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
Cancer Epigenetics Laboratory, Department of Clinical Oncology, The Chinese University of Hong Kong, Hong Kong.
Br J Haematol. 2007 Mar;136(6):829-32. doi: 10.1111/j.1365-2141.2007.06512.x.
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.
肿瘤抑制基因（TSG）的表观遗传沉默会使TSG功能失活。此前，我们将PCDH10鉴定为癌组织中发生甲基化的TSG。在此，我们在淋巴瘤细胞系中检测到其频繁沉默和甲基化，包括100%的伯基特淋巴瘤、100%的弥漫性大B细胞淋巴瘤、86%的霍奇金淋巴瘤、100%的鼻型自然杀伤/T细胞淋巴瘤以及1/3的白血病细胞系，并且在原发性肿瘤中也有发现，但在正常外周血单个核细胞或淋巴结中未检测到。用5-氮杂-2'-脱氧胞苷进行去甲基化可逆转PCDH10的沉默。在14%的霍奇金淋巴瘤血清中进一步检测到甲基化。因此，PCDH10甲基化频繁参与淋巴瘤的发生，可作为肿瘤特异性生物标志物。
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