BMC Cancer | |
Deletion of the TNFAIP3/A20 gene detected by FICTION analysis in classical Hodgkin lymphoma | |
Junko Nomoto6  Nobuhiro Hiramoto4  Motohiro Kato7  Masashi Sanada7  Akiko Miyagi Maeshima2  Hirokazu Taniguchi2  Fumie Hosoda3  Yoshitaka Asakura4  Wataru Munakata4  Naohiro Sekiguchi4  Dai Maruyama4  Takashi Watanabe4  Hitoshi Nakagama5  Kengo Takeuchi1  Kensei Tobinai4  Seishi Ogawa7  Yukio Kobayashi4  | |
[1] Pathology Project for Molecular Targets, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan | |
[2] Pathology Division, National Cancer Center Hospital, Tokyo, Japan | |
[3] Cancer Genomics Division, National Cancer Center Research Institute, Tokyo, Japan | |
[4] Hematology Division, National Cancer Center Hospital, Tokyo, Japan | |
[5] Early Carcinogenetic Division, Research Institute, National Cancer Center Hospital, Tokyo, Japan | |
[6] Section of Microbiology and Immunology, Tokyo Medical and Dental University Graduate School of Health Care Sciences, Tokyo, Japan | |
[7] Cancer Genomics, Faculty of Medicine, The University of Tokyo, Tokyo, Japan | |
关键词: Homozygous deletion; TNFAIP3 gene; Hodgkin lymphoma; FICTION analysis; | |
Others : 1080152 DOI : 10.1186/1471-2407-12-457 |
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received in 2012-05-30, accepted in 2012-10-02, 发布年份 2012 | |
【 摘 要 】
Background
The TNFAIP3 gene, which encodes a ubiquitin-modifying enzyme (A20) involved in the negative regulation of NF-κB signaling, is frequently inactivated by gene deletions/mutations in a variety of B-cell malignancies. However, the detection of this in primary Hodgkin lymphoma (HL) specimens is hampered by the scarcity of Hodgkin Reed-Sternberg (HR-S) cells even after enrichment by micro-dissection.
Methods
We used anti-CD30 immunofluorescence with fluorescence in-situ hybridization (FISH) to evaluate the relative number of TNFAIP3/CEP6 double-positive signals in CD30-positive cells.
Results
From a total of 47 primary classical Hodgkin lymphoma (cHL) specimens, 44 were evaluable. We found that the relative numbers of TNFAIP3/CD30 cells were distributed among three groups, corresponding to those having homozygous (11%), heterozygous (32%), and no (57%) deletions in TNFAIP3. This shows that TNFAIP3 deletions could be sensitively detected using our chosen methods.
Conclusions
Comparing the results with mutation analysis, TNFAIP3 inactivation was shown to have escaped detection in many samples with homozygous deletions. This suggests that TNFAIP3 inactivation in primary cHL specimens might be more frequent than previously reported.
【 授权许可】
2012 Nomoto et al.; licensee BioMed Central Ltd.
【 预 览 】
Files | Size | Format | View |
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20141202230107206.pdf | 445KB | download | |
Figure 1. | 106KB | Image | download |
【 图 表 】
Figure 1.
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