Safety and Clinical Usage of Newcastle Disease Virus in  Cancer Therapy

Lam, Han Yuen; Yeap, Swee Keong; Rasoli, Mehdi; Omar, Abdul Rahman; Yusoff, Khatijah; Suraini, Abd Aziz; Alitheen, Noorjahan Banu

doi:10.1155/2011/718710

Cited by 78 publications

(80 citation statements)

References 83 publications

(181 reference statements)

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“…NDV is inherently tumor selective and oncolytic. The tumor selective property of NDV, coupled with compelling preclinical and phase I/II studies in human subjects, has identified NDV as an attractive virotherapy candidate (9,24,27).…”

mentioning

confidence: 99%

Incorporation of Host Complement Regulatory Proteins into Newcastle Disease Virus Enhances Complement Evasion

Biswas

Johnson

Kumar

et al. 2012

J Virol

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bNewcastle disease virus (NDV), an avian paramyxovirus, is inherently tumor selective and is currently being considered as a clinical oncolytic virus and vaccine vector. In this study, we analyzed the effect of complement on the neutralization of NDV purified from embryonated chicken eggs, a common source for virus production. Fresh normal human serum (NHS) neutralized NDV by multiple pathways of complement activation, independent of neutralizing antibodies. Neutralization was associated with C3 deposition and the activation of C2, C3, C4, and C5 components. Interestingly, NDV grown in mammalian cell lines was resistant to complement neutralization by NHS. To confirm whether the incorporation of regulators of complement activity (RCA) into the viral envelope afforded complement resistance, we grew NDV in CHO cells stably transfected with CD46 or HeLa cells, which strongly express CD46 and CD55. NDV grown in RCA-expressing cells was resistant to complement by incorporating CD46 and CD55 on virions. Mammalian CD46 and CD55 molecules on virions exhibited homologous restriction, since chicken sera devoid of neutralizing antibodies to NDV were able to effectively neutralize these virions. The incorporation of chicken RCA into NDV produced in embryonated eggs similarly provided species specificity toward chicken sera.

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mentioning

confidence: 99%

Incorporation of Host Complement Regulatory Proteins into Newcastle Disease Virus Enhances Complement Evasion

Biswas

Johnson

Kumar

et al. 2012

J Virol

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“…54 Depending on the mode of oncolysis, NDVs have been evaluated and classified as lytic or non lytic strains. The lytic strains cause syncytia formation to induce changes in the plasma membrane resulting in lysis of target cells.…”

Section: Mode Of Actionmentioning

confidence: 99%

Application of Oncolytic Viruses for Cure of Colorectal Cancer

Davis¹

2015

CRJ

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Abstract:Colorectal cancer is one of the most commonly diagnosed and lethal cancers worldwide. It is the resultant of multistep processes caused by the accumulation of genetic/epigenetic aberrations. The different therapeutic strategies like radiotherapy, chemotherapy and surgery, used individually or in different combinations, do not remove tumors or their progression all the time. Besides, these procedures involve surrounding cells and tissues. In case of surgery, which is possible only before metastasis, even a single cancer cell left out during surgery, cause further cancer. Focus has been laid in developing agents that could specifically target the cancer cells and leave out the remaining normal cells. This also attempt at total recovery. This was how the focus was laid on viral agents. Over the last two decades, due to various advancements in molecular biology, virotherapy has seen various developments. A special class of viruses called oncolytic viruses have been used as a therapeutic strategy against cancer. These agents have various inherent and engineered factors like enhanced tissue tropism, thereby providing high selectivity; armed with transgenes to deliver therapeutic genes and to perform tumor selective replication, all these factors proving them improved and evolved mechanisms, when compared with other cancer therapeutics. These oncolytic viruses provide greater protection in association with herbal remedies. The purpose of this paper is to provide a detailed account of some of the current observations, developments and insights made in the field of oncolytic virotherapy for targeting colorectal cancer cells. A panel of five oncolytic viruses i.e. adenovirus, herpes virus, reovirus, vaccinia virus and new castle disease virus that are under clinical studies for targeting colorectal cancer cells have been discussed.

