The Experts below are selected from a list of 4227 Experts worldwide ranked by ideXlab platform
Xinyuan Liu - One of the best experts on this subject based on the ideXlab platform.
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Oncolytic Adenovirus Complexes Coated with Lipids and Calcium Phosphate for Cancer Gene Therapy.
ACS nano, 2016Co-Authors: Jianhua Chen, Xinyuan Liu, Liang Chu, Pei Gao, Sujing Yuan, Li Ding, Ying Sun, Yourong DuanAbstract:Oncolytic Adenovirus (OncoAd) is a promising therapeutic agent for treating cancer. However, the therapeutic potential of OncoAd is hindered by hepatic sequestration and the host immune response in vivo. Here, we constructed a PEG/Lipids/calcium phosphate (CaP)-OncoAd (PLC-OncoAd) delivery system for ZD55-IL-24, an Oncolytic Adenovirus that carries the IL-24 gene. The negatively charged PLC-ZD55-IL-24 were disperse and resisted serum-induced aggregation. Compared to naked ZD55-IL-24, the systemic administration of PLC-ZD55-IL-24 in BALB/c mice resulted in reduced liver sequestration and systemic toxicity and evaded the innate immune response. In addition, masking the surface of OncoAd protected it from neutralization by pre-existing neutralizing antibody. PLC-OncoAd achieved efficient targeted delivery in Huh-7-bearing nude mice, and intravenous administration of a high dose of PLC-ZD55-IL-24 increased therapeutic efficacy without inducing toxicity. The developed PLC-OncoAd delivery system represents a pr...
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Targeting lung cancer stem-like cells with TRAIL gene armed Oncolytic Adenovirus.
Journal of cellular and molecular medicine, 2015Co-Authors: Yu Yang, Weidan Huang, Miao Ding, Jing Xiao, Dongmei Yang, Xinyuan Liu, Liang ChuAbstract:Lung cancer stem cell (LCSC) is critical in cancer initiation, progression, drug resistance and relapse. Disadvantages showed in conventional lung cancer therapy probably because of its existence. In this study, lung cancer cell line A549 cells propagated as spheroid bodies (named as A549 sphere cells) in growth factors-defined serum-free medium. A549 sphere cells displayed CSC properties, including chemo-resistance, increased proportion of G0/G1 cells, slower proliferation rate, ability of differentiation and enhanced tumour formation ability in vivo. Oncolytic Adenovirus ZD55 carrying EGFP gene, ZD55-EGFP, infected A549 sphere cells and inhibited cell growth. Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) armed Oncolytic Adenovirus, ZD55-TRAIL, exhibited enhanced cytotoxicity and induced A549 sphere cells apoptosis through mitochondrial pathway. Moreover, small molecules embelin, LY294002 and resveratrol improved the cytotoxicity of ZD55-TRAIL. In the A549 sphere cells xenograft models, ZD55-TRAIL significantly inhibited tumour growth and improved survival status of mice. These results suggested that gene armed Oncolytic Adenovirus is a potential approach for lung cancer therapy through targeting LCSCs.
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Tumor suppressor in lung cancer-1 (TSLC1) mediated by dual-regulated Oncolytic Adenovirus exerts specific antitumor actions in a mouse model.
Acta pharmacologica Sinica, 2013Co-Authors: Wen Lei, Xiumei Zhou, Ke-ni Guo, Yu-long Xia, Hong-bin Liu, Shibing Wang, Shui-di Zheng, Wen-song Tan, Xinyuan LiuAbstract:Tumor suppressor in lung cancer-1 (TSLC1) mediated by dual-regulated Oncolytic Adenovirus exerts specific antitumor actions in a mouse model
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Overexpression of tumor suppressor TSLC1 by a survivin-regulated Oncolytic Adenovirus significantly inhibits hepatocellular carcinoma growth.
