Oncolytic Virotherapy最新文献

{"title":"Oncolytic virus delivery: from nano-pharmacodynamics to enhanced oncolytic effect.","authors":"Raquel Yokoda,&nbsp;Bolni M Nagalo,&nbsp;Brent Vernon,&nbsp;Rahmi Oklu,&nbsp;Hassan Albadawi,&nbsp;Thomas T DeLeon,&nbsp;Yumei Zhou,&nbsp;Jan B Egan,&nbsp;Dan G Duda,&nbsp;Mitesh J Borad","doi":"10.2147/OV.S145262","DOIUrl":"https://doi.org/10.2147/OV.S145262","url":null,"abstract":"<p><p>With the advancement of a growing number of oncolytic viruses (OVs) to clinical development, drug delivery is becoming an important barrier to overcome for optimal therapeutic benefits. Host immunity, tumor microenvironment and abnormal vascularity contribute to inefficient vector delivery. A number of novel approaches for enhanced OV delivery are under evaluation, including use of nanoparticles, immunomodulatory agents and complex viral-particle ligands along with manipulations of the tumor microenvironment. This field of OV delivery has quickly evolved to bioengineering of complex nanoparticles that could be deposited within the tumor using minimal invasive image-guided delivery. Some of the strategies include ultrasound (US)-mediated cavitation-enhanced extravasation, magnetic viral complexes delivery, image-guided infusions with focused US and targeting photodynamic virotherapy. In addition, strategies that modulate tumor microenvironment to decrease extracellular matrix deposition and increase viral propagation are being used to improve tumor penetration by OVs. Some involve modification of the viral genome to enhance their tumoral penetration potential. Here, we highlight the barriers to oncolytic viral delivery, and discuss the challenges to improving it and the perspectives of establishing new modes of active delivery to achieve enhanced oncolytic effects.</p>","PeriodicalId":19491,"journal":{"name":"Oncolytic Virotherapy","volume":"6 ","pages":"39-49"},"PeriodicalIF":6.7,"publicationDate":"2017-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/OV.S145262","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35292488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Curative effect of HF10 on liver and peritoneal metastasis mediated by host antitumor immunity.","authors":"Yoshihiro Hotta,&nbsp;Hideki Kasuya,&nbsp;Itzel Bustos,&nbsp;Yoshinori Naoe,&nbsp;Toru Ichinose,&nbsp;Maki Tanaka,&nbsp;Yasuhiro Kodera","doi":"10.2147/OV.S127179","DOIUrl":"https://doi.org/10.2147/OV.S127179","url":null,"abstract":"<p><strong>Background: </strong>HF10 is a highly attenuated type 1 herpes simplex virus (HSV) with proven effective oncolytic effect. Previous investigations have demonstrated that colon cancer mice model treated with HF10 not only had better survival but were also resistant to the reimplantation of the antitumor effect mediated by host antitumor immunity. Importantly, it has also been noted that in mice with antitumors implanted on both sides of the back, an injection of HF10 on only one side strongly restrains not only the injected antitumor but also the non-injected ones.</p><p><strong>Materials and methods: </strong>MC26 colon cancer cells were injected subcutaneously into the back, spleen, and intraperitoneal region of metastasis model mice. Antitumor volume and survival rate were monitored. To measure cytotoxic T lymphocytes (CTL) cytotoxicity against MC26, lymphocytes were extracted from the spleens of the peritoneal metastasis model mice as well as from the thymus of the liver metastasis model mice. The expression of interferon gamma was examined by enzyme-linked immunospot assay. Samples from the liver metastasis model mice were subjected to polymerase chain reaction to quantify the level of HSV genomes.</p><p><strong>Results: </strong>HF10 was injected only on the back antitumor; however, a antitumor-suppressor effect was observed against liver and peritoneal metastases. When HF10 genome was measured, we observed lower genome on liver metastases compared to back antitumor genome quantity. CTL activity against MC26 was also observed. These results indicate that local administration of HF10 exerts a curative effect on systemic disease, mediated by host antitumor immunity.</p><p><strong>Conclusion: </strong>HF10 local administration stimulates antitumor immunity to recognize antitumor-specific antigen, which then improves systemic disease. Metastatic antitumors lysis, on the other hand, appears to be mediated by the host immune system, rather than by virus-mediated direct oncolysis.