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Absence of human herpesvirus‐8 and Epstein–Barr virus in inflammatory myofibroblastic tumor with anaplastic large cell lymphoma kinase fusion gene
Author(s) -
Yamamoto Hidetaka,
Kohashi Kenichi,
Oda Yoshinao,
Tamiya Sadafumi,
Takahashi Yukiko,
Kinoshita Yoshiaki,
Ishizawa Shin,
Kubota Masayuki,
Tsuneyoshi Masazumi
Publication year - 2006
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.2006.02012.x
Subject(s) - anaplastic lymphoma kinase , immunohistochemistry , pathology , biology , anaplastic large cell lymphoma , lymphoma , cd30 , virus , epstein–barr virus , pathogenesis , cancer research , virology , medicine , malignant pleural effusion , lung cancer
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.