Absence of human herpesvirus-8 and Epstein-Barr virus in inflammatory myofibroblastic tumor with anaplastic large cell lymphoma kinase fusion gene.
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.
Yamamoto
Hidetaka
H
Department of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. hidetaka@surgpath.med.kyushu-u.ac.jp
Kohashi
Kenichi
K
Oda
Yoshinao
Y
Tamiya
Sadafumi
S
Takahashi
Yukiko
Y
Kinoshita
Yoshiaki
Y
Ishizawa
Shin
S
Kubota
Masayuki
M
Tsuneyoshi
Masazumi
M
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
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