</p>","PeriodicalId":19491,"journal":{"name":"Oncolytic Virotherapy","volume":"6 ","pages":"31-38"},"PeriodicalIF":6.7,"publicationDate":"2017-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/OV.S127179","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34845629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proinflammatory response induced by Newcastle disease virus in tumor and normal cells.","authors":"Teridah Ernala Ginting,&nbsp;Jeremiah Suryatenggara,&nbsp;Salomo Christian,&nbsp;George Mathew","doi":"10.2147/OV.S123292","DOIUrl":"https://doi.org/10.2147/OV.S123292","url":null,"abstract":"<p><strong>Purpose: </strong>To investigate the specific role of immune responses induced by lentogenic Newcastle disease virus (NDV) for its antitumor effect.</p><p><strong>Materials and methods: </strong>NDV LaSota strain was used to infect the following human cells: non-small cell lung carcinoma (A549), glioblastoma (U87MG and T98G), mammary gland adenocarcinoma (MCF7 and MDA-MB-453), hepatocellular carcinoma (Huh7), transformed embryonic kidney cells (HEK293), primary monocytes, lung fibroblast (HF19), skin fibroblast (NB1RGB) and rat astroglia (RCR-1) at 0.001 multiplicity of infection. NDV-induced cytotoxicity and expression of proinflammatory cytokines were analyzed using 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide assay and multiplex enzyme-linked immunosorbent assay, respectively.</p><p><strong>Results: </strong>Tumor cells (A549, U87MG, T98G, Huh7, MDA-MB-453, and MCF7) showed viability of <44%, while normal cell lines HEK293, NB1RGB, and RCR-1 showed 84%, 73%, and 69% viability at 72 hours postinfection, respectively. Proinflammatory cytokine profiling showed that NDV mainly induced the secretion of interferon (IFN)-α, IFN-β, and IFN-λ in tumor cells and only IFN-λ in normal cells. In addition, NDV infection induced the production of interleukin (IL)-6 in most cells.</p><p><strong>Conclusion: </strong>Our findings suggest a new perspective regarding the role of IFN-λ and IL-6 in the mechanism of tumor selectivity and oncolysis of NDV.</p>","PeriodicalId":19491,"journal":{"name":"Oncolytic Virotherapy","volume":"6 ","pages":"21-30"},"PeriodicalIF":6.7,"publicationDate":"2017-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/OV.S123292","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34812148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial announcing PubMed indexing of <i>Oncolytic Virotherapy</i>.","authors":"Faris Farassati","doi":"10.2147/OV.S128720","DOIUrl":"https://doi.org/10.2147/OV.S128720","url":null,"abstract":"php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). Oncolytic Virotherapy 2017:6 19–20 Oncolytic Virotherapy Dovepress","PeriodicalId":19491,"journal":{"name":"Oncolytic Virotherapy","volume":"6 ","pages":"19-20"},"PeriodicalIF":6.7,"publicationDate":"2017-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/OV.S128720","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34769541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oncolytic virotherapy including Rigvir and standard therapies in malignant melanoma","authors":"H. Babiker, I. Riaz, M. Husnain, M. Borad","doi":"10.2147/OV.S100072","DOIUrl":"https://doi.org/10.2147/OV.S100072","url":null,"abstract":"The treatment of metastatic melanoma has evolved from an era where interferon and chemotherapy were the mainstay of treatments to an era where immunotherapy has become the frontline. Ipilimumab (IgG1 CTLA-4 inhibitor), nivolumab (IgG4 PD-1 inhibitor), pembrolizumab (IgG4 PD-1 inhibitor) and nivolumab combined with ipilimumab have become first-line therapies in patients with metastatic melanoma. In addition, the high prevalence of BRAF mutations in melanoma has led to the discovery and approval of targeted molecules, such as vemurafenib (BRAF kinase inhibitor) and trametinib (MEK inhibitor), as they yielded improved responses and survival in malignant melanoma patients. This is certainly a burgeoning time in immunotherapy drug development, and the aforementioned efforts along with the recent US Food and Drug Administration approval of talimogene laherparepvec (T-VEC), a recombinant oncolytic herpes virus, have paved the way to exploring the role of additional oncolytic viruses, such as the echovirus