Journal of cancer research and clinical oncology, 2012Co-Authors: Wen Lei, Xinyuan Liu, Xiumei Zhou, Kang-jian Zhang, Shibin Wang, Ruijuan Xiao, Ke-ni Guo, Yu-long Xia, Yigang WangAbstract:Hepatocellular carcinoma (HCC) is one of the most common malignant tumors worldwide. Oncolytic viruses represent a promising therapeutic agent or vehicle to human cancers due to their ability of selectively lysing cancer cells but not in normal cells. TSLC1, a novel tumor suppressor gene, was loss in many human cancers including HCC, not in normal cells. The current study is focused on the antitumor effect of TSLC1-armed survivin-regulated Oncolytic Adenovirus for HCC and to explore their molecular mechanism. The expression of tumor suppressor TSLC1 and survivin was detected by quantitative PCR. The recombinant virus Ad.SP-E1A-E1B((Delta 55))-TSLC1 (brief name as SD55-TSLC1) was constructed by inserting TSLC1 gene into the dual-regulated Oncolytic Adenovirus vector Ad.SP-E1A-E1B((Delta 55)). Then, we performed the antitumor experiments of SD55-TSLC1 in vitro and in nude mice xenografted with Huh7 liver cancer. The expression of TSLC1 was lower in HCC cells than in normal cells, which implied TSLC1 is a tumor suppressor of liver cancer. Survivin expression is higher in detected HCC cells than in normal cells. The SD55-TSLC1 exhibited an excellent antitumor effect on HCC cell growth in vitro but does no or little damage to normal liver cells. Animal experiment further confirmed that SD55-TSLC1 achieved significant inhibition of Huh7 liver cancer xenografted growth. Furthermore, the mechanism of antitumor efficacy by SD55-TSLC1 was elucidated to be due to the activation of caspase apoptotic pathway including the inducement of caspase-3, caspase-8, and poly (ADP-ribose) polymerase cleavage. This is the first report of TSLC1 by Oncolytic Adenovirus with an excellent antitumor effect to liver cancer growth. These data suggest that an Oncolytic Adenovirus expressing TSLC1 is effective and support that SD55-TSLC1 may be a potent antitumoral agent for future clinical trials of liver cancer.
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The antitumor efficacy of IL-24 mediated by E1A and E1B triple regulated Oncolytic Adenovirus
Cancer biology & therapy, 2010Co-Authors: Lian Li Xiao, Yigang Wang, Kang-jian Zhang, Jing Qian, Yuan Tan, Guo Liang Xie, Xiao Yuan Jia, Xinyuan LiuAbstract:Background: IL-24 (interleukin-24) is a promising, multi-functional anti-cancer agent able to selectively induce tumor cell apoptosis while sparing normal cells. Additionally, IL-24 can enhance the immune response to tumors and suppress tumor angiogenesis. In this study, we introduced IL-24 into the Oncolytic Adenovirus, Ad·sp·E1A(∆24·E1B(∆55)·IL-24. in which E1A was engineered to target Rb (retinoblastoma) deficient or dysfunctional tumors. The survivin promoter (sp), was used to drive expression of IL-24, thereby allowing it to target most tumors. Finally, the 55 KDa gene of E1B was also deleted, thereby preventing replication in normal cells.Results: Ad·sp·E1A(∆24)·E1B(∆55)·IL-24 showed enhanced anti-tumor effects over the E1, singly regulated Oncolytic Adenovirus, ONYX-015, in in vitro experiments. Furthermore, Ad·sp·E1A(∆24)·E1B(∆55)·IL-24 could effectively inhibit the progression of NCI-H460 lung carcinoma xenografts in nude mice. Methods: The antitumor effect of Ad·sp·E1A(∆24)·E1B(∆55)·IL-24 was as...
Ramon Alemany - One of the best experts on this subject based on the ideXlab platform.
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Evolving Status of Clinical Immunotherapy with Oncolytic Adenovirus.
Clinical cancer research : an official journal of the American Association for Cancer Research, 2021Co-Authors: Marti Farrera-sal, Miriam Bazan-peregrino, Laura Moya-borrego, Ramon AlemanyAbstract:Cancer immunotherapy targeting immune checkpoint inhibitors shows efficacy in several human cancers, but "cold tumors" that lack immune cells are typically unresponsive. Among the potential therapeutic approaches that could "heat" or promote lymphocyte infiltration of cold tumors, Oncolytic viruses have attracted interest for their lytic and immunogenic mechanisms of action. Here we review the use of Oncolytic Adenoviruses in cancer immunotherapy, with a particular focus on pre-clinical and clinical data of Oncolytic Adenovirus-triggered immune responses against tumor antigens. We also discuss parameters to consider in clinical trial design and the combination of Oncolytic Adenoviruses with conventional treatments or other immunotherapies.
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Correction: Characterization of the Antiglioma Effect of the Oncolytic Adenovirus VCN-01.
