Hayashi K, Chen W G, Chen Y Y, Bacchi M M, Bacchi C E, Alvarenga M, Abreu E S, Chang K L, Weiss L M
Department of Pathology, City of Hope National Medical Center, Duarte, CA 91010, USA.
Hum Pathol. 1997 Dec;28(12):1408-14. doi: 10.1016/s0046-8177(97)90231-8.
A 30-basepair (bp) deletion in the Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) gene has been reported in nasopharyngeal carcinoma and EBV-associated malignant lymphomas. Prior studies have found the deletion in about 10% to 28% of cases of Hodgkin's disease (HD), particularly in cases with aggressive histology. We studied the prevalence of 30-bp LMP1 gene deletion in EBV-positive HD in the United States (US) (12 cases) and Brazil (26 cases) with comparison to reactive lymphoid tissues (21 cases) and HD without EBV-positive Reed-Sternberg cells (15 cases). We studied the status of the LMP1 gene by Southern blot hybridization of polymerase chain reaction (PCR) products obtained after amplification with primers spanning the site of the deletion. We also performed EBV typing, EBER1 in situ hybridization, and LMP1 protein immunohistochemistry. EBV was detected in 12/26 (46%) cases of HD from the US and 26/27 (96%) cases of Brazilian HD. The 30-bp LMP1 gene deletion was observed in 4/12 (33%) cases of EBV-positive HD from US, and 12/26 (46%) cases of Brazilian EBV-positive HD, including 3 cases of type B EBV, as compared with 12/21 (57%) reactive lymphoid tissues and 9/15 (60%) cases of EBV-negative HD. US and Brazilian HD showed a higher prevalence of the 30-bp LMP1 gene deletion, compared with studies of others. The unexpected finding of high incidence of 30-bp deletion in LMP1 gene in reactive lymphoid tissue and HD without EBV-positive Reed-Sternberg cells suggests that this deletion may not be relevant to HD pathogenesis in most cases.
在鼻咽癌和EB病毒（EBV）相关的恶性淋巴瘤中，已报道过EB病毒潜伏膜蛋白1（LMP1）基因存在一个30碱基对（bp）的缺失。先前的研究发现，在约10%至28%的霍奇金淋巴瘤（HD）病例中存在该缺失，尤其是在组织学表现侵袭性的病例中。我们研究了美国（12例）和巴西（26例）EBV阳性HD中30-bp LMP1基因缺失的患病率，并与反应性淋巴组织（21例）和无EBV阳性里德-斯腾伯格细胞的HD（15例）进行比较。我们通过对用跨越缺失位点的引物扩增后获得的聚合酶链反应（PCR）产物进行Southern印迹杂交，来研究LMP1基因的状态。我们还进行了EBV分型、EBER1原位杂交和LMP1蛋白免疫组织化学检测。在美国的12/26（46%）例HD病例和巴西的26/27（96%）例HD病例中检测到了EBV。在美国的4/12（33%）例EBV阳性HD病例和巴西的12/26（46%）例EBV阳性HD病例中观察到了30-bp LMP1基因缺失，其中包括3例B型EBV，与之相比，反应性淋巴组织中有12/21（57%）例，无EBV阳性里德-斯腾伯格细胞的HD中有9/15（60%）例。与其他研究相比，美国和巴西的HD显示出30-bp LMP1基因缺失的患病率更高。在反应性淋巴组织和无EBV阳性里德-斯腾伯格细胞的HD中LMP1基因30-bp缺失的高发生率这一意外发现表明，在大多数情况下，这种缺失可能与HD的发病机制无关。
