title: Absence of human herpesvirus-8 and Epstein-Barr virus in inflammatory myofibroblastic tumor with anaplastic large cell lymphoma kinase fusion gene.
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.
authors.affiliation: Department of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. hidetaka@surgpath.med.kyushu-u.ac.jp
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Yamamoto
authors.forename: Kenichi
authors.initials: K
authors.lastname: Kohashi
authors.forename: Yoshinao
authors.initials: Y
authors.lastname: Oda
authors.forename: Sadafumi
authors.initials: S
authors.lastname: Tamiya
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Takahashi
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Kinoshita
authors.forename: Shin
authors.initials: S
authors.lastname: Ishizawa
authors.forename: Masayuki
authors.initials: M
authors.lastname: Kubota
authors.forename: Masazumi
authors.initials: M
authors.lastname: Tsuneyoshi
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000077548:Anaplastic Lymphoma Kinase; D000956:Antigens, Viral / Q000235:genetics / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D033922:Clathrin Heavy Chains / Q000235:genetics / Q000378:metabolism; D020031:Epstein-Barr Virus Infections / Q000150:complications* / Q000235:genetics / Q000473:pathology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D015967:Gene Expression Regulation, Viral; D006566:Herpesviridae Infections / Q000150:complications* / Q000235:genetics / Q000473:pathology; D004854:Herpesvirus 4, Human / Q000235:genetics / Q000472:pathogenicity*; D019288:Herpesvirus 8, Human / Q000235:genetics / Q000472:pathogenicity*; D006801:Humans; D007223:Infant; D008297:Male; D008875:Middle Aged; D009379:Neoplasms, Muscle Tissue / Q000209:etiology / Q000235:genetics* / Q000473:pathology / Q000821:virology*; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism; D015514:Oncogene Proteins, Fusion / Q000235:genetics; D011505:Protein-Tyrosine Kinases / Q000235:genetics* / Q000378:metabolism; D020794:Receptor Protein-Tyrosine Kinases; D014335:Tropomyosin / Q000235:genetics / Q000378:metabolism
chemical_list: D000956:Antigens, Viral; D009687:Nuclear Proteins; D015514:Oncogene Proteins, Fusion; C498783:TPM3 protein, human; C501213:TPM4 protein, human; D014335:Tropomyosin; C109540:latency-associated nuclear antigen; D033922:Clathrin Heavy Chains; C000626173:ALK protein, human; D000077548:Anaplastic Lymphoma Kinase; D011505:Protein-Tyrosine Kinases; D020794:Receptor Protein-Tyrosine Kinases