High viral load of Merkel cell polyomavirus DNA sequences in Langerhans cell sarcoma tissues.
High viral load of Merkel cell polyomavirus DNA sequences in Langerhans cell sarcoma tissues.
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DOI：
10.1186/1750-9378-9-15
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发表时间：
2014
影响因子：
3.7
通讯作者：
Yoshino T
中科院分区：
文献类型：
--
作者：
Murakami I;Matsushita M;Iwasaki T;Kuwamoto S;Kato M;Horie Y;Hayashi K;Gogusev J;Jaubert F;Nakamoto S;Yamakawa M;Nakamine H;Takata K;Oka T;Yoshino T
朗格汉斯细胞肉瘤（LC）是一种高度恶性肿瘤，具有明显的恶性细胞学特征和LC表型。我们最近提出，LC作为常见的亲皮性默克尔细胞多瘤病毒（MCPyV）的储库，并确定了LC组织细胞增生症（LCH）（具有潜在的致癌能力）与MCPyV之间的关系，MCPyV是反应过程而不是肿瘤过程的触发因素。我们建议LC是一个水库MCPyV和假设，一些LCS亚型可能与MCPyV代理。我们用多重定量PCR（Q-PCR）和免疫组织化学方法检测了7例LCS组织中的抗MCPyV大T（LT）抗原抗体。使用Q-PCR在43%（3/7）的组织中检测到MCPyV DNA序列的高病毒载量（病毒载量= MCPyV的相对水平）（0.328-0.772拷贝/细胞（默克尔细胞癌（MCC）= 1.0）），但未观察到LT抗原表达（0/7）。频繁的MCPyV-DNA扩增提示部分患者的LCS可能与MCPyV感染有关。LCS的病毒载量（中位数0.453拷贝/细胞）高于低载量的LCH（中位数0.003，12例）（P < 0.01），提示某些LCS可能存在病毒诱导的致瘤过程。虽然LT抗原表达的缺乏可能表明MCPyV在这种病理学中的不同作用，但LCS的一些亚型可能在MCPyV感染的LC的背景下发展。据我们所知，这是第一次报道MCPyV和LCS之间的关系。最近发现的MCPyV为MCC开辟了新的治疗途径。这些数据为LCS的治疗干预开辟了新的可能性。
Langerhans cell (LC) sarcoma (LCS) is a high-grade neoplasm with overtly malignant cytologic features and an LC phenotype. We very recently suggested that LC behaves as a reservoir for common dermotropic Merkel cell polyomavirus (MCPyV) and determined the relationship between LC histiocytosis (LCH), which has an underlining oncogenic capacity, and MCPyV as a trigger for a reactive process rather than a neoplastic process. We propose LC to be a reservoir for MCPyV and hypothesize that some LCS subtypes may be related to the MCPyV agent. We examined seven LCS tissues using multiplex quantitative PCR (Q-PCR) and immunohistochemistry with anti MCPyV large-T (LT) antigen antibody. High viral loads of MCPyV DNA sequences (viral load = relative levels of MCPyV) were detected (0.328–0.772 copies/cell (Merkel cell carcinoma (MCC) = 1.0)) using Q-PCR in 43% (3/7) tissues, but LT antigen expression was not observed (0/7). Frequent MCPyV-DNA amplification suggests that LCS in some patients may be related to MCPyV infection. Moreover, the higher viral load of LCS (median, 0.453 copies/cell) than low load of LCH (0.003, median of 12 cases) (P < 0.01) may suggest a virally induced tumorigenic process in some LCS. Although the absence of LT antigen expression may indicate a different role for MCPyV in this pathology, some subtypes of LCS may develop in the background of MCPyV-infected LC. To the best of our knowledge, this is the first report on the relationship between MCPyV and LCS. The recent discovery of MCPyV opened new therapeutic avenues for MCC. These data open novel possibilities for therapeutic interventions against LCS.
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影响因子：
3.3
作者：
Kuwamoto, Satoshi
通讯作者：
Kuwamoto, Satoshi
影响因子：
4.6
作者：
Matsushita, Michiko;Kuwamoto, Satoshi;Hayashi, Kazuhiko
通讯作者：
Hayashi, Kazuhiko
DOI：
10.1097/pas.0b013e3181aa30a5
发表时间：
2009-09
期刊：
The American journal of surgical pathology
影响因子：
--
作者：
Busam KJ;Jungbluth AA;Rekthman N;Coit D;Pulitzer M;Bini J;Arora R;Hanson NC;Tassello JA;Frosina D;Moore P;Chang Y
通讯作者：
Chang Y
影响因子：
15.3
作者：
Grosjean, I;Caux, C;Kaiserlian, D
通讯作者：
Kaiserlian, D
影响因子：
3.3
作者：
Kuwamoto, Satoshi;Higaki, Hiromi;Hayashi, Kazuhiko
通讯作者：
Hayashi, Kazuhiko