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Significant Growth Inhibition of Canine Mammary Carcinoma Xenografts following Treatment with Oncolytic Vaccinia Virus GLV-1h68.

Gentschev I, Ehrig K, Donat U, Hess M, Rudolph S, Chen N, Yu YA, Zhang Q, Bullerdiek J, Nolte I, Stritzker J, Szalay AA - J Oncol (2010)

Bottom Line: Therefore, there is an urgent need to identify novel agents for therapy of this disease.Finally, infection with GLV-1h68 led to strong inflammatory and oncolytic effects resulting in significant growth inhibition of the tumors.In summary, the data showed that the GLV-1h68 virus strain has promising potential for effective treatment of canine mammary carcinoma.

View Article: PubMed Central - PubMed

Affiliation: Genelux Corporation, San Diego Science Center, San Diego, CA 92109, USA.

ABSTRACT
Canine mammary carcinoma is a highly metastatic tumor that is poorly responsive to available treatment. Therefore, there is an urgent need to identify novel agents for therapy of this disease. Recently, we reported that the oncolytic vaccinia virus GLV-1h68 could be a useful tool for therapy of canine mammary adenoma in vivo. In this study we analyzed the therapeutic effect of GLV-1h68 against canine mammary carcinoma. Cell culture data demonstrated that GLV-1h68 efficiently infected and destroyed cells of the mammary carcinoma cell line MTH52c. Furthermore, after systemic administration, this attenuated vaccinia virus strain primarily replicated in canine tumor xenografts in nude mice. Finally, infection with GLV-1h68 led to strong inflammatory and oncolytic effects resulting in significant growth inhibition of the tumors. In summary, the data showed that the GLV-1h68 virus strain has promising potential for effective treatment of canine mammary carcinoma.

No MeSH data available.


Related in: MedlinePlus

Cytotoxicity (a) and replication (b) of the GLV-1h68 virus in canine mammary MTH52c cells. (a) Viability of MTH52c cells after GLV-1h68 infection using MOIs of 0.1 and 1 was monitored over 96 hours. The amount of viable cells after infection with GLV-1h68 was measured in triplicate. Values are shown as percentages of respective uninfected controls. (b) Viral titer analysis in MTH52c cell culture after infection with GLV-1h68 at an MOI of 0.1. Cells and supernatant of virally treated cells were collected at various times post infection. Viral titers were determined as pfu per well in triplicate by plaque assay in CV-1 cell monolayers. Average plus standard deviations plotted.
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fig1: Cytotoxicity (a) and replication (b) of the GLV-1h68 virus in canine mammary MTH52c cells. (a) Viability of MTH52c cells after GLV-1h68 infection using MOIs of 0.1 and 1 was monitored over 96 hours. The amount of viable cells after infection with GLV-1h68 was measured in triplicate. Values are shown as percentages of respective uninfected controls. (b) Viral titer analysis in MTH52c cell culture after infection with GLV-1h68 at an MOI of 0.1. Cells and supernatant of virally treated cells were collected at various times post infection. Viral titers were determined as pfu per well in triplicate by plaque assay in CV-1 cell monolayers. Average plus standard deviations plotted.

Mentions: In order to test the ability of the GLV-1h68 virus to infect and lyse MTH52c cells in cell culture, we first performed a cell viability assay, as described in Materials and Methods. Ninety-six hours after GLV-1h68 infection at an MOI of 0.1 and 1.0, the MTH52c cells were eradicated, with only 2.4 ± 1.04% and 206 ± 0.68%surviving the treatment, respectively (Figure 1(a)). These results indicate that GLV-1h68 virus infection leads to an efficient eradication of the carcinoma MTH52c cells in culture.


Significant Growth Inhibition of Canine Mammary Carcinoma Xenografts following Treatment with Oncolytic Vaccinia Virus GLV-1h68.

Gentschev I, Ehrig K, Donat U, Hess M, Rudolph S, Chen N, Yu YA, Zhang Q, Bullerdiek J, Nolte I, Stritzker J, Szalay AA - J Oncol (2010)

Cytotoxicity (a) and replication (b) of the GLV-1h68 virus in canine mammary MTH52c cells. (a) Viability of MTH52c cells after GLV-1h68 infection using MOIs of 0.1 and 1 was monitored over 96 hours. The amount of viable cells after infection with GLV-1h68 was measured in triplicate. Values are shown as percentages of respective uninfected controls. (b) Viral titer analysis in MTH52c cell culture after infection with GLV-1h68 at an MOI of 0.1. Cells and supernatant of virally treated cells were collected at various times post infection. Viral titers were determined as pfu per well in triplicate by plaque assay in CV-1 cell monolayers. Average plus standard deviations plotted.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2902752&req=5

fig1: Cytotoxicity (a) and replication (b) of the GLV-1h68 virus in canine mammary MTH52c cells. (a) Viability of MTH52c cells after GLV-1h68 infection using MOIs of 0.1 and 1 was monitored over 96 hours. The amount of viable cells after infection with GLV-1h68 was measured in triplicate. Values are shown as percentages of respective uninfected controls. (b) Viral titer analysis in MTH52c cell culture after infection with GLV-1h68 at an MOI of 0.1. Cells and supernatant of virally treated cells were collected at various times post infection. Viral titers were determined as pfu per well in triplicate by plaque assay in CV-1 cell monolayers. Average plus standard deviations plotted.
Mentions: In order to test the ability of the GLV-1h68 virus to infect and lyse MTH52c cells in cell culture, we first performed a cell viability assay, as described in Materials and Methods. Ninety-six hours after GLV-1h68 infection at an MOI of 0.1 and 1.0, the MTH52c cells were eradicated, with only 2.4 ± 1.04% and 206 ± 0.68%surviving the treatment, respectively (Figure 1(a)). These results indicate that GLV-1h68 virus infection leads to an efficient eradication of the carcinoma MTH52c cells in culture.

Bottom Line: Therefore, there is an urgent need to identify novel agents for therapy of this disease.Finally, infection with GLV-1h68 led to strong inflammatory and oncolytic effects resulting in significant growth inhibition of the tumors.In summary, the data showed that the GLV-1h68 virus strain has promising potential for effective treatment of canine mammary carcinoma.

View Article: PubMed Central - PubMed

Affiliation: Genelux Corporation, San Diego Science Center, San Diego, CA 92109, USA.

ABSTRACT
Canine mammary carcinoma is a highly metastatic tumor that is poorly responsive to available treatment. Therefore, there is an urgent need to identify novel agents for therapy of this disease. Recently, we reported that the oncolytic vaccinia virus GLV-1h68 could be a useful tool for therapy of canine mammary adenoma in vivo. In this study we analyzed the therapeutic effect of GLV-1h68 against canine mammary carcinoma. Cell culture data demonstrated that GLV-1h68 efficiently infected and destroyed cells of the mammary carcinoma cell line MTH52c. Furthermore, after systemic administration, this attenuated vaccinia virus strain primarily replicated in canine tumor xenografts in nude mice. Finally, infection with GLV-1h68 led to strong inflammatory and oncolytic effects resulting in significant growth inhibition of the tumors. In summary, the data showed that the GLV-1h68 virus strain has promising potential for effective treatment of canine mammary carcinoma.

No MeSH data available.


Related in: MedlinePlus