HDM2 overexpression and focal loss of p14/ARF expression may deregulate the p53 tumour suppressor pathway in meningeal haemangiopericytomas. Study by double immunofluorescence and laser scanning confocal microscopy

Histopathology. 2005 Feb;46(2):184-94. doi: 10.1111/j.1365-2559.2005.02074.x.

Abstract

Aims: To investigate the p53 pathway in meningeal haemangiopericytomas (MHPCs), p14/ARF, p53 protein expression and two wild-type (wt) p53-induced proteins (HDM2 and p21/WAF1) were studied in 18 MHPCs, 11 primary, four of them recurrent on one, one, two and four occasions.

Methods: Immunohistochemical detection of p14/ARF, p53, p21/WAF1, HDM2 and Ki67 proliferative index (PI) protein expression.

Results: Ki67 index was > 5% in eight out 18 cases (44.4%). The PI in recurrent cases increased with neoplastic progression. Simultaneous p53 and wt p53 transactivated gene (p21/WAF, HDM2) expression occurred in all cases. This argues against p53 mutation. HDM2 overexpression was observed in 10 cases (55.5%). Double-immunofluorescence staining and laser scanning confocal microscopy (LSCM) displayed HDM2 and p53 colocalization. This strongly suggests that HDM2 binds and inactivates p53 that could be pathogenic for MHPCs, by a different mechanism than point mutation. p14/ARF expression > 5% was observed in 12 cases (66.6%). A normal (diffuse) pattern of expression was seen in 13 cases (72.2%). Focal loss of expression was observed in five patients (27.7%): three primary cases and two recurrences. Therefore, p14/ARF down-regulation may also contribute to the development of MHPC.

Conclusion: HDM2 overexpression, sometimes combined with focal loss of p14/ARF expression, may play a pathogenic role in MHPCs.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Cycle Proteins / analysis
  • Cyclin-Dependent Kinase Inhibitor p21
  • Fluorescent Antibody Technique / methods
  • Hemangiopericytoma / metabolism
  • Hemangiopericytoma / pathology*
  • Humans
  • Immunohistochemistry
  • Ki-67 Antigen / analysis
  • Meningeal Neoplasms / metabolism
  • Meningeal Neoplasms / pathology*
  • Microscopy, Confocal
  • Neoplasm Proteins / biosynthesis*
  • Nuclear Proteins / biosynthesis
  • Proto-Oncogene Proteins / biosynthesis
  • Proto-Oncogene Proteins c-mdm2
  • Tumor Suppressor Protein p14ARF / biosynthesis
  • Tumor Suppressor Protein p53 / biosynthesis

Substances

  • CDKN1A protein, human
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p21
  • Ki-67 Antigen
  • Neoplasm Proteins
  • Nuclear Proteins
  • Proto-Oncogene Proteins
  • Tumor Suppressor Protein p14ARF
  • Tumor Suppressor Protein p53
  • MDM2 protein, human
  • Proto-Oncogene Proteins c-mdm2