フルテキストファイル
著者
Matsushita Michiko Department of Pathobiological Science and Technology, School of Health Science, Tottori University Faculty of Medicine 鳥取大学研究者総覧 KAKEN研究者をさがす
Iwasaki Takeshi Department of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University
Nonaka Daisuke Department of Histopathology, The Christie NHS Foundation Trust
Kuwamoto Satoshi Division of Molecular Pathology, Department of Pathology, Tottori University Faculty of Medicine 鳥取大学研究者総覧 KAKEN研究者をさがす
Nagata Keiko Division of Molecular Pathology, Department of Pathology, Tottori University Faculty of Medicine 鳥取大学研究者総覧 KAKEN研究者をさがす
Kato Masako Division of Molecular Pathology, Department of Pathology, Tottori University Faculty of Medicine 鳥取大学研究者総覧 KAKEN研究者をさがす
Kitamura Yukisato Department of Pathobiological Science and Technology, School of Health Science, Tottori University Faculty of Medicine 鳥取大学研究者総覧 KAKEN研究者をさがす
Hayashi Kazuhiko Division of Molecular Pathology, Department of Pathology, Tottori University Faculty of Medicine 鳥取大学研究者総覧 KAKEN研究者をさがす
キーワード
activation-induced cytidine deaminase
Merkel cell carcinoma
Merkel cell polyomavirus
抄録
[Background] Merkel cell carcinomas (MCCs), clinically aggressive neuroendocrine skin cancers, are divided into Merkel cell polyomavirus (MCPyV)-positive and-negative tumors, which show different clinicopathological features and may develop through different mechanisms of carcinogenesis. Aberrant expression of activation-induced cytidine deaminase (AID) as a genomic modulator was demonstrated through pathogen-related NF-κB signal in Helicobacter pylori-associated gastric cancer, adult T cell leukemia/lymphoma (HTLV-1), hepatoma(HCV), and Burkitt lymphoma (EBV).
[Methods] To elucidate the relation of aberrant AID expression in MCPyV-positive and -negative MCCs, we evaluated immunohistochemical expressions of AID and AID-regulating factors between 24 MCPyV-positive and 17 MCPyV-negative MCCs.
[Results] AID expression was significantly higher in MCPyV-negative MCCs than MCPyV-positive ones (P = 0.026), although expression of NF-κB p65 (phospho S536) (AID-enhancer) was significantly higher in MCPyV-positive MCCs than MCPyV-negative ones (P = 0.034). Expressions of PAX5 and c-Myb were not significantly different between these subgroups. Expressions of AID and AID-regulating factors were not correlated to prognosis of MCC patients.
[Conclusion] Our findings suggest that although pathogen-induced AID expression through upregulationof NF-κB may be relevant to carcinogenesis of MCPyV-positive MCCs, the significantly higher aberrant AID expression in MCPyV-negative MCCs is consistent with the fact that MCPyV-negative MCCs have an extremely extremely higher mutation burden than MCPyV-positive ones.
出版者
Tottori University Faculty of Medicine
資料タイプ
学術雑誌論文
外部リンク
ISSN・ISBN
1346-8049
書誌ID
AA00892882
掲載誌名
Yonago Acta Medica
最新掲載誌名
Yonago Acta Medica
60
3
開始ページ
145
終了ページ
153
発行日
2017-09-15
著者版フラグ
出版社版
掲載情報
Yonago Acta Medica. 2017, 60(3), 145-153
部局名
医学部・医学系研究科・医学部附属病院
言語
英語