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Antisense Vector

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P E Lacy – One of the best experts on this subject based on the ideXlab platform.

  • expression of functional human epstein barr virus c3d receptor cr2 cd21 on insulinoma cell line induction of tumor rejection but not diabetes in syngeneic rats
    Diabetes, 1991
    Co-Authors: Jean-claude Carel, V. Michael Holers, William L. Chick, Dan R Littman, P E Lacy

    Abstract:

    We stably expressed human complement receptor 2 ([CR2] CD21 C3d/Epstein-Barr virus [EBV] receptor) on the rat insulinoma cell line RINm5F with a recombinant retroviral Vector. CR2-expressing RINm5F cells secreted 78–33% less insulin than parental cells or cells transduced with an Antisense Vector and could be infected with high-titer EBV. We tested whether human CR2 expression on RINm5F cells would affect tumorigenesis after transplantation to syngeneic New England Deaconess Hospital rats. Non-CR2–expressing Antisense-transduced RINm5F cells rapidly grew tumors and caused hypoglycemia, hyperinsulinemia, and the death of the animals after 15.7 ± 0.7 days. CR2-expressing RINm5F cells were infiltrated by mononuclear cells at an early stage and eventually caused noninfiltrated tumors and the death of the animals after 33.0 ± 0.4 days. These tumors were CR2− and are believed to have arisen from a minor CR2− population of tumor cells. The pancreatic islets were histologically normal at all time points. We conclude that expression of a xenoantigen on a rat insulinoma cell line induces an immune response in syngeneic rats but does not result in breakage of tolerance to parental or revertant cells.

  • Expression of functional human Epstein-Barr virus/C3d receptor ([CR2] CD21) on insulinoma cell line. Induction of tumor rejection but not diabetes in syngeneic rats.
    Diabetes, 1991
    Co-Authors: Jean-claude Carel, V. Michael Holers, Dan R Littman, Chick Wl, P E Lacy

    Abstract:

    We stably expressed human complement receptor 2 ([CR2] CD21 C3d/Epstein-Barr virus [EBV] receptor) on the rat insulinoma cell line RINm5F with a recombinant retroviral Vector. CR2-expressing RINm5F cells secreted 78–33% less insulin than parental cells or cells transduced with an Antisense Vector and could be infected with high-titer EBV. We tested whether human CR2 expression on RINm5F cells would affect tumorigenesis after transplantation to syngeneic New England Deaconess Hospital rats. Non-CR2–expressing Antisense-transduced RINm5F cells rapidly grew tumors and caused hypoglycemia, hyperinsulinemia, and the death of the animals after 15.7 ± 0.7 days. CR2-expressing RINm5F cells were infiltrated by mononuclear cells at an early stage and eventually caused noninfiltrated tumors and the death of the animals after 33.0 ± 0.4 days. These tumors were CR2− and are believed to have arisen from a minor CR2− population of tumor cells. The pancreatic islets were histologically normal at all time points. We conclude that expression of a xenoantigen on a rat insulinoma cell line induces an immune response in syngeneic rats but does not result in breakage of tolerance to parental or revertant cells.

  • Expression of functional human Epstein-Barr virus/C3d receptor ([CR2] CD21) on insulinoma cell line. Induction of tumor rejection but not diabetes in syngeneic rats.
    Diabetes, 1991
    Co-Authors: Jean-claude Carel, V. Michael Holers, Dan R Littman, Chick Wl, P E Lacy

    Abstract:

    We stably expressed human complement receptor 2 ([CR2] CD21 C3d/Epstein-Barr virus [EBV] receptor) on the rat insulinoma cell line RINm5F with a recombinant retroviral Vector. CR2-expressing RINm5F cells secreted 78–33% less insulin than parental cells or cells transduced with an Antisense Vector and could be infected with high-titer EBV. We tested whether human CR2 expression on RINm5F cells would affect tumorigenesis after transplantation to syngeneic New England Deaconess Hospital rats. Non-CR2–expressing Antisense-transduced RINm5F cells rapidly grew tumors and caused hypoglycemia, hyperinsulinemia, and the death of the animals after 15.7 ± 0.7 days. CR2-expressing RINm5F cells were infiltrated by mononuclear cells at an early stage and eventually caused noninfiltrated tumors and the death of the animals after 33.0 ± 0.4 days. These tumors were CR2− and are believed to have arisen from a minor CR2− population of tumor cells. The pancreatic islets were histologically normal at all time points. We conclude that expression of a xenoantigen on a rat insulinoma cell line induces an immune response in syngeneic rats but does not result in breakage of tolerance to parental or revertant cells.

R. Jude Samulski – One of the best experts on this subject based on the ideXlab platform.

  • Adeno-associated virus (AAV) Vector Antisense gene transfer in vivo decreases GABAAα1 containing receptors and increases inferior collicular seizure sensitivity
    Brain Research, 1997
    Co-Authors: Xiao Xiao, Thomas J. Mccown, George R. Breese, A. Leslie Morrow, R. Jude Samulski

    Abstract:

    Abstract In the inferior colliculus, adeno-associated virus (AAV) Vectors are capable of gene transfer and stable, long-term expression, but it remained to be shown if this in vivo gene transfer could alter focal seizure sensitivity in the inferior colliculus. Because GABA receptors directly modulate inferior collicular seizures, AAV Vectors were constructed with a cytomegalovirus (CMV) promoter and a truncated, human GABAAα1 cDNA in both the sense and Antisense orientations. Seven days after collicular microinjection of the sense Vectors (1 μl; 3×109 particles/μl), neurons exhibited GABAAα-like immunoreactivity in amounts far exceeding endogenous concentrations. Unilateral or bilateral sense Vector infusion had no effect on inferior collicular seizure parameters or on [3H]zolpidem binding. In contrast, bilateral infusion of the Antisense AAV-GABAAα1 Vector (1 μl; 3×108 particles/μl) caused a 137% increase in the seizure duration. Moreover, unilateral Antisense Vector infusion produced a localized, 48% decrease in [3H]zolpidem binding. Thus, in the inferior colliculus, Antisense AAV-CMV Vectors can reduce a specific receptor subunit protein and change receptor function that directly influences in vivo seizure sensitivity.

