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Alpha2a Interferon
The Experts below are selected from a list of 249351 Experts worldwide ranked by ideXlab platform
Andrew Symonds – One of the best experts on this subject based on the ideXlab platform.
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down regulation of nitric oxide production by droloxifene and toremifene in human breast cancer cells
Oncology Reports, 2003Co-Authors: Jan Martin, Andrew Symonds, Sunita ChohanAbstract:We investigated the effect of tamoxifen, 4-OH tamoxifen, toremifene droloxifene, Interferon–Alpha2a, Interferon-alpha2b and Interferon-alpha2c, singly and in combination, for their effect on nitric oxide production by MCF-7 and ZR-75-1 human breast cancer cells. Tamoxifen and 4-OH tamoxifen singly had no effect on nitric oxide production by either cell line. However, treatment with droloxifene or toremifene significantly reduced nitric oxide production by both MCF-7 and ZR-75-1 human breast cancer cell lines. Combination treatment with anti-estrogens and Interferon–Alpha2a Interferon-alpha2b or Interferon-alpha2c had no synergistic or additive effect compared to each drug singly.
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Synergistic antitumour effect of a combination of toremifene and Interferon-alpha on ZR-75-1 human breast cancer cells: dependence on Interferon-alpha subtype.
Oncology reports, 2002Co-Authors: Jan Martin, Andrew SymondsAbstract:We investigated the effect of toremifene, Interferon–Alpha2a, Interferon-alpha2b and Interferon-alpha2c, singly and in combination for their effect on the growth of ZR-75-1 human breast cancer cells. Median effect analysis was used to determine synergistic or additive effects. Anti-proliferative studies showed that the growth of ZR-75-1 cells was inhibited to a greater extent by combination treatment with toremifene plus Interferon–Alpha2a, resulting in a synergistic interaction (CI
Jan Martin – One of the best experts on this subject based on the ideXlab platform.
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down regulation of nitric oxide production by droloxifene and toremifene in human breast cancer cells
Oncology Reports, 2003Co-Authors: Jan Martin, Andrew Symonds, Sunita ChohanAbstract:We investigated the effect of tamoxifen, 4-OH tamoxifen, toremifene droloxifene, Interferon–Alpha2a, Interferon-alpha2b and Interferon-alpha2c, singly and in combination, for their effect on nitric oxide production by MCF-7 and ZR-75-1 human breast cancer cells. Tamoxifen and 4-OH tamoxifen singly had no effect on nitric oxide production by either cell line. However, treatment with droloxifene or toremifene significantly reduced nitric oxide production by both MCF-7 and ZR-75-1 human breast cancer cell lines. Combination treatment with anti-estrogens and Interferon–Alpha2a Interferon-alpha2b or Interferon-alpha2c had no synergistic or additive effect compared to each drug singly.
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Synergistic antitumour effect of a combination of toremifene and Interferon-alpha on ZR-75-1 human breast cancer cells: dependence on Interferon-alpha subtype.
Oncology reports, 2002Co-Authors: Jan Martin, Andrew SymondsAbstract:We investigated the effect of toremifene, Interferon–Alpha2a, Interferon-alpha2b and Interferon-alpha2c, singly and in combination for their effect on the growth of ZR-75-1 human breast cancer cells. Median effect analysis was used to determine synergistic or additive effects. Anti-proliferative studies showed that the growth of ZR-75-1 cells was inhibited to a greater extent by combination treatment with toremifene plus Interferon–Alpha2a, resulting in a synergistic interaction (CI
Sunita Chohan – One of the best experts on this subject based on the ideXlab platform.
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down regulation of nitric oxide production by droloxifene and toremifene in human breast cancer cells
Oncology Reports, 2003Co-Authors: Jan Martin, Andrew Symonds, Sunita ChohanAbstract:We investigated the effect of tamoxifen, 4-OH tamoxifen, toremifene droloxifene, Interferon–Alpha2a, Interferon-alpha2b and Interferon-alpha2c, singly and in combination, for their effect on nitric oxide production by MCF-7 and ZR-75-1 human breast cancer cells. Tamoxifen and 4-OH tamoxifen singly had no effect on nitric oxide production by either cell line. However, treatment with droloxifene or toremifene significantly reduced nitric oxide production by both MCF-7 and ZR-75-1 human breast cancer cell lines. Combination treatment with anti-estrogens and Interferon–Alpha2a Interferon-alpha2b or Interferon-alpha2c had no synergistic or additive effect compared to each drug singly.
Bruno Bergamasco – One of the best experts on this subject based on the ideXlab platform.
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Systemic high-dose recombinant-alpha-2a-Interferon therapy modulates lymphokine production in multiple sclerosis.
