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在对 3 个黑色素瘤转移灶的全长转录组测序中,未发现病毒基因组的证据。

No evidence of viral genomes in whole-transcriptome sequencing of three melanoma metastases.

出版信息

Exp Dermatol. 2011 Sep;20(9):766-8. doi: 10.1111/j.1600-0625.2011.01312.x. Epub 2011 Jun 14.

Abstract

Several viruses are known to cause cancer, such as human herpes virus 8 in Kaposi sarcoma and human papilloma viruses in cervical cancer. Recently, Merkel cell polyoma virus (MCPyV) has been described in 80% of Merkel cell carcinomas (MCC). Similarly to MCC and Kaposi sarcoma, melanoma incidence is increased in immunosuppressed patients. We asked whether infection by known or yet unknown viruses may play a role in melanoma development as well. To detect viral sequences expressed in melanoma cells, we analysed three melanoma metastases by whole-transcriptome sequencing and digital transcriptome subtraction. None of the samples investigated harboured viral sequences. In contrast, artificial viral sequences and MCPyV transcripts used as a positive control for the bioinformatics analysis were detected. This renders it less likely that viruses are frequently involved in melanoma induction. A larger number of melanoma transcriptome sequencings are required to rule out viruses as a relevant pathogen.

摘要

已知有几种病毒可导致癌症,例如卡波西肉瘤中的人类疱疹病毒 8 和宫颈癌中的人乳头瘤病毒。最近,Merkel 细胞多瘤病毒(MCPyV)已在 80%的 Merkel 细胞癌(MCC)中被描述。与 MCC 和卡波西肉瘤类似,免疫抑制患者的黑色素瘤发病率增加。我们想知道已知或未知的病毒感染是否也可能在黑色素瘤的发展中起作用。为了检测黑色素瘤细胞中表达的病毒序列,我们通过全转录组测序和数字转录组消减分析了三个黑色素瘤转移灶。未检测到研究样本中存在病毒序列。相比之下,用作生物信息学分析阳性对照的人工病毒序列和 MCPyV 转录本被检测到。这使得病毒频繁参与黑色素瘤诱导的可能性降低。需要更多的黑色素瘤转录组测序来排除病毒作为相关病原体的可能性。

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