P53 mutation and MDM2 amplification frequency in pediatric rhabdomyosarcoma tumors and cell lines

Med Pediatr Oncol. 2000 Aug;35(2):96-103. doi: 10.1002/1096-911x(200008)35:2<96::aid-mpo2>3.0.co;2-z.

Abstract

Background: The p53 tumor suppressor gene is the most commonly mutated gene in human cancer, and mutations arise in a wide variety of tumor types. Wild-type p53 functions as a regulator of apoptosis, so mutations in the p53 gene are generally associated with aggressive tumors and a poor prognosis.

Procedure: We have investigated the p53 mutation and MDM2 amplification frequencies in biopsies from pediatric rhabdomyosarcoma (RMS) tumors and cell lines by SSCP and Southern analyses.

Results: A mutation was detected in only 1 of 20 tumor specimens (5%), whereas the frequency in established RMS cell lines was significantly higher (6/10, 60%). p53 Mutations were more common in cell lines derived from tumors previously exposed to chemotherapy compared to those derived from tumors at di-agnosis, and it is likely that these mutations enhanced the probability of successful long-term culture. The frequency of MDM2 gene amplification in patient biopsies was also low (2/20, 10%). Interestingly, complete responses to treatment were obtained in the two patients with tumors that demonstrated amplification of MDM2. The response to treatment of patients with tumors wild-type for p53 and without MDM2 amplification was quite varied, indicating that expression of a wild-type p53 gene at diagnosis cannot always facilitate a favorable outcome.

Conclusions: p53 mutation and MDM2 gene amplification frequencies are extremely low in RMS tumors, but a wild-type p53 genotype is not always associated with a favorable prognosis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adolescent
  • Adult
  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use
  • Blotting, Southern
  • Cell Line
  • Child
  • Child, Preschool
  • Combined Modality Therapy
  • Exons
  • Gene Amplification
  • Humans
  • Infant
  • Mutation
  • Neoplasm Proteins / genetics*
  • Nuclear Proteins*
  • Polymorphism, Single-Stranded Conformational
  • Prognosis
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins c-mdm2
  • Rhabdomyosarcoma / drug therapy
  • Rhabdomyosarcoma / genetics*
  • Rhabdomyosarcoma / pathology
  • Tumor Suppressor Protein p53 / genetics*

Substances

  • Neoplasm Proteins
  • Nuclear Proteins
  • Proto-Oncogene Proteins
  • Tumor Suppressor Protein p53
  • MDM2 protein, human
  • Proto-Oncogene Proteins c-mdm2