mdm2 protein is observed in various human malignancies, indicating its oncogenic role.

Purpose of the Study:

  • To review clinical, cellular, and biochemical studies on the mdm2 oncogene.
  • To present a proposed role for mdm2 in cell cycle regulation pathways.

Main Methods:

  • Literature review of existing studies on mdm2.
  • Analysis of mdm2 interactions with p53 and retinoblastoma protein (pRb).

Main Results:

  • mdm2 overexpression inhibits p53's tumor suppressive functions, including transactivation, cell cycle arrest, and apoptosis.

Related Experiment Videos

  • A feedback loop between mdm2 and p53 regulates normal cell cycling, but disruption can lead to genomic instability.
  • mdm2 also interacts with pRb and E2F-1/DP1, suggesting p53-independent roles in proliferation.

    • Conclusions:

    • Elevated mdm2 levels impair p53's ability to control cell cycle progression during cellular insults, promoting tumor evolution.
    • mdm2 plays a critical role in human carcinogenesis through both p53-dependent and -independent pathways.