The emergence of combinatorial strategies in the development of RNA oncolytic virus therapies

被引:25
作者
Nguyen, Thi Lien-Anh [1 ,2 ]
Tumilasci, Vanessa Fonseca [1 ,2 ]
Singhroy, Diane [1 ,2 ]
Arguello, Meztli [1 ]
Hiscott, John [1 ,2 ,3 ]
机构
[1] Jewish Gen Hosp, Terry Fox Mol Oncol Grp, Lady Davis Inst, Montreal, PQ H3T 1E2, Canada
[2] McGill Univ, Dept Microbiol & Immunol, Montreal, PQ, Canada
[3] McGill Univ, Dept Med, Montreal, PQ, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
VESICULAR STOMATITIS-VIRUS; NEWCASTLE-DISEASE-VIRUS; HISTONE DEACETYLASE INHIBITORS; SEMLIKI-FOREST-VIRUS; T-CELL THERAPY; CHRONIC LYMPHOCYTIC-LEUKEMIA; TUMOR SELECTIVE REPLICATION; INNATE ANTIVIRAL RESPONSE; SINDBIS VIRAL VECTORS; HERPES-SIMPLEX-VIRUS;
D O I
10.1111/j.1462-5822.2009.01317.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Oncolytic viruses (OVs) represent an exciting new biological approach to cancer therapy. In particular, RNA viruses have emerged as potent agents for oncolytic virotherapy because of their capacity to specifically target and destroy tumour cells while sparing normal cells and tissues. Several barriers remain in the development of OV therapy, including poor penetration into the tumour mass, inefficient virus replication in primary cancers, and tumour-specific resistance to OV-mediated killing. The combination of OVs with cytotoxic agents, such as small molecule inhibitors of signalling or immunomodulators, as well as stealth delivery of therapeutic viruses have shown promise as novel experimental strategies to overcome resistance to viral oncolysis. These agents complement OV therapy by unblocking host pathways, delivering viruses with greater efficiency and/or increasing virus proliferation at the tumour site. In this review, we summarize recent development of these concepts, the potential obstacles, and future prospects for the clinical utilization of RNA OVs in cancer therapy.
引用
收藏
页码:889 / 897
页数:9
相关论文
共 90 条
[1]   Oncolytic viral therapies - the clinical experience [J].
Aghi, M ;
Martuza, RL .
ONCOGENE, 2005, 24 (52) :7802-7816
[2]   Defective translational control facilitates vesicular stomatitis virus oncolysis [J].
Balachandran, S ;
Barber, GN .
CANCER CELL, 2004, 5 (01) :51-65
[3]   Vesicular stomatitis virus (VSV) therapy of tumors [J].
Balachandran, S ;
Barber, GN .
IUBMB LIFE, 2000, 50 (02) :135-138
[4]   VSV-tumor selective replication and protein translation [J].
Barber, GN .
ONCOGENE, 2005, 24 (52) :7710-7719
[5]  
Bergmann M, 2001, CANCER RES, V61, P8188
[6]   Novel three-pronged strategy to enhance cancer cell killing in glioblastoma cell lines:: Histone deacetylase inhibitor, chemotherapy, and oncolytic adenovirus dl520 [J].
Bieler, A ;
Mantwill, K ;
Dravits, T ;
Bernshausen, A ;
Glockzin, G ;
Köhler-Vargas, N ;
Lage, H ;
Gansbacher, B ;
Holm, PS .
HUMAN GENE THERAPY, 2006, 17 (01) :55-70
[7]   Early Steps of the Virus Replication Cycle Are Inhibited in Prostate Cancer Cells Resistant to Oncolytic Vesicular Stomatitis Virus [J].
Carey, Brooke L. ;
Ahmed, Maryam ;
Puckett, Shelby ;
Lyles, Douglas S. .
JOURNAL OF VIROLOGY, 2008, 82 (24) :12104-12115
[8]   Reprogrammed viruses as cancer therapeutics: targeted, armed and shielded [J].
Cattaneo, Roberto ;
Miest, Tanner ;
Shashkova, Elena V. ;
Barry, Michael A. .
NATURE REVIEWS MICROBIOLOGY, 2008, 6 (07) :529-540
[9]   Bcl-2 overexpression enhances tumor-specific T-cell survival [J].
Charo, J ;
Finkelstein, SE ;
Grewal, N ;
Restifo, NP ;
Robbins, PF ;
Rosenberg, SA .
CANCER RESEARCH, 2005, 65 (05) :2001-2008
[10]   Reovirus therapy of tumors with activated Ras pathway [J].
Coffey, MC ;
Strong, JE ;
Forsyth, PA ;
Lee, PWK .
SCIENCE, 1998, 282 (5392) :1332-1334