PloS one, 2016Co-Authors: Beatriz Vera, Ramon Alemany, Manel Cascallo, Naiara Martínez-vélez, Enric Xipell, Arlet Acanda De La Rocha, Ana Patiño-garcía, Javier S. Castresana, Marisol Gonzalez-huarriz, Marta M. AlonsoAbstract:The sixth author’s name is misspelled. The correct name is: Javier S. Castresana. The correct citation is: Vera B, Martinez-Velez N, Xipell E, Acanda de la Rocha A, Patino-Garcia A, Castresana JS, et al. (2016) Characterization of the Antiglioma Effect of the Oncolytic Adenovirus VCN-01. PLoS ONE 11(1): e0147211. doi:10.1371/journal.pone.0147211
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662. An Oncolytic Adenovirus Gene Therapy Targeting Both Tumor Cell Survival and Desmoplasia in Pancreatic Cancer
Molecular Therapy, 2016Co-Authors: Ioanna Milenova, Ramon Alemany, Emma Eriksson, Rafael Moreno, Angelica LoskogAbstract:An Oncolytic Adenovirus Gene Therapy Targeting Both Tumor Cell Survival and Desmoplasia in Pancreatic Cancer
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516. A Novel Oncolytic Adenovirus Expressing Tumor Microenvironment Stimulators to Evoke and Facilitate Anti-Tumor Immune Responses
Molecular Therapy, 2016Co-Authors: Jessica Wenthe, Ramon Alemany, Ioanna Milenova, Emma Eriksson, Rafael Moreno, Angelica LoskogAbstract:A Novel Oncolytic Adenovirus Expressing Tumor Microenvironment Stimulators to Evoke and Facilitate Anti-Tumor Immune Responses
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Safety and Efficacy of VCN-01, an Oncolytic Adenovirus Combining Fiber HSG-Binding Domain Replacement with RGD and Hyaluronidase Expression
Clinical cancer research : an official journal of the American Association for Cancer Research, 2014Co-Authors: Alba Rodriguez-garcia, Rafael Moreno, Marta Giménez-alejandre, Juan J. Rojas, Miriam Bazan-peregrino, Manel Cascallo, Ramon AlemanyAbstract:Purpose: Tumor targeting upon intravenous administration and subsequent intratumoral virus dissemination are key features to improve Oncolytic Adenovirus therapy. VCN-01 is a novel Oncolytic Adenovirus that combines selective replication conditional to pRB pathway deregulation, replacement of the heparan sulfate glycosaminoglycan putative-binding site KKTK of the fiber shaft with an integrin-binding motif RGDK for tumor targeting, and expression of hyaluronidase to degrade the extracellular matrix. In this study, we evaluate the safety and efficacy profile of this novel Oncolytic Adenovirus. Experimental Design: VCN-01 replication and potency were assessed in a panel of tumor cell lines. VCN-01 tumor-selective replication was evaluated in human fibroblasts and pancreatic islets. Preclinical toxicity, biodistribution, and efficacy studies were conducted in mice and Syrian hamsters. Results: Toxicity and biodistribution preclinical studies support the selectivity and safety of VCN-01. Antitumor activity after intravenous or intratumoral administration of the virus was observed in all tumor models tested, including melanoma and pancreatic adenocarcinoma, both in immunodeficient mice and immunocompetent hamsters. Conclusions: Oncolytic Adenovirus VCN-01 characterized by the expression of hyaluronidase and the RGD shaft retargeting ligand shows an efficacy–toxicity prolife in mice and hamsters by intravenous and intratumoral administration that warrants clinical testing. Clin Cancer Res; 21(6); 1406–18. ©2014 AACR .
Yigang Wang - One of the best experts on this subject based on the ideXlab platform.
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A novel Golgi protein (GOLPH2)-regulated Oncolytic Adenovirus exhibits potent antitumor efficacy in hepatocellular carcinoma.
