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巨细胞病毒是唾液腺肿瘤的诱因之一

2011/11/17 来源:Biologynews
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南加州大学遗传发育实验室的一项重要新研究证实:巨细胞病毒(CMV)是最常见唾液腺肿瘤的诱因之一。CMV列在已识别致癌病毒组成的病毒库中,它们的数量不超过10个,其中包括HPV。

南加州大学遗传发育实验室的一项重要新研究证实:巨细胞病毒(CMV)是最常见唾液腺肿瘤的诱因之一。CMV列在已识别致癌病毒组成的病毒库中,它们的数量不超过10个,其中包括HPV。

这项研究发表在《实验和分子病理学》(Experimental and Molecular Pathology)期刊上,它是由南加州大学研究人员开展的一系列研究中的最新进展。研究人员揭示了诱癌病毒CMV的功能:既能诱导健康细胞癌变,又能“开采”突变细胞的缺陷,以促使肿瘤的形成。

南加州大学奥斯特鲁夫牙科学院的遗传发育教授Michael Melnick 称:“CMV是一种诱癌基因,这一结论是在对人类唾液腺瘤和产后小鼠唾液腺两者的严格研究后做出的。”

CMV作为诱癌病毒的分类对人类健康具有重要的提醒意义。这一病毒广泛地分布在人体中,能引起免疫系统受损病人的严重疾病和死亡。当女性怀孕时,如果首次接触CMV很有可能导致胎儿缺陷。Melnick 补充道:“CMV也可能引起除唾液腺瘤之外的其它肿瘤。”

“CMV广泛存在简直令人难以置信;大多数人很可能携带这种病毒,只因为我们接触过它。”他说,“在免疫系统正常的携带者中,这一病毒保持休眠状态并驻守在唾液腺上,没有人知道什么因素能重新激活它。”

这项研究不仅表明CMV在肿瘤细胞是活跃的,还发现分泌病毒蛋白的量与肿瘤恶性程度的关联性强。

研究小组不仅发现CMV关联于粘液表皮样瘤和最常见的唾液腺瘤,还识别出特定的分子信号途径,CMV能借助该途径诱导肿瘤。Melnick 称:“通常情况下,这一途径只有在胚胎生长发育过程中激活,但是,当CMV干扰该途径时,恶性肿瘤由此产生,并合成越来越多的CMV病毒。”(生物探索译)

相关英文论文摘要:

Human Cytomegalovirus and Mucoepidermoid Carcinoma of Salivary Glands: Cell-Specific Localization of Active Viral and Oncogenic Signaling Proteins is Confirmatory of a Causal Relationship

Human cytomegalovirus (hCMV) infection is common. Although still controversial, there is growing evidence that active hCMV infection is associated with a variety of malignancies, including brain, breast, lung, colon, and prostate. Given that hCMV is frequently resident in salivary gland (SG) ductal epithelium, we hypothesized that hCMV would be important to the pathogenesis of SG mucoepidermoid carcinoma (MEC). This was initially supported by our finding that purified CMV induces malignant transformation in SG cells in an in vitro mouse model, and utilizes a pathogenic pathway previously reported for human MEC. Here we present the histologic and molecular characterization of 39 human SG MECs selected randomly from a repository of cases spanning 2004–2011. Serial sections were obtained from formalin-fixed, paraffin embedded, tissue blocks from previous incisional or excisional biopsies. Immunohistochemical assays were performed for active hCMV proteins (IE1 and pp65) and the activated COX/AREG/EGFR/ERK signaling pathway. All four prospective causal criteria for viruses and cancer are fully satisfied: (1) protein markers for active hCMV are present in 97% of MECs; (2) markers of active hCMV are absent in non-neoplastic SG tissues; (3) hCMV-specific proteins (IE1, pp65) are in specific cell types and expression is positively correlated with severity; (4) hCMV correlates and colocalizes with an upregulation and activation of an established oncogenic signaling pathway (COX/AREG/EGFR/ERK). Thus, the evidential support reported here and previously in a mouse model is strongly confirmatory of a causal relationship between hCMV and SG mucoepidermoid carcinoma. To our knowledge, this is the first demonstration of hCMV's role in human oncogenesis that fully responds to all of Koch's Postulates as revised for viruses and cancer. In the absence of any contrary evidence, hCMV can reasonably be designated an “oncovirus.”

英文论文链接: http://www.sciencedirect.com/science/article/pii/S0014480011001869

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