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The MDM2 gene amplification database

J Momand1, D Jung, S Wilczynski

  • 1Department of Cell and Tumor Biology, Beckman Research Institute, National Medical Center, 1450 East Duarte Road, Duarte, CA 91010-3000, USA. jmomand@coh.org

Nucleic Acids Research
|July 22, 1998
PubMed
Summary

The MDM2 gene is amplified in 7% of human tumors, particularly soft tissue tumors, osteosarcomas, and esophageal carcinomas. Amplification of MDM2 and p53 mutations rarely occur together, suggesting distinct carcinogenic pathways.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The p53 tumor suppressor gene is crucial for preventing cancer and is inactivated through various mechanisms in human tumors.
  • Key mechanisms of p53 inactivation include gene mutation, association with viral proteins, and interaction with the MDM2 oncoprotein.
  • The MDM2 gene itself is frequently upregulated in tumors via gene amplification, increased transcription, and enhanced translation.

Purpose of the Study:

  • To review the spectrum of MDM2 abnormalities in human tumors.
  • To compare the tissue distribution of MDM2 amplification and p53 mutation frequencies.
  • To investigate the relationship between MDM2 amplification and p53 mutations within the same tumors.

Main Methods:

  • A comprehensive review of previously published data examining MDM2 amplification.

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  • Analysis of 3889 tumor samples from 28 distinct tumor types for MDM2 amplification.
  • Comparison of MDM2 amplification frequencies with p53 mutation data across different tumor types.

    • Main Results:

    • MDM2 amplification was observed in 7% of the analyzed human tumors across 19 tumor types.
    • The highest frequencies of MDM2 amplification were found in soft tissue tumors (20%), osteosarcomas (16%), and esophageal carcinomas (13%).
    • MDM2 amplification and p53 mutations were generally mutually exclusive, with 29 out of 33 MDM2 amplification-positive tumors exhibiting wild-type p53.

    Conclusions:

    • MDM2 amplification is a significant mechanism of p53 regulation in human cancers.
    • Certain tumor types, including soft tissue tumors, testicular germ cell cancers, and neuroblastomas, show a higher incidence of MDM2 amplification than p53 mutation.
    • The inverse relationship between MDM2 amplification and p53 mutation suggests that distinct etiological factors or carcinogens may drive these different inactivation pathways.