生物
BK病毒
癌变
移植
梅克尔多元癌细胞病毒
癌症
癌症研究
基因
人病毒体
多瘤病毒感染
肿瘤病毒
基因组
病毒学
病毒
梅克尔细胞癌
癌
遗传学
肾
肾移植
外科
医学
作者
Yuchen Wang,Yanna Liu,Wen-feng Deng,Fangxiang Fu,Susha Yan,Hongwei Yang,Rumin Liu,Jiao Geng,Jian Xu,Yihan Wu,Junfeng Ma,Jun Zhou,Na Liu,Yu Jin,Renfei Xia,Nahel Elias,Richard J. Lee,Adam S. Feldman,Michael L. Blute,Robert B. Colvin,Chin‐Lee Wu,Yun Miao
出处
期刊:Oncogene
[Springer Nature]
日期:2020-07-28
卷期号:39 (35): 5734-5742
被引量:16
标识
DOI:10.1038/s41388-020-01398-6
摘要
BK polyomavirus (BKPyV)-associated cancer after transplantation has gained increasing attention. However, the role of BKPyV integration on oncogenesis is still unclear. In this study, next-generation virome capture sequencing of primary and metastatic tumors were performed in three patients with BKPyV-associated urothelial carcinoma after renal transplantation. As a result, a total of 332 viral integration sites were identified in the six tumors. Integration of BKPyV in both primary and metastatic tumors followed the mechanism of microhomology-mediated end joining mostly, since microhomologies between human and BKPyV genomes were significantly enriched in flanking regions of 84% of the integration sites. Viral DNA breakpoints were nonrandom and tended to assemble in large T gene, small T gene and viral protein 2 gene. There were three, one and one consensus integration sites between the primary and metastatic tumors, which affected LINC01924, eIF3c, and NEIL2 genes in the three cases respectively. Thus, we concluded that integration of BKPyV was a continuous process occurring in both primary and metastatic tumors, generating heterogenous tumor cell populations. Through this ongoing process, certain cell populations might have gained growth advantage or metastatic potential, as a result of viral integration either affecting the cellular genes where the viral DNA integrated to or altering the expression or function of the viral genes.
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