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Sally J. Denardo - One of the best experts on this subject based on the ideXlab platform.

  • survival benefit associated with human anti mouse antibody hama in patients with b cell malignancies
    Cancer Immunology Immunotherapy, 2006
    Co-Authors: Ignacio Azinovic, Gary R. Mirick, Bonnie M. Bradt, Gerald L. Denardo, Kathleen R Lamborn, Desiree S Goldstein, Sally J. Denardo
    Abstract:

    Background: About one-third of patients with relapsed B-cell malignancies develop human anti-mouse antibody (HAMA) following mouse antibody treatment. The purpose of this study was to assess the relationship between HAMA and survival in patients given a mouse anti-lymphoma monoclonal antibody (mAb), Lym-1, directed against a unique epitope of HLA-DR Antigen that is up-regulated on malignant B-cells. Methods: ELISA was used to quantify HAMA in 51 patients with B-cell malignancies treated with iodine-131 (131I) labeled Lym-1. Sera were collected prior to and following radioimmunotherapy (RIT) with 131I-Lym-1 until documented to be HAMA negative or throughout lifetime. Univariate, then multivariate analyses including other risk factors, were used to analyze the relationship of HAMA to survival. The relationships of HAMA to prior chemotherapies and to absolute lymphocyte counts prior to RIT were also assessed. Results: Eighteen of 51 patients (35%) developed HAMA following RIT (range of ultimate maximum titers, 6.6–1,802 μg/ml). Using the time dependent Cox proportional hazards model, maximum HAMA titers were associated with survival (P=0.02). HAMA continued to be significant for survival in multivariate analyses that included known risk factors. In Landmark analysis of 39 patients that survived at least 16 weeks, median survival of patients with HAMA less than 5 μg/ml was 61 versus 103 weeks for patients with HAMA equal or greater than 5 μg/ml at 16 weeks (P=0.02). The median survival of the five patients with highest maximum HAMA titers was 244 weeks. At 16 weeks, there was an inverse correlation between the maximum HAMA titer and the number of previous chemotherapies (P<0.003). Absolute lymphocyte counts prior to 131I-Lym-1 treatment for patients that seroconverted were higher than those for patients that did not seroconvert (P=0.01). Conclusions: Patients with B-cell malignancies that developed high HAMA titers had longer survival that was not explained by risk factors or histologic grade, suggesting the importance of the immune system.

  • survival benefit associated with human anti mouse antibody hama in patients with b cell malignancies
    Cancer Immunology Immunotherapy, 2006
    Co-Authors: Ignacio Azinovic, Gary R. Mirick, Bonnie M. Bradt, Gerald L. Denardo, Kathleen R Lamborn, Desiree S Goldstein, Sally J. Denardo
    Abstract:

    Background: About one-third of patients with relapsed B-cell malignancies develop human anti-mouse antibody (HAMA) following mouse antibody treatment. The purpose of this study was to assess the relationship between HAMA and survival in patients given a mouse anti-lymphoma monoclonal antibody (mAb), Lym-1, directed against a unique epitope of HLA-DR Antigen that is up-regulated on malignant B-cells. Methods: ELISA was used to quantify HAMA in 51 patients with B-cell malignancies treated with iodine-131 (131I) labeled Lym-1. Sera were collected prior to and following radioimmunotherapy (RIT) with 131I-Lym-1 until documented to be HAMA negative or throughout lifetime. Univariate, then multivariate analyses including other risk factors, were used to analyze the relationship of HAMA to survival. The relationships of HAMA to prior chemotherapies and to absolute lymphocyte counts prior to RIT were also assessed. Results: Eighteen of 51 patients (35%) developed HAMA following RIT (range of ultimate maximum titers, 6.6–1,802 μg/ml). Using the time dependent Cox proportional hazards model, maximum HAMA titers were associated with survival (P=0.02). HAMA continued to be significant for survival in multivariate analyses that included known risk factors. In Landmark analysis of 39 patients that survived at least 16 weeks, median survival of patients with HAMA less than 5 μg/ml was 61 versus 103 weeks for patients with HAMA equal or greater than 5 μg/ml at 16 weeks (P=0.02). The median survival of the five patients with highest maximum HAMA titers was 244 weeks. At 16 weeks, there was an inverse correlation between the maximum HAMA titer and the number of previous chemotherapies (P<0.003). Absolute lymphocyte counts prior to 131I-Lym-1 treatment for patients that seroconverted were higher than those for patients that did not seroconvert (P=0.01). Conclusions: Patients with B-cell malignancies that developed high HAMA titers had longer survival that was not explained by risk factors or histologic grade, suggesting the importance of the immune system.

