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首页> 外文期刊>Medical and Pediatric Oncology: The Official Journal of the American Association for Cancer Education >Epigenetic changes in the DAP-kinase CpG island in pediatric lymphoma.
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Epigenetic changes in the DAP-kinase CpG island in pediatric lymphoma.

机译：小儿淋巴瘤中DAP激酶CpG岛的表观遗传变化。

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BACKGROUND: Hypermethylation of CpG islands in the promoter region of death-associated protein kinase (DAP-kinase) coupled with the loss of gamma-interferon-induced apoptosis have been reported in B-cell malignancies suggesting a role in pathogenesis or prognosis. Along with B-cell malignancies, pediatric lymphomas also include T-cell non-Hodgkin lymphoma (NHL), anaplastic large cell lymphoma, and Hodgkin disease, each with unique prognoses. The purpose of this study was to elucidate epigenetic changes in the DAP-kinase promoter region of pediatric cases to determine associations with aberrant hypermethylation. PROCEDURES: Thirty-nine cases of different lymphoid pathology [10 Burkitt lymphoma, 1 B-cell NHL; 7 T-cell lymphoblastic lymphoma; 4 anaplastic large cell lymphoma (LCL); 2 B-cell LCL; 14 nodular sclerosing Hodgkin disease (NSHD); and 1 B-cell acute lymphoblastic leukemia (ALL)] had methylation-specific polymerase chain reaction performed on bisulfite-treated DNA, which distinguishes the methylation status of the promoter region, and DAP-kinase mRNA expression assays performed on available specimens. RESULTS: In normal lymphocytes, the CpG islands in the promoter region were unmethylated, as were the T-cell lymphoblastic lymphoma and anaplastic LCL. In contrast, 100% of the Burkitt lymphoma (10/10) and B-cell ALL (1/1) were hypermethylated. Of the specimens with mRNA available, 7/8 Burkitt lymphoma had no DAP-kinase mRNA expression compared to normal expression in 3/3 and 4/4 T-cell lymphoblastic lymphoma and NSHD, respectively. CONCLUSIONS: In these pediatric lymphoid tumors, hypermethylation of the DAP-kinase promoter region with associated loss of DAP-kinase gene expression was associated with B-cell malignancies and thus may be important in the development and/or provide a prognostic tool in B- cell lymphomas.
机译：背景：在B细胞恶性肿瘤中，已经报道了死亡相关蛋白激酶（DAP-激酶）启动子区域CpG岛的超甲基化，以及γ-干扰素诱导的细胞凋亡的丧失，提示其在发病机理或预后中的作用。除B细胞恶性肿瘤外，小儿淋巴瘤还包括T细胞非霍奇金淋巴瘤（NHL），间变性大细胞淋巴瘤和霍奇金病，每种预后均独特。这项研究的目的是阐明小儿科病例的DAP激酶启动子区域的表观遗传学变化，以确定与异常高甲基化的关联。程序：39例不同的淋巴病理学病例[10伯基特淋巴瘤，1个B细胞NHL; 7例T细胞淋巴母细胞淋巴瘤; 4间变性间变性大细胞淋巴瘤（LCL）; 2个B单元LCL; 14例结节性硬化性霍奇金病（NSHD）;和1个B细胞急性淋巴细胞白血病（ALL）]在亚硫酸氢盐处理的DNA上进行了甲基化特异性聚合酶链反应，从而区分了启动子区域的甲基化状态，并在现有标本上进行了DAP激酶mRNA表达测定。结果：在正常淋巴细胞中，启动子区域的CpG岛未甲基化，T细胞淋巴母细胞淋巴瘤和间变性LCL也未甲基化。相反，Burkitt淋巴瘤（10/10）和B细胞ALL（1/1）被100％甲基化。与3/3和4/4 T细胞淋巴母细胞淋巴瘤和NSHD中的正常表达相比，在具有可用mRNA的标本中，7/8伯基特淋巴瘤没有DAP激酶mRNA表达。结论：在这些小儿淋巴样肿瘤中，DAP激酶启动子区域的高甲基化以及相关的DAP激酶基因表达的丧失与B细胞恶性肿瘤有关，因此可能对B-细胞的发展和/或提供预后工具具有重要意义。细胞淋巴瘤。

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