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“…Over the past century, a number of oncolytic viruses have been discovered, such as mumps, measles, adenovirus, reovirus, Newcastle disease virus (NDV), and others. 3,4 Newcastle disease virus as a vector for gene therapy is under clinical evaluation. 5 Newcastle disease virus is a member of the Avulavirus genus in the Paramyxoviridae family.…”

Section: Introductionmentioning

confidence: 99%

“…The inherent viral oncolytic properties are believed to be derived from defective IFN signaling pathways in tumor cells. 3,5,8 The development of reverse genetics technology for NDV enable us to modify the NDV genome as well as introduce foreign sequences to refine the antitumor activity. [9][10][11][12][13] Previous studies in our laboratory showed that recombinant NDVs (rNDVs) expressing Trail, interleukin (IL) 15, and IL-2 are promising antitumor agents.…”

Section: Introductionmentioning

confidence: 99%

Recombinant Newcastle Disease Virus Encoding IL-12 and/or IL-2 as Potential Candidate for Hepatoma Carcinoma Therapy

Ren

Tian

Liu

et al. 2016

Technol Cancer Res Treat

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Interleukins as immunomodulators are promising therapeutic agents for cancer therapy. Previous studies showed that there was an improved antitumor immunity in tumor-bearing mice using recombinant Newcastle disease virus carrying for interleukin-2. Interleukin-12 is a promising antitumor cytokine too. So we investigated and compared the antitumor effect of genetically engineered Newcastle disease virus strains expressing both interleukin-12 and/or interleukin-2 (rClone30-interleukin-2, rClone30-interleukin-12, and rClone30-interleukin-12-interleukin-2). In vitro studies showed that rClone30s could efficiently infect tumor cells and express interleukin-12 and/or interleukin-2. 3-(4,5-Dimethylthiazol-2-y)-2,5-diphenyl-tetrazolium bromide results showed rClone30s possessed strong cytotoxic activities against multiple tumor cell lines (U251, HepG2, A549, and Hela). Animal studies showed that rClone30-interleukin-12-interleukin-2 was more effective in inhibition of murine hepatoma carcinoma tumors, with the mean tumor volume (day 14) of 141.70 mm 3 comparing 165.67 mm 3 of rClone30-interleukin-12 group, 210.47 mm 3 of rClone30-interleukin-2 group, 574.70 mm 3 of rClone30 group, and 1206.83 mm 3 of phosphate-buffered saline group. Moreover, the rClone30-interleukin-12-interleukin-2 treated mice secreted more interferon g (333.518 pg/mL) and its downstream cytokine interferon-g induced protein 10 (16.006 pg/mL) in tumor than the rClone30-interleukin-12 group (interferon g: 257.548 pg/mL; interferon-g induced protein 10: 13.601 pg/mL), rClone30-interleukin2 group (interferon g: 124.601 pg/mL; interferon-g induced protein 10: 9.779 pg/mL), or rClone30 group (interferon g: 48.630 pg/mL; interferon-g induced protein 10:1.650 pg/mL). For the survival study, rClone30-interleukin12-interleukin2 increased the survival rate (12 of 16) of the tumor-bearing mice versus 11 of 16 in rClone30-interleukin-12 group, 10 of 16 in rClone30-interleukin-2 group, 7 of 16 in Clone30 group, and 0/16 in phosphate-buffered saline group, respectively. To determine whether the mice treated with recombinant virus developed protective immune response, the mice were rechallenged with the same tumor cells. The results showed that viral-treated mice were significantly protected from rechallenge. These results suggest that expressing both interleukin-2 and/or interleukin-12 could be ideal approaches to enhance the antitumor ability of Newcastle disease virus, and rClone30-interleukin-12-interleukin-2 is slightly superior over rClone30-interleukin-12 and rClone30-interleukin-2 alone.

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Safety and Clinical Usage of Newcastle Disease Virus in Cancer Therapy

Cited by 78 publications

References 83 publications

Incorporation of Host Complement Regulatory Proteins into Newcastle Disease Virus Enhances Complement Evasion

Incorporation of Host Complement Regulatory Proteins into Newcastle Disease Virus Enhances Complement Evasion

Application of Oncolytic Viruses for Cure of Colorectal Cancer

Recombinant Newcastle Disease Virus Encoding IL-12 and/or IL-2 as Potential Candidate for Hepatoma Carcinoma Therapy

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