Mary M - One of the best experts on this subject based on the ideXlab platform.

  • development of a receptor peptide antagonist to human γ interferon and characterization of its ligand bound conformation using transferred nuclear overhauser effect spectroscopy
    Journal of Biological Chemistry, 1995
    Co-Authors: Gail F Seelig, Winifred W Prosise, Julio C Hawkins, Mary M
    Abstract:

    Abstract Polyclonal anti-idiotypic antibody raised to a synthetic discontinuous peptide derived from the human -interferon (huIFN-) sequence recognizes soluble human -interferon receptor (Seelig, G. F., Prosise, W. W., and Taremi, S. S. (1994) J. Biol. Chem. 269, 358-363). We sought to use this reagent to identify a ligand-binding domain within IFN--receptor. To do this, the neutralizing anti-idiotypic antibody was used to probe overlapping linear peptide octamers of the extracellular domain of the huIFN- receptor. A 22-amino-acid residue receptor segment 120-141 identified by the antibody was synthesized. CD and NMR analysis indicates that peptide 120-141 has no apparent secondary structure in water or in water containing 50% trifluoroethanol. The synthetic receptor peptide inhibited huIFN- induced expression of HLA/DR Antigen on Colo 205 cells with an approximate ICof 35 μ M. Immobilized peptide specifically bound recombinant huIFN- but did not bind human granulocyte-macrophage colony-stimulating factor on a microtiter plate in a direct binding enzyme-linked immunosorbent assay. The binding results are supported by two-dimensional transferred nuclear Over-hauser effect (TRNOE) NMR data obtained on the peptide in the presence of recombinant huIFN-. Characterization of the conformation of the bound peptide by TRNOE suggests that this peptide assumes a distinct conformation. Intramolecular interactions within the bound peptide were detected at two non-contiguous regions and at a third region comprising a β-turn formed by the sequence DIRK. We believe that this represents the structure of the receptor within the ligand-binding domain.

  • development of a receptor peptide antagonist to human interferon and characterization of its ligand bound conformation using transferred nuclear overhauser effect spectroscopy
    Journal of Biological Chemistry, 1995
    Co-Authors: Gail F Seelig, Winifred W Prosise, Julio C Hawkins, Mary M
    Abstract:

    Abstract Polyclonal anti-idiotypic antibody raised to a synthetic discontinuous peptide derived from the human -interferon (huIFN-) sequence recognizes soluble human -interferon receptor (Seelig, G. F., Prosise, W. W., and Taremi, S. S. (1994) J. Biol. Chem. 269, 358-363). We sought to use this reagent to identify a ligand-binding domain within IFN--receptor. To do this, the neutralizing anti-idiotypic antibody was used to probe overlapping linear peptide octamers of the extracellular domain of the huIFN- receptor. A 22-amino-acid residue receptor segment 120-141 identified by the antibody was synthesized. CD and NMR analysis indicates that peptide 120-141 has no apparent secondary structure in water or in water containing 50% trifluoroethanol. The synthetic receptor peptide inhibited huIFN- induced expression of HLA/DR Antigen on Colo 205 cells with an approximate ICof 35 μ M. Immobilized peptide specifically bound recombinant huIFN- but did not bind human granulocyte-macrophage colony-stimulating factor on a microtiter plate in a direct binding enzyme-linked immunosorbent assay. The binding results are supported by two-dimensional transferred nuclear Over-hauser effect (TRNOE) NMR data obtained on the peptide in the presence of recombinant huIFN-. Characterization of the conformation of the bound peptide by TRNOE suggests that this peptide assumes a distinct conformation. Intramolecular interactions within the bound peptide were detected at two non-contiguous regions and at a third region comprising a β-turn formed by the sequence DIRK. We believe that this represents the structure of the receptor within the ligand-binding domain.

