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Related Experiment Video

Updated: Jun 8, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

A high-frequency regulatory polymorphism in the p53 pathway accelerates tumor development.

Sean M Post¹, Alfonso Quintás-Cardama, Vinod Pant

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

|September 14, 2010

Summary

The MDM2(SNP309G) allele elevates MDM2 levels, reducing p53 and apoptosis, which increases tumor risk. This SNP potentiates cancer development, particularly in individuals with p53 mutations.

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Area of Science:

Molecular Biology
Cancer Genetics
Oncology

Background:

MDM2 negatively regulates p53, a crucial tumor suppressor.
Elevated MDM2 levels are observed in many cancers with wild-type p53.
A specific MDM2 promoter single nucleotide polymorphism (SNP309) enhances Sp1 binding and increases MDM2 expression.

Purpose of the Study:

To investigate the impact of the MDM2(SNP309G) allele on tumorigenesis.
To determine if the MDM2(SNP309G) allele increases cancer risk.
To assess the effect of the MDM2(SNP309G) allele on tumor development in the context of p53 mutations.

Main Methods:

Generation of genetically engineered mice with MDM2(SNP309T) and MDM2(SNP309G) alleles.
Analysis of Mdm2 and p53 levels, and apoptosis in Mdm2(SNP309G/G) cells.
Evaluation of tumor incidence and spectrum in Mdm2(SNP309G/G) mice, including those with a p53 mutation.

Main Results:

Mdm2(SNP309G/G) cells displayed elevated Mdm2, reduced p53, and decreased apoptosis.
A subset of Mdm2(SNP309G/G) mice developed tumors before one year of age.
The MDM2(SNP309G) allele exacerbated tumor development and altered the tumor spectrum in mice with a p53 mutation.

Conclusions:

The MDM2(SNP309G) allele is causally linked to increased cancer risk.
This SNP contributes to tumorigenesis by disrupting the p53 pathway.
The findings highlight the clinical relevance of MDM2 genetic variations in cancer predisposition.