Oncotarget, 2015Co-Authors: Yigang Wang, Tao Liu, Huang Panpan, Hongfang Zhao, Rong Zhang, Kan Chen, Fang Huang, Xiumei Zhou, Caixia CuiAbstract:// Yigang Wang 1 , Tao Liu 1, * , Panpan Huang 1, * , Hongfang Zhao 1 , Rong Zhang 1 , Buyun Ma 1 , Kan Chen 1 , Fang Huang 4 , Xiumei Zhou 1 , Caixia Cui 3 , Xinyuan Liu 1, 2 1 Xinyuan Institute of Medicine and Biotechnology, School of Life Sciences, Zhejiang Sci-Tech University, Hangzhou 310018, PR China 2 Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, PR China 3 Otorhinolaryngology Head and Neck Surgery, The Affiliated Hospital of Hangzhou Normal University, Hangzhou 310015, PR China 4 School of Public Health, Zhejiang University, Hangzhou 310058, China * These authors have contributed equally to this work Correspondence to: Yigang Wang, e-mail: wangyigang43@163.com Xinyuan Liu, e-mail: xyliu@sibs.ac.cn Keywords: GOLPH2, hepatocellular carcinoma, Oncolytic Adenovirus, anticancer capacity Received: February 10, 2015 Accepted: April 10, 2015 Published: April 23, 2015 ABSTRACT Golgi apparatus is the organelle mainly functioning as protein processing and secretion. GOLPH2 is a resident Golgi glycoprotein, usually called GP73. Recent data displayed that GOLPH2 is a superb hepatocellular carcinoma (HCC) marker candidate, and even its specificity is better than liver cancer marker AFP. Oncolytic Adenoviruses are broadly used for targeting cancer therapy due to their selective tumor-killing effect. However, it was reported that traditionally Oncolytic Adenovirus lack the HCC specificity. In this study, a novel dual-regulated Oncolytic Adenovirus GD55 targeting HCC was first constructed based on our cancer targeted gene-viral therapeutic strategy. To verify the targeting and effectiveness of GOLPH2-regulated Oncolytic Adenovirus GD55 in HCC, the anticancer capacity was investigated in HCC cell lines and animal model. The results proved that the novel GOLPH2-regulated GD55 conferred higher Adenovirus replication and infectivity for liver cancer cells than Oncolytic Adenovirus ZD55. The GOLPH2-regulated GD55 exerted a significant grow-suppressing effect on HCC cells in vitro but little damage to normal liver cells. In animal experiment, antitumor effect of GD55 was more effective in HCC xenograft of nude mice than that of ZD55. Thus GOLPH2-regulated GD55 may be a promising Oncolytic virus agent for future liver cancer treatment.
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Overexpression of tumor suppressor TSLC1 by a survivin-regulated Oncolytic Adenovirus significantly inhibits hepatocellular carcinoma growth.
Journal of cancer research and clinical oncology, 2012Co-Authors: Wen Lei, Xinyuan Liu, Xiumei Zhou, Kang-jian Zhang, Shibin Wang, Ruijuan Xiao, Ke-ni Guo, Yu-long Xia, Yigang WangAbstract:Hepatocellular carcinoma (HCC) is one of the most common malignant tumors worldwide. Oncolytic viruses represent a promising therapeutic agent or vehicle to human cancers due to their ability of selectively lysing cancer cells but not in normal cells. TSLC1, a novel tumor suppressor gene, was loss in many human cancers including HCC, not in normal cells. The current study is focused on the antitumor effect of TSLC1-armed survivin-regulated Oncolytic Adenovirus for HCC and to explore their molecular mechanism. The expression of tumor suppressor TSLC1 and survivin was detected by quantitative PCR. The recombinant virus Ad.SP-E1A-E1B((Delta 55))-TSLC1 (brief name as SD55-TSLC1) was constructed by inserting TSLC1 gene into the dual-regulated Oncolytic Adenovirus vector Ad.SP-E1A-E1B((Delta 55)). Then, we performed the antitumor experiments of SD55-TSLC1 in vitro and in nude mice xenografted with Huh7 liver cancer. The expression of TSLC1 was lower in HCC cells than in normal cells, which implied TSLC1 is a tumor suppressor of liver cancer. Survivin expression is higher in detected HCC cells than in normal cells. The SD55-TSLC1 exhibited an excellent antitumor effect on HCC cell growth in vitro but does no or little damage to normal liver cells. Animal experiment further confirmed that SD55-TSLC1 achieved significant inhibition of Huh7 liver cancer xenografted growth. Furthermore, the mechanism of antitumor efficacy by SD55-TSLC1 was elucidated to be due to the activation of caspase apoptotic pathway including the inducement of caspase-3, caspase-8, and poly (ADP-ribose) polymerase cleavage. This is the first report of TSLC1 by Oncolytic Adenovirus with an excellent antitumor effect to liver cancer growth. These data suggest that an Oncolytic Adenovirus expressing TSLC1 is effective and support that SD55-TSLC1 may be a potent antitumoral agent for future clinical trials of liver cancer.