  • Adeno-associated virus (AAV) Vector Antisense gene transfer in vivo decreases GABA(A) alpha1 containing receptors and increases inferior collicular seizure sensitivity.
    Brain research, 1997
    Co-Authors: Xiao Xiao, Thomas J. Mccown, George R. Breese, A. Leslie Morrow, R. Jude Samulski

    Abstract:

    In the inferior colliculus, adeno-associated virus (AAV) Vectors are capable of gene transfer and stable, long-term expression, but it remained to be shown if this in vivo gene transfer could alter focal seizure sensitivity in the inferior colliculus. Because GABA receptors directly modulate inferior collicular seizures, AAV Vectors were constructed with a cytomegalovirus (CMV) promoter and a truncated, human GABA(A) alpha1 cDNA in both the sense and Antisense orientations. Seven days after collicular microinjection of the sense Vectors (1 microl; 3 x 10(9) particles/microl), neurons exhibited GABA(A) alpha-like immunoreactivity in amounts far exceeding endogenous concentrations. Unilateral or bilateral sense Vector infusion had no effect on inferior collicular seizure parameters or on [3H]zolpidem binding. In contrast, bilateral infusion of the Antisense AAV-GABA(A) alpha1 Vector (1 microl; 3 x 10(8) particles/microl) caused a 137% increase in the seizure duration. Moreover, unilateral Antisense Vector infusion produced a localized, 48% decrease in [3H]zolpidem binding. Thus, in the inferior colliculus, Antisense AAV-CMV Vectors can reduce a specific receptor subunit protein and change receptor function that directly influences in vivo seizure sensitivity.

D L Shawler – One of the best experts on this subject based on the ideXlab platform.

  • Phase I clinical trial of a TGF-β Antisense-modified tumor cell vaccine in patients with advanced glioma
    Cancer Gene Therapy, 2006
    Co-Authors: H Fakhrai, J C Mantil, L Liu, G L Nicholson, C S Murphy-satter, J Ruppert, D L Shawler

    Abstract:

    We performed a phase I clinical trial in grade IV astrocytoma to assess the safety of a whole-cell vaccine comprising autologous tumor cells genetically modified by a transforming growth factor- β 2 (TGF- β 2) Antisense Vector. Blocking secretion of the immunosuppressive molecule TGF- β in this manner should inhibit one of the major mechanisms by which tumor cells evade immune surveillance and should lead to clinically effective antitumor immunity. Six patients with progressive WHO grade IV astrocytoma were enrolled in the trial. Patients received 2–7 subcutaneous injections of 5 × 10^6–2 × 10^7 autologous tumor cells per injection. TGF- β 2 secretion by the tumor cells used to vaccinate patients was inhibited by 53–98%. Treatment was well tolerated with only low-grade, transient treatment-related toxicities reported. Two patients had partial regressions and two had stable disease following therapy. The overall median survival was 68 weeks. Median survival of the responding patients was 78 weeks, compared to a historic value of 47 weeks for glioma patients treated conventionally. There were indications of humoral and cellular immunity induced by the vaccine. These findings support further clinical evaluation of vaccines comprised of TGF- β Antisense-modified tumor cells.

  • Phase I clinical trial of a TGF-beta Antisense-modified tumor cell vaccine in patients with advanced glioma.
    Cancer gene therapy, 2006
    Co-Authors: H Fakhrai, J C Mantil, L Liu, G L Nicholson, C S Murphy-satter, J Ruppert, D L Shawler

    Abstract:

    We performed a phase I clinical trial in grade IV astrocytoma to assess the safety of a whole-cell vaccine comprising autologous tumor cells genetically modified by a transforming growth factor-beta2 (TGF-beta2) Antisense Vector. Blocking secretion of the immunosuppressive molecule TGF-beta in this manner should inhibit one of the major mechanisms by which tumor cells evade immune surveillance and should lead to clinically effective antitumor immunity. Six patients with progressive WHO grade IV astrocytoma were enrolled in the trial. Patients received 2-7 subcutaneous injections of 5 x 10(6)-2 x 10(7) autologous tumor cells per injection. TGF-beta2 secretion by the tumor cells used to vaccinate patients was inhibited by 53-98%. Treatment was well tolerated with only low-grade, transient treatment-related toxicities reported. Two patients had partial regressions and two had stable disease following therapy. The overall median survival was 68 weeks. Median survival of the responding patients was 78 weeks, compared to a historic value of 47 weeks for glioma patients treated conventionally. There were indications of humoral and cellular immunity induced by the vaccine. These findings support further clinical evaluation of vaccines comprised of TGF-beta Antisense-modified tumor cells.