High prevalence of the MYD88 mutation in testicular lymphoma: Immunohistochemical and genetic analyses.
High prevalence of the MYD88 mutation in testicular lymphoma: Immunohistochemical and genetic analyses.
复制标题
睾丸淋巴瘤中 MYD88 突变的高患病率：免疫组织化学和遗传分析。
DOI：
10.1111/pin.12336
复制
发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Katoh R.
中科院分区：
文献类型：
--
作者：
Oishi N;Kondo T;Nakazawa T;Mochizuki K;Tanioka F;Oyama T;Yamamoto T;Iizuka J;Tanabe K;Shibata N;Kirito K;Katoh R.
弥漫性大B细胞淋巴瘤(DLBCL)中已发现MYD88基因的激活突变。我们研究了23例睾丸DLBCL中MYD88基因的突变情况及其基因扩增和蛋白表达。为了检测MYD88突变，我们采用了等位基因特异性的聚合酶链式反应和Sanger测序，并分别用定量聚合酶链式反应和免疫组织化学方法分析了MYD88基因的扩增和蛋白表达。17例原发睾丸DLBCL中，94%(16/17)为非生发中心B细胞亚型，82%(14/17)为MYD88L265P，65%(11/17)为MYD88强表达。与正常淋巴结相比，MYD88在睾丸DLBCL中显著扩增。然而，扩增状态与其突变状态或蛋白表达无相关性。此外，MYD88突变状态和表达模式都不影响总的存活率。6例为继发性睾丸DLBCL，非GCB亚型和MYD88L265P亚型的发生率分别为83%(5/6)和80%(4/5)。总之，我们发现非GCB亚型和常见的MYD88L265P基因在原发和继发性睾丸DLBCL中都有很高的患病率。我们的数据表明，MYD88突变是睾丸DLBCL中相当一致的遗传特征。
The activating mutation ofMYD88has been identified in diffuse large B‐cell lymphoma (DLBCL). We investigated the mutational status and both the gene amplification and protein expression ofMYD88in 23 cases of testicular DLBCL. To detect theMYD88mutations, we employed the allele‐specific PCR and Sanger sequencing.MYD88gene amplification and protein expression were analyzed by quantitative PCR and by immunohistochemistry, respectively. There were 17 cases of primary testicular DLBCL: 94% (16/17) exhibited a non‐Germinal center B‐cell (non‐GCB) subtype, 82% (14/17) showed theMYD88L265P, and 65% (11/17) had intense expression ofMYD88. When compared with normal lymph nodes, theMYD88is significantly amplified in primary testicular DLBCL. However, the amplification status showed no correlation with its mutational status or protein expression. Moreover, neither theMYD88mutational status nor the expression pattern affected overall survival. Six cases were secondary testicular DLBCL with an 83% (5/6) and an 80% (4/5) incidence of the non‐GCB subtype and of theMYD88L265P, respectively. In conclusion, we demonstrated a high prevalence of the non‐GCB subtype and the commonMYD88L265P in both primary and secondary testicular DLBCL. Our data suggest that theMYD88mutation is a fairly consistent genetic feature in testicular DLBCL.