Rigvir, as new and innovative treatment modalities in patients with melanoma. Herein, we discuss the current standard of care treatment in melanoma with an emphasis on immunotherapy and oncolytic viruses in development.","PeriodicalId":19491,"journal":{"name":"Oncolytic Virotherapy","volume":"6 1","pages":"11 - 18"},"PeriodicalIF":6.7,"publicationDate":"2017-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/OV.S100072","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45944516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel oncolytic viral therapies in patients with thoracic malignancies","authors":"Zeeshan Ahmad, R. Kratzke","doi":"10.2147/OV.S116012","DOIUrl":"https://doi.org/10.2147/OV.S116012","url":null,"abstract":"Oncolytic virotherapy is the use of replication-competent viruses to treat malignancies. The potential of oncolytic virotherapy as an approach to cancer therapy is based on historical evidence that certain viral infections can cause spontaneous remission of both hematologic and solid tumor malignancies. Oncolytic virotherapy may eliminate cancer cells through either direct oncolysis of infected tumor cells or indirect immune-mediated oncolysis of uninfected tumor cells. Recent advances in oncolytic virotherapy include the development of a wide variety of genetically attenuated RNA viruses with precise cellular tropism and the identification of cell-surface receptors that facilitate viral transfer to the tissue of interest. Current research is also focused on targeting metastatic disease by sustaining the release of progeny viruses from infected tumor cells and understanding indirect tumor cell killing through immune-mediated mechanisms of virotherapy. The purpose of this review is to critically evaluate recent evidence on the clinical development of tissue-specific viruses capable of targeting tumor cells and eliciting secondary immune responses in lung cancers and mesothelioma.","PeriodicalId":19491,"journal":{"name":"Oncolytic Virotherapy","volume":"6 1","pages":"1 - 9"},"PeriodicalIF":6.7,"publicationDate":"2016-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/OV.S116012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68450670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CXCL12 retargeting of an adenovirus vector to cancer cells using a bispecific adapter","authors":"Shilpa Bhatia, Samia M. O'Bryan, A. A. Rivera, D. Curiel, J. Mathis","doi":"10.2147/OV.S112107","DOIUrl":"https://doi.org/10.2147/OV.S112107","url":null,"abstract":"Ad vectors are promising delivery vehicles for cancer therapeutic interventions. However, their application is limited by promiscuous tissue tropism and hepatotoxicity. This limitation can be avoided by altering the native tropism of Ads so that they can be redirected to the target cells through alternate cellular receptors. The CXCR4 chemokine receptor belongs to a large superfamily of G-protein-coupled receptors and is known to be upregulated in a wide variety of cancers, including breast cancer and melanoma. These receptors have been associated with cancer cell survival, progression, and metastasis. In the current study, an Ad to cancer cells overexpressing CXCR4 by using a bispecific adapter, sCAR-CXCL12, was retargeted. The sCAR-CXCL12 adapter contained the soluble ectodomain form of the native Ad5 receptor (sCAR), which was fused to a mature human chemokine ligand, CXCL12, through a short peptide linker. A dramatic increase in the infectivity of cancer cells using a targeted Ad vector compared with an untargeted vector was observed. Furthermore, sCAR-CXCL12 attenuated Ad infection of liver ex vivo and in vivo and enhanced Ad vector infection of xenograft tumors implanted in immunodeficient SCID-bg mice. Thus, the sCAR-CXCL12 adapter could be used to retarget Ad vectors to chemokine receptor-positive tumors.","PeriodicalId":19491,"journal":{"name":"Oncolytic Virotherapy","volume":"5 1","pages":"99 - 113"},"PeriodicalIF":6.7,"publicationDate":"2016-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/OV.S112107","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68450649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spotlight on talimogene laherparepvec for the treatment of melanoma lesions in the skin and lymph nodes","authors":"M. Orloff","doi":"10.2147/OV.S99532","DOIUrl":"https://doi.org/10.2147/OV.S99532","url":null,"abstract":"On