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Frequent epigenetic silencing of protocadherin 10 by methylation in multiple haematologic malignancies
Author(s) -
Ying Jianming,
Gao Zifen,
Li Hongyu,
Srivastava Gopesh,
Murray Paul G.,
Goh Hwee Koon,
Lim Chai Yen,
Wang Yajun,
Marafioti Teresa,
Mason David Y.,
Ambinder Richard F.,
Chan Anthony T. C.,
Tao Qian
Publication year - 2007
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2007.06512.x
Subject(s) - gene silencing , methylation , cancer research , lymphoma , epigenetics , biology , dna methylation , deoxycytidine , peripheral blood mononuclear cell , tumor suppressor gene , cancer , immunology , gene , carcinogenesis , genetics , gene expression , in vitro , gemcitabine
Summary Epigenetic silencing of tumour suppressor genes (TSG) inactivates TSG functions. Previously, we identified PCDH10 as a methylated TSG in carcinomas. Here, we detected its frequent silencing and methylation in lymphoma cell lines including 100% Burkitt, 100% diffuse large B cell, 86% Hodgkin, 100% nasal natural killer/T‐cell lymphoma and 1/3 of leukaemia cell lines, and in primary tumours but not in normal peripheral blood mononuclear cells or lymph nodes. PCDH10 silencing could be reversed by demethylation with 5‐aza‐2′‐deoxycytidine. Methylation was further detected in 14% of Hodgkin lymphoma sera. Thus, PCDH10 methylation is frequently involved in lymphomagenesis and could serve as a tumour‐specific biomarker.