Journal of the Neurological Sciences, 1996Co-Authors: M. R. Bongioanni, Luca Durelli, B Ferrero, D. Imperiale, A. Oggero, E. Verdun, G. Aimo, Roberto Pagni, Massimo Geuna, Bruno BergamascoAbstract:Chronic systemic high-dose recombinant Alpha2a–Interferon (rIFNA) therapy reduces exacerbation rate and MRI signs of disease activity in relapsing/remitting multiple sclerosis (RR MS) patients. In order to clarify the possible mechanisms underlying the clinical efficacy of rIFNA in MS, several immunologic studies were performed as a part of a pilot clinical trial. Twenty RR MS patients were treated with 9 × 106 IU of rIFNA (n = 12) or placebo (n = 8) intramuscularly every other day for 6 months. Cytokine production by cultured lymphocytes, major histocompatibility complex class II (MHC-II) antigen expression on cultured macrophages, peripheral blood (PB) and cerebrospinal fluid (CSF) lymphocyte phenotype, and IgG and beta2 microglobulin levels were studied before therapy, after 6 months of therapy, and 6 months after stopping therapy. rIFNA therapy was associated with reduction of Interferon-gamma and tumor necrnecrosistor-alpha production by PB lymphocytes (p < 0.04), and with slight, not significant, increase of transforming growth factor-beta2 or interleukin (IL)-10 production. IL-4 was undetectable in the culture supernatants both before and after therapy. rIFNA therapy had no effect on macrophage MHC-II molecule expression. An increased percentage of CD8 +, CD8 + high CD11b + low, and CD3 − CD16 + CD56 + cells, and of CD4 + absolute cell number was observed in CSF after rIFNA therapy. After rIFNA administration, IgG level significantly increased both systemically (p < 0.02) and intrathecally (p < 0.001). Serum beta2 microglobulin level increased (p < 0.01), as well. Only 1 out of the 12 rIFNA treated patients developed neutralizing antibodies against rIFNA during therapy. Six months after stopping therapy all the immunologic changes returned to baseline. These data suggest that the beneficial effect of rIFNA therapy on MS disease activity is probably mediated by a downregulation of proinflammatory cytokine synthesis by PB lymphocytes rather than by macrophage MHC-II antigen expression. The immunologic effects of high-dose systemic rIFNA therapy are temporary and restricted to the period of drug administration.
M. R. Bongioanni – One of the best experts on this subject based on the ideXlab platform.
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Systemic high-dose recombinant-alpha-2a-Interferon therapy modulates lymphokine production in multiple sclerosis.
Journal of the Neurological Sciences, 1996Co-Authors: M. R. Bongioanni, Luca Durelli, B Ferrero, D. Imperiale, A. Oggero, E. Verdun, G. Aimo, Roberto Pagni, Massimo Geuna, Bruno BergamascoAbstract:Chronic systemic high-dose recombinant Alpha2a–Interferon (rIFNA) therapy reduces exacerbation rate and MRI signs of disease activity in relapsing/remitting multiple sclerosis (RR MS) patients. In order to clarify the possible mechanisms underlying the clinical efficacy of rIFNA in MS, several immunologic studies were performed as a part of a pilot clinical trial. Twenty RR MS patients were treated with 9 × 106 IU of rIFNA (n = 12) or placebo (n = 8) intramuscularly every other day for 6 months. Cytokine production by cultured lymphocytes, major histocompatibility complex class II (MHC-II) antigen expression on cultured macrophages, peripheral blood (PB) and cerebrospinal fluid (CSF) lymphocyte phenotype, and IgG and beta2 microglobulin levels were studied before therapy, after 6 months of therapy, and 6 months after stopping therapy. rIFNA therapy was associated with reduction of Interferon-gamma and tumor necrosis factor-alpha production by PB lymphocytes (p < 0.04), and with slight, not significant, increase of transforming growth factor-beta2 or interleukin (IL)-10 production. IL-4 was undetectable in the culture supernatants both before and after therapy. rIFNA therapy had no effect on macrophage MHC-II molecule expression. An increased percentage of CD8 +, CD8 + high CD11b + low, and CD3 − CD16 + CD56 + cells, and of CD4 + absolute cell number was observed in CSF after rIFNA therapy. After rIFNA administration, IgG level significantly increased both systemically (p < 0.02) and intrathecally (p < 0.001). Serum beta2 microglobulin level increased (p < 0.01), as well. Only 1 out of the 12 rIFNA treated patients developed neutralizing antibodies against rIFNA during therapy. Six months after stopping therapy all the immunologic changes returned to baseline. These data suggest that the beneficial effect of rIFNA therapy on MS disease activity is probably mediated by a downregulation of proinflammatory cytokine synthesis by PB lymphocytes rather than by macrophage MHC-II antigen expression. The immunologic effects of high-dose systemic rIFNA therapy are temporary and restricted to the period of drug administration.