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High expression of MDM2 protein and low rate of p21(WAF1/CIP1) expression in SCID mice Epstein Barr virus-induced

S El Mansouri1, A Martin, A Mercadier

  • 1Service d'Hématologie Biologique, EA 1625, and Service d'Anatomie Pathologique, Hôpital Avicenne, UFR SMBH Léonard de Vinci, Université Paris XIII, Bobigny, France.

The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society
|September 18, 1999
PubMed

Insights

Epstein-Barr virus (EBV) lymphoproliferation in SCID mice shows high proliferation, but not due to p53 mutations. Overexpressed MDM2, not p53 inactivation, may drive this EBV-driven cancer growth.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Epstein-Barr virus (EBV) can induce lymphoproliferation in severe combined immunodeficient (SCID) mice.
  • The role of p53 and its regulators, MDM2 and p21(WAF1/CIP1), in this process is not fully understood.

Purpose of the Study:

  • To investigate the prevalence of p53 inactivation and the expression of MDM2 and p21(WAF1/CIP1) in EBV-induced lymphoproliferation in SCID mice.

Main Methods:

  • Analysis of 19 SCID mouse samples with EBV-induced lymphoproliferation.
  • Immunohistochemistry to assess Ki-67, p53, MDM2, and p21(WAF1/CIP1) expression.
  • Functional yeast assay to screen for p53 mutations.

Main Results:

  • High Ki-67 expression indicated a significant proliferative index in all samples.
  • Only one sample showed a p53-inactivating mutation; p53 protein accumulation was observed in 6/19 samples.
  • MDM2 nuclear accumulation was detected in all samples, while p21 expression was found in 7/19 samples without correlation to p53 levels.

Conclusions:

  • High proliferation in SCID mice EBV-induced lymphoproliferation is not driven by p53 mutation.
  • Overexpression of MDM2, potentially via a p53-independent pathway, may contribute to the observed lymphoproliferation.

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