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The antitumor efficacy of IL-24 mediated by E1A and E1B triple regulated Oncolytic Adenovirus
Cancer biology & therapy, 2010Co-Authors: Lian Li Xiao, Yigang Wang, Kang-jian Zhang, Jing Qian, Yuan Tan, Guo Liang Xie, Xiao Yuan Jia, Xinyuan LiuAbstract:Background: IL-24 (interleukin-24) is a promising, multi-functional anti-cancer agent able to selectively induce tumor cell apoptosis while sparing normal cells. Additionally, IL-24 can enhance the immune response to tumors and suppress tumor angiogenesis. In this study, we introduced IL-24 into the Oncolytic Adenovirus, Ad·sp·E1A(∆24·E1B(∆55)·IL-24. in which E1A was engineered to target Rb (retinoblastoma) deficient or dysfunctional tumors. The survivin promoter (sp), was used to drive expression of IL-24, thereby allowing it to target most tumors. Finally, the 55 KDa gene of E1B was also deleted, thereby preventing replication in normal cells.Results: Ad·sp·E1A(∆24)·E1B(∆55)·IL-24 showed enhanced anti-tumor effects over the E1, singly regulated Oncolytic Adenovirus, ONYX-015, in in vitro experiments. Furthermore, Ad·sp·E1A(∆24)·E1B(∆55)·IL-24 could effectively inhibit the progression of NCI-H460 lung carcinoma xenografts in nude mice. Methods: The antitumor effect of Ad·sp·E1A(∆24)·E1B(∆55)·IL-24 was as...
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Enhancement of tumor cell death by combining cisplatin with an Oncolytic Adenovirus carrying MDA-7/IL-24
Acta pharmacologica Sinica, 2009Co-Authors: Kang-jian Zhang, Xue-tian Yue, Yi-qiang Wang, Yi Yang, Yigang WangAbstract:Enhancement of tumor cell death by combining cisplatin with an Oncolytic Adenovirus carrying MDA-7/IL-24
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Potent antitumor activity of double‐regulated Oncolytic Adenovirus‐mediated ST13 for colorectal cancer
Cancer science, 2009Co-Authors: De Bin Yu, Yigang Wang, Su Yang Zhong, Min Yang, Qi Jun Qian, Shu Zheng, Xinyuan LiuAbstract:Following targeted gene virotherapy, the suppression of tumorigenicity 13 (ST13) gene was inserted into the double-regulated Oncolytic Adenovirus SG500 to ensure more safety and potent antitumor activity against colorectal cancer in vitro and in vivo. We generated the ST13-expressing Oncolytic Adenovirus SG500-ST13, with which colorectal carcinoma cell lines SW620 and HCT116, and the lung fibroblast cell line WI38, were infected. Crystal violet staining was carried out to detect the cytopathic effect in cells, and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method was used to assay cell viability. The effect of apoptosis induced by SG500-ST13 was confirmed by Hoechst staining and the TdT-mediated dUTP-biotin nick-end labeling method. To further identify the antitumor effects of SG500-ST13 on HCT116 xenografts in Balb/c nude mice, the induction of cell death was assessed by hematoxylin-eosin staining. Immunohistochemical study was also carried out.
Naoto Endo - One of the best experts on this subject based on the ideXlab platform.
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Efficient virotherapy for osteosarcoma by telomerase-specific Oncolytic Adenovirus
Journal of cancer research and clinical oncology, 2010Co-Authors: Hiroyuki Kawashima, Toshiyoshi Fujiwara, Akira Ogose, Takashi Ariizumi, Tetsuo Hotta, Yasuo Urata, Naoto EndoAbstract:Purpose A telomerase-specific Oncolytic Adenovirus, Telomelysin, can selectively kill cancer cells, and be attenuated in normal cells. We herein describe the Oncolytic effect of Telomelysin on human osteosarcoma both in vitro and in vivo.
Cheng Qian - One of the best experts on this subject based on the ideXlab platform.
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Targeting eradication of chronic myeloid leukemia using chimeric Oncolytic Adenovirus to drive IL-24 expression.
