欢欣鼓舞一下:据中新网,广州中山大学发现逆天病毒,专杀癌细胞对正常细胞无害

【广州中山大学发现逆天病毒，专杀癌细胞对正常细胞无害！[震惊]】据中新网，广东中山大学医学院研究发现，一种被称为“天然病毒M1”的病毒，能选择性地感染并杀伤肝癌、结直肠癌、膀胱癌、黑色素瘤等多种体外培养的癌细胞，但对正常细胞却没有毒副作用！据悉，课题组已在动物身上证实了该病毒的效力！

论文链接:
http://m.pnas.org/content/early/2014/10/02/1408759111.abstract

Identification and characterization of alphavirus M1 as a selective oncolytic virus targeting ZAP-defective human cancers

 Authors  Yuan Lin

Significance

Although oncolytic virotherapy is showing great promise in clinical trials, not all patients are benefiting. Identifying predictors of therapeutic effectiveness for each oncolytic virus would provide a good chance to increase response rate. Here, we describe an alphavirus (M1) that possesses selective and potent antitumor activity through intravenous infusion, whereas its replication is controlled by the zinc-finger antiviral protein (ZAP) gene. A survey of cancer tissue banks reveals that ZAP is commonly deficient in human cancers, suggesting extensive application prospects of M1. Our work provides an example of a potentially personalized cancer therapy using a targeted oncolytic virus that can be selectively administered to patients with ZAP-deficient tumors. We predict that such agents will form the armamentarium of cancer therapy in the future.

Abstract

Oncolytic virotherapy is a growing treatment modality that uses replicating viruses as selective antineoplastic agents. Safety and efficacy considerations dictate that an ideal oncolytic agent would discriminate between normal and cancer cells on the basis of common genetic abnormalities in human cancers. Here, we identify a naturally occurring alphavirus (M1) as a novel selective killer targeting zinc-finger antiviral protein (ZAP)-deficient cancer cells. In vitro, in vivo, and ex vivo studies showed potent oncolytic efficacy and high tumor tropism of M1. We showed that the selectivity depends on ZAP deficiency by systematic identification. A large-scale multicenter pathology study using tissue microarrays reveals that ZAP is commonly deficient in human cancers, suggesting extensive application prospects for M1. Additionally, M1 killed cancer cells by inducing endoplasmic reticulum stress-mediated apoptosis. Our report provides novel insights into potentially personalized cancer therapy using oncolytic viruses.