Absence of human herpesvirus-8 and Epstein-Barr virus in inflammatory myofibroblastic tumor with anaplastic large cell lymphoma kinase fusion gene

Pathol Int. 2006 Oct;56(10):584-90. doi: 10.1111/j.1440-1827.2006.02012.x.

Abstract

Inflammatory myofibroblastic tumor (IMT) is clinically and histologically characterized by inflammation. Some populations of IMT have anaplastic large cell lymphoma kinase (ALK) gene rearrangements. Infection with Epstein-Barr virus (EBV) and human herpesvirus-8 (HHV-8) in tumor cells of IMT has been reported; these reports, however, have been limited to ALK-negative IMT. The purpose of the present paper was to evaluate 21 cases of IMT for the presence of EBV and HHV-8. Immunohistochemically, 15 cases were ALK positive and six were negative. Of eight cases analyzed using reverse transcription-polymerase chain reaction, tropomyosin 3 (TPM3)-ALK, TPM4-ALK and clathrin heavy chain-ALK fusion genes were detected in one, two and two cases, respectively. All 21 IMT, irrespective of ALK expression, were negative for EBV by in situ hybridization for EBV-encoded RNA and immunohistochemical stain for latent membrane antigen-1. HHV-8 was also negative in all IMT by PCR for HHV-8 DNA sequence (KS330/233) and immunohistochemical stain for latent nuclear antigen. These results suggest that IMT may be a heterogeneous group in terms of pathogenesis, and EBV and HHV-8 do not play a major role in the pathogenesis of ALK-positive tumor.

Publication types

  • Evaluation Study

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Anaplastic Lymphoma Kinase
  • Antigens, Viral / genetics
  • Antigens, Viral / metabolism
  • Child
  • Child, Preschool
  • Clathrin Heavy Chains / genetics
  • Clathrin Heavy Chains / metabolism
  • Epstein-Barr Virus Infections / complications*
  • Epstein-Barr Virus Infections / genetics
  • Epstein-Barr Virus Infections / pathology
  • Female
  • Gene Expression Regulation, Neoplastic / genetics
  • Gene Expression Regulation, Viral
  • Herpesviridae Infections / complications*
  • Herpesviridae Infections / genetics
  • Herpesviridae Infections / pathology
  • Herpesvirus 4, Human / genetics
  • Herpesvirus 4, Human / pathogenicity*
  • Herpesvirus 8, Human / genetics
  • Herpesvirus 8, Human / pathogenicity*
  • Humans
  • Infant
  • Male
  • Middle Aged
  • Neoplasms, Muscle Tissue / etiology
  • Neoplasms, Muscle Tissue / genetics*
  • Neoplasms, Muscle Tissue / pathology
  • Neoplasms, Muscle Tissue / virology*
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism
  • Oncogene Proteins, Fusion / genetics
  • Protein-Tyrosine Kinases / genetics*
  • Protein-Tyrosine Kinases / metabolism
  • Receptor Protein-Tyrosine Kinases
  • Tropomyosin / genetics
  • Tropomyosin / metabolism

Substances

  • Antigens, Viral
  • Nuclear Proteins
  • Oncogene Proteins, Fusion
  • TPM3 protein, human
  • TPM4 protein, human
  • Tropomyosin
  • latency-associated nuclear antigen
  • Clathrin Heavy Chains
  • ALK protein, human
  • Anaplastic Lymphoma Kinase
  • Protein-Tyrosine Kinases
  • Receptor Protein-Tyrosine Kinases