October 27, 2015, talimogene laherparepvec (T-VEC), a first in class intralesional oncolytic virotherapy, was granted the US Food and Drug Administration approval for the treatment of melanoma in the skin and lymph nodes. Its approval has added yet another therapeutic option to the growing list of effective therapies for melanoma. Though the Phase III OPTiM trial has demonstrated its efficacy as a single agent, the target patient population remains narrow. With numerous effective and tolerable treatments available for unresectable and metastatic melanoma, intralesional therapies such as T-VEC are still finding their niche. T-VEC is now widely accepted as option for treatment; however, its combination with various other agents in an effort to expand its use and synergize with other interventions is still being explored. This article will review the pre-clinical and clinical work that eventually led to the Food and Drug Administration approval of this first-in-class agent, as well as address concerns about clinical application and ongoing research.","PeriodicalId":19491,"journal":{"name":"Oncolytic Virotherapy","volume":"5 1","pages":"91 - 98"},"PeriodicalIF":6.7,"publicationDate":"2016-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/OV.S99532","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68450955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oncolytic Seneca Valley Virus: past perspectives and future directions","authors":"M. Burke","doi":"10.2147/OV.S96915","DOIUrl":"https://doi.org/10.2147/OV.S96915","url":null,"abstract":"Seneca Valley Virus isolate 001 (SVV-001) is an oncolytic RNA virus of the Picornaviridae family. It is also the first picornavirus discovered of the novel genus Senecavirus. SVV-001 replicates through an RNA intermediate, bypassing a DNA phase, and is unable to integrate into the host genome. SVV-001 was originally discovered as a contaminant in the cell culture of fetal retinoblasts and has since been identified as a potent oncolytic virus against tumors of neuroendocrine origin. SVV-001 has a number of features that make it an attractive oncolytic virus, namely, its ability to target and penetrate solid tumors via intravenous administration, inability for insertional mutagenesis, and being a self-replicating RNA virus with selective tropism for cancer cells. SVV-001 has been studied in both pediatric and adult early phase studies reporting safety and some clinical efficacy, albeit primarily in adult tumors. This review summarizes the current knowledge of SVV-001 and what its future as an oncolytic virus may hold.","PeriodicalId":19491,"journal":{"name":"Oncolytic Virotherapy","volume":"5 1","pages":"81 - 89"},"PeriodicalIF":6.7,"publicationDate":"2016-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/OV.S96915","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68450903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oncolytic virotherapy for pediatric malignancies: future prospects.","authors":"Alicia M Waters,&nbsp;Gregory K Friedman,&nbsp;Eric K Ring,&nbsp;Elizabeth A Beierle","doi":"10.2147/OV.S96932","DOIUrl":"https://doi.org/10.2147/OV.S96932","url":null,"abstract":"<p><p>Pediatric solid tumors remain a major health concern, with nearly 16,000 children diagnosed each year. Of those, ~2,000 succumb to their disease, and survivors often suffer from lifelong disability secondary to toxic effects of current treatments. Countless multimodality treatment regimens are being explored to make advances against this deadly disease. One targeted treatment approach is oncolytic virotherapy. Conditionally replicating viruses can infect tumor cells while leaving normal cells unharmed. Four viruses have been advanced to pediatric clinical trials, including herpes simplex virus-1, Seneca Valley virus, reovirus, and vaccinia virus. In this review, we discuss the mechanism of action of each virus, pediatric preclinical studies conducted to date, past and ongoing pediatric clinical trials, and potential future direction for these novel viral therapeutics. </p>","PeriodicalId":19491,"journal":{"name":"Oncolytic Virotherapy","volume":"5 ","pages":"73-80"},"PeriodicalIF":6.7,"publicationDate":"2016-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/OV.S96932","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34350218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}