Literature DB >> 11965046

Expression of minor histocompatibility antigen, HA-1, in solid tumor cells.

Nobuharu Fujii1, Akio Hiraki, Kazuma Ikeda, Yasushi Ohmura, Isao Nozaki, Katsuji Shinagawa, Fumihiko Ishimaru, Katsuyuki Kiura, Nobuyoshi Shimizu, Mitsune Tanimoto, Mine Harada.   

Abstract

BACKGROUND: Minor histocompatibility antigen (mHag) induces and mounts graft-versus-host disease after allogeneic hematopoietic stem cell transplantation. Among several mHags, HA-1 is one that acts alone and is the most studied. It is suggested that HA-1 may be one of the immunodominant antigens inducing not only graft-versus-host disease but also graft-versus-malignancy effects. There are some reports that mHag HA-1-specific cytotoxic T lymphocytes generated from an HA-1-negative donor can lyse HA-1-positive leukemic cells. However, the tissue distribution of HA-1 has been described as restricted to the cells of the hematopoietic lineage.
METHODS: We examined the HA-1 expression in peripheral blood mononuclear cells (PBMNC), leukemia/lymphoma cell lines, solid tumor cell lines, and paired samples of tumor and normal tissues from individual cancer patients by quantitative reverse-transcription polymerase chain reaction.
RESULTS: We found that mRNA of HA-1 is expressed in all leukemia/lymphoma cell lines and PBMNC. Most of the leukemia/lymphoma cell lines have the same levels of HA-1 expression as a leukemia/lymphoma cell line, Raji. The expression levels of human PBMNC were 14- to 19-fold higher than those of Raji. Among 32 solid tumor cell lines, 7 showed >50% expression levels compared with Raji.
CONCLUSIONS: HA-1 expression in the mRNA level is higher in cells of hematopoietic origin, but this tissue distribution is not strictly restricted. Some solid tumor cells and tissues express HA-1 gene equal to hematopoietic cells.

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Year:  2002        PMID: 11965046     DOI: 10.1097/00007890-200204150-00022

Source DB:  PubMed          Journal:  Transplantation        ISSN: 0041-1337            Impact factor:   4.939


  11 in total

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Journal:  PLoS Genet       Date:  2007-06       Impact factor: 5.917

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