International journal of clinical and experimental pathology, 2015Co-Authors: Xubin Wei, Li Liu, Gang Wang, Cheng Qian, Jimin ShaoAbstract:Chronic myeloid leukemia (CML) is a clonal disorder in which cells of the myeloid lineage undergo massive clonal expansion as well as resistance to conventional chemotherapy. Gene therapy hold a great promise for treatment of malignancies based on the transfer of genetic material to the tissues. In this study, we explore whether chimeric Oncolytic Adenovirus-mediated transfer of human interleukin-24 (IL-24) gene induce the enhanced antitumor potency. Our results showed that chimeric Oncolytic Adenovirus carrying hIL-24 (AdCN205-11-IL-24) could produce high levels of hIL-24 in CML cancer cells, as compared with constructed double-regulated Oncolytic Adenovirus expressing hIL-24 (AdCN205-IL-24). AdCN205-11-IL-24 could specifically induce cytotoxocity to CML cancer cells, but little or no effect on normal cell lines. AdCN205-11-IL-24 exhibited remarkable anti-tumor activities and induce higher antitumor activity to CML cancer cells by inducing apoptosis in vitro. Our study may provides a potent and safe tool for CML gene therapy.
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136. The Oncolytic Adenovirus Targeting to TERT and Rb Pathway Induced Specific Cytotoxicity to Tumor Cells
Molecular Therapy, 2006Co-Authors: Rong Cai, Xinyuan Liu, Aiwen Dong, Wei Zhang, Kai Chen, Songbo Qiu, Cheng QianAbstract:Overexpression of human telomerase reverse transcriptase (hTERT) and dysfunction of retinoblastoma (Rb) have been implicated in the most types of malignancies. Oncolytic viruses have been used widely for therapy of cancers. In order to develop specific recombinant Adenovirus with strict tumor specificity, we engineered Oncolytic Adenovirus to target both of TERT and Rb pathways. The CR2 region of adenoviral E1a protein interacts with Rb and allows virus replication. Therefore, we have constructed double-controlled recombinant Adenovirus with CR2 deleted E1a driven by hTERT promoter (AdTC). As control vectors, we generated single-controlled recombinant Adenovirus with either CR2 deleted E1a (AdC) or wild-type of E1a driven by hTERT promoter (AdT). Firstly, different length and modification of hTERT promoter have been studied to find out the appropriated hTERT promoter with better tumor specificity. With this modified hTERT promoter, we found that double-controlled Oncolytic Adenovirus AdTC has strictly tumor-specific cytotoxicity, as compared with single-controlled Oncolytic Adenoviruses of either AdC or AdT. This cytotoxicity was observed in the different types of tumor cells. There was dramatic reduction of cytotoxicity in normal cell infected with AdTC. Production of viral particles in tumor cells infected with AdTC as measured by progeny assay was similar as cells infected either with AdC or AdT. This dada indicated that Oncolytic Adenovirus to target both of TERT and Rb pathways provides safe and potent vector for therapy cancers.
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A novel Oncolytic Adenovirus targeting to telomerase activity in tumor cells with potent
Oncogene, 2004Co-Authors: Weiguo Zou, Cheng Qian, Zilai Zhang, Chun-xia Luo, Jing Liu, Zifei Pei, Xinyuan LiuAbstract:Telomerase is a therapeutic target for cancer. Human telomerase reverse transcriptase (hTERT), the catalytic subunit of the telomerase, is transcriptionaly upregulated exclusively in about 90% of cancer cells. Previous studies have demonstrated that hTERT promoter can control the expression of exogenous genes to the telomerase-positive cancer cells, thus hTERT promoter is an excellent candidate for generating cancer-specific Oncolytic Adenovirus. In this study, we devised a novel Oncolytic Adenovirus (Ad.TERT) by replacing the normal E1A regulatory elements with hTERT promoter. Ad.TERT displays cancer-specific E1A expression, virus replication and cytolysis in in vitro experiments. In animal experiments, intratumoral administration of Ad.TERT demonstrates potent antitumoral efficacy at least in two xenograft models (Bcap37 and BEL7404). Ad.TERT was targeted by the telomerase activity in cancer cells and has potent antitumoral efficacy in vivo, and since telomerase activity is a wide-ranged tumor marker, Ad.TERT could be a powerful therapeutic agent for a variety of cancers.
