检测到慢性淋巴细胞白血病细胞中新型截断的 Merkel 细胞多瘤病毒大 T 抗原缺失。
Detection of a novel truncating Merkel cell polyomavirus large T antigen deletion in chronic lymphocytic leukemia cells.
机构信息
Institute of Pathology, University Hospital Freiburg, Freiburg, Germany.
出版信息
Blood. 2010 Dec 9;116(24):5280-4. doi: 10.1182/blood-2010-02-269829. Epub 2010 Sep 3.
Merkel cell polyomavirus (MCPyV) is detected in approximately 80% of Merkel cell carcinomas (MCC). Yet, clonal integration and truncating mutations of the large T antigen (LTAg) of MCPyV are restricted to MCC. We tested the presence and mutations of MCPyV in highly purified leukemic cells of 70 chronic lymphocytic leukemia (CLL) patients. MCPyV was detected in 27.1% (n = 19) of these CLL cases. In contrast, MCPyV was detected only in 13.4% of normal controls (P < .036) in which no LTAg mutations were found. Mutational analyses revealed a novel 246bp LTAg deletion in the helicase gene in 6 of 19 MCPyV-positive CLL cases. 2 CLL cases showed concomitant mutated and wild-type MCPyV. Immunohistochemistry revealed protein expression of the LTAg in MCPyV-positive CLL cases. The detection of MCPyV, including LTAg deletions and LTAg expression in CLL cells argues for a potential role of MCPyV in a significant subset of CLL cases.
默克尔细胞多瘤病毒（Merkel cell polyomavirus，MCPyV）在大约 80%的默克尔细胞癌（Merkel cell carcinoma，MCC）中被检测到。然而，MCPyV 的大 T 抗原（large T antigen，LTAg）的克隆整合和截断突变仅限于 MCC。我们检测了 70 例慢性淋巴细胞白血病（chronic lymphocytic leukemia，CLL）患者高度纯化的白血病细胞中 MCPyV 的存在和突变。在这些 CLL 病例中，27.1%（n=19）检测到 MCPyV。相比之下，在 13.4%的正常对照中（P<0.036）仅检测到 MCPyV，并且在这些对照中没有发现 LTAg 突变。突变分析显示，在 19 例 MCPyV 阳性的 CLL 病例中有 6 例存在新的 246bp LTAg 缺失。在 2 例 CLL 病例中同时存在突变型和野生型 MCPyV。免疫组化显示 MCPyV 阳性的 CLL 病例中存在 LTAg 蛋白表达。CLL 细胞中 MCPyV 的检测，包括 LTAg 缺失和 LTAg 表达，表明 MCPyV 在 CLL 病例的一个重要亚群中可能发挥作用。
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