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Frequent expression of CD30 antigen in the primary gastric non‐B, non‐Hodgkin lymphomas
Author(s) -
IwamizuWatanabe Sachiko,
Yamashita Yoriko,
Yatabe Yasushi,
Nakamura Shigeo,
Mori Naoyoshi
Publication year - 2004
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.1440-1827.2004.01657.x
Subject(s) - cd30 , lymphoma , pathology , anaplastic large cell lymphoma , anaplastic lymphoma kinase , immunostaining , medicine , large cell , immunohistochemistry , gastric lymphoma , cd8 , antigen , cancer , immunology , adenocarcinoma , malignant pleural effusion , lung cancer
Most primary gastric lymphomas are of B‐cell origin. Fourteen cases of primary gastric non‐B, non‐Hodgkin lymphomas were studied to evaluate their clinicopathological and immunophenotypic findings. The cases were comprised of 11 men and three women, with a median age of 56.5 years. Most patients underwent surgery either with or without chemotherapy, exhibiting a 5 year survival rate of 57.5%. Morphologically, the neoplastic cells showed various histological features, such as anaplastic large cell lymphoma (ALCL) ( n  = 3), peripheral T‐cell lymphoma, unspecified, large ( n  = 4), medium‐sized ( n  = 2) and mixed cell ( n  = 5). Two cases displayed a non‐B, non‐T cell phenotype, whereas the remaining cases displayed a T‐cell phenotype. Six cases were CD4+, while two were CD8+. The neoplastic cells were CD30+ in 10 cases. TIA‐1 was positive in six cases. In one case, anaplastic large cell lymphoma kinase (ALK) was identified with immunostaining and chromosomal rearrangement of ALK was detected by fluorescence in situ hybridization (FISH). In conclusion, although the mechanism of CD30 expression is unknown, primary gastric non‐B, non‐Hodgkin lymphomas tend to express CD30. We consider that some of the cases in the present study may be derived from cytotoxic T cells, similar to systemic and cutaneous ALCL, the majority of which exhibit TIA‐1.

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