Enhanced inhibition of syngeneic murine tumors by combinatorial therapy with genetically engineered HSV-1 expressing CCL2 and IL-12

Parker, J.B.; Meleth, Sreelatha; Hughes, Kenneth B; Gillespie, G. Yancey; Whitley, Richard J.; Markert, James M.

doi:10.1038/sj.cgt.7700784

Cited by 59 publications

(53 citation statements)

References 40 publications

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“…26 The group also demonstrated that the virus selected after in vivo serial passage of M002 in tumors of a D54-MG human malignant glioma cell line improved survival in two independent murine brain tumor models compared to the parent M002. 27 This enhanced antitumor efficacy was not due to restoration of protein synthesis or early US11 expression.…”

Section: © 2 0 0 8 L a N D E S B I O S C I E N C E D O N O T D I S mentioning

confidence: 99%

“Armed” oncolytic herpes simplex viruses for brain tumor therapy

Todo¹

2008

Cell Adhesion & Migration

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Section: © 2 0 0 8 L a N D E S B I O S C I E N C E D O N O T D I S mentioning

confidence: 99%

“Armed” oncolytic herpes simplex viruses for brain tumor therapy

Todo¹

2008

Cell Adhesion & Migration

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“…T cells were stained with CFDA, washed once with T-cell medium and adjusted to 5x10 5 cells/ml in the same medium. An aliquot (100 µl) of the cell suspension containing 5x10 4 T cells was placed in the top chamber of the Transwell. Supernatant obtained from WM3450 or WM35 cell culture or chemokine, prepared at the indicated concentration in T-cell medium (500 µl total volume), was added to the bottom chamber of the Transwell.…”

Section: Methodsmentioning

confidence: 99%

“…[1][2][3] Such studies have provided potent tumor vaccines based on ex vivo transduction of chemokines into tumor cells, inducing tumor rejection mediated by infiltrating T cells at the vaccine site in mice. 1,4 Other approaches, including the fusion of chemokines to tumor Ag-specific antibody to attract adoptively transferred or endogenous T cells to the tumor site, or incorporation of chemokines into Ag vaccines to attract T cells to the vaccine site, have also resulted in tumor destruction in mouse models. 5,6 Development of immunotherapeutic strategies for cancer patients based on chemokines and their receptors awaits a better definition of the role of these molecules in T-cell migration toward tumor cells of patients.…”

Section: Introductionmentioning

confidence: 99%

Preferential involvement of CX chemokine receptor 4 and CX chemokine ligand 12 in T-Cell migration toward melanoma cells

Zhang

Somasundaram²,

Berking³

et al. 2006

Cancer Biology & Therapy

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Our previous analysis of the role of chemokines in T lymphocyte trafficking toward human tumor cells revealed the migration of a melanoma patient's cytotoxic T lymphocytes (CTL) toward autologous tumor cells, resulting in tumor cell apoptosis, in an organotypic melanoma culture. CTL migration was mediated by CX chemokine receptor (CXCR) 4 expressed by the CTL and CX chemokine ligand (CXCL) 12 secreted by the tumor cells, as evidenced by blockage of CTL migration by antibodies to CXCL12 or CXCR4, high concentrations of CXCL12 or small molecule CXCR4 antagonist. Here, we present the results of T cell migration in one additional melanoma patient and T cell and tumor cell analyses for CXCR4 and CXCL12 expression, respectively, in 12 additional melanoma patients, indicating the preferential role of CXCR4 and CXCL12 in CTL migration toward melanoma cells. These studies add to the increasing body of evidence suggesting that CXCL12 is a potent chemoattractant for T cells.

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“…The data were analyzed for statistical significance using a linear mixed model, as described previously. 32 …”

Section: Hsv-1 Expressing CD For Brain Tumor Therapy Mb Guffey Et Almentioning

confidence: 99%

Engineered herpes simplex virus expressing bacterial cytosine deaminase for experimental therapy of brain tumors

et al. 2006

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Lack of effective therapy of primary brain tumors has promoted the development of novel experimental approaches utilizing oncolytic viruses combined with gene therapy. Towards this end, we have assessed a conditionally replication-competent, g 1 34.5-deleted herpes simplex virus type 1 (HSV-1) expressing cytosine deaminase (CD) for treatment of malignant brain tumors. Our results are summarized as follows: (i) a recombinant HSV (M012) was constructed in which both copies of the g 1 34.5 gene were replaced with the bacterial CD gene, under the control of the cellular promoter Egr-1; (ii) M012-infected cells in vitro efficiently convert 5-fluorocytosine (5-FC) to 5-fluorouracil, thereby enhancing cytotoxicity of neighboring, uninfected cells; (iii) both direct and bystander cytotoxicity of murine neuroblastoma and human glioma cell lines after infection with M012 were demonstrated; (iv) direct intracerebral inoculation of A/J mice demonstrated lack of neurotoxicity at doses similar to G207, a g 1 34.5-deleted HSV with demonstrated safety in human patient trials and (v) intratumoral injection of M012 into Neuro-2a flank tumors in combination with 5-FC administration significantly reduced tumor growth versus tumors treated with R3659 combined with 5-FC, or treated with M012 alone. Thus, M012 is a promising new oncolytic HSV vector with an enhanced prodrug-mediated, antineoplastic effect that is safe for intracranial administration.

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Enhanced inhibition of syngeneic murine tumors by combinatorial therapy with genetically engineered HSV-1 expressing CCL2 and IL-12

Cited by 59 publications

References 40 publications

“Armed” oncolytic herpes simplex viruses for brain tumor therapy

“Armed” oncolytic herpes simplex viruses for brain tumor therapy

Preferential involvement of CX chemokine receptor 4 and CX chemokine ligand 12 in T-Cell migration toward melanoma cells

Engineered herpes simplex virus expressing bacterial cytosine deaminase for experimental therapy of brain tumors

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