Ignacio Azinovic - One of the best experts on this subject based on the ideXlab platform.

  • survival benefit associated with human anti mouse antibody hama in patients with b cell malignancies
    Cancer Immunology Immunotherapy, 2006
    Co-Authors: Ignacio Azinovic, Gary R. Mirick, Bonnie M. Bradt, Gerald L. Denardo, Kathleen R Lamborn, Desiree S Goldstein, Sally J. Denardo
    Abstract:

    Background: About one-third of patients with relapsed B-cell malignancies develop human anti-mouse antibody (HAMA) following mouse antibody treatment. The purpose of this study was to assess the relationship between HAMA and survival in patients given a mouse anti-lymphoma monoclonal antibody (mAb), Lym-1, directed against a unique epitope of HLA-DR Antigen that is up-regulated on malignant B-cells. Methods: ELISA was used to quantify HAMA in 51 patients with B-cell malignancies treated with iodine-131 (131I) labeled Lym-1. Sera were collected prior to and following radioimmunotherapy (RIT) with 131I-Lym-1 until documented to be HAMA negative or throughout lifetime. Univariate, then multivariate analyses including other risk factors, were used to analyze the relationship of HAMA to survival. The relationships of HAMA to prior chemotherapies and to absolute lymphocyte counts prior to RIT were also assessed. Results: Eighteen of 51 patients (35%) developed HAMA following RIT (range of ultimate maximum titers, 6.6–1,802 μg/ml). Using the time dependent Cox proportional hazards model, maximum HAMA titers were associated with survival (P=0.02). HAMA continued to be significant for survival in multivariate analyses that included known risk factors. In Landmark analysis of 39 patients that survived at least 16 weeks, median survival of patients with HAMA less than 5 μg/ml was 61 versus 103 weeks for patients with HAMA equal or greater than 5 μg/ml at 16 weeks (P=0.02). The median survival of the five patients with highest maximum HAMA titers was 244 weeks. At 16 weeks, there was an inverse correlation between the maximum HAMA titer and the number of previous chemotherapies (P<0.003). Absolute lymphocyte counts prior to 131I-Lym-1 treatment for patients that seroconverted were higher than those for patients that did not seroconvert (P=0.01). Conclusions: Patients with B-cell malignancies that developed high HAMA titers had longer survival that was not explained by risk factors or histologic grade, suggesting the importance of the immune system.

  • survival benefit associated with human anti mouse antibody hama in patients with b cell malignancies
    Cancer Immunology Immunotherapy, 2006
    Co-Authors: Ignacio Azinovic, Gary R. Mirick, Bonnie M. Bradt, Gerald L. Denardo, Kathleen R Lamborn, Desiree S Goldstein, Sally J. Denardo
    Abstract:

    Background: About one-third of patients with relapsed B-cell malignancies develop human anti-mouse antibody (HAMA) following mouse antibody treatment. The purpose of this study was to assess the relationship between HAMA and survival in patients given a mouse anti-lymphoma monoclonal antibody (mAb), Lym-1, directed against a unique epitope of HLA-DR Antigen that is up-regulated on malignant B-cells. Methods: ELISA was used to quantify HAMA in 51 patients with B-cell malignancies treated with iodine-131 (131I) labeled Lym-1. Sera were collected prior to and following radioimmunotherapy (RIT) with 131I-Lym-1 until documented to be HAMA negative or throughout lifetime. Univariate, then multivariate analyses including other risk factors, were used to analyze the relationship of HAMA to survival. The relationships of HAMA to prior chemotherapies and to absolute lymphocyte counts prior to RIT were also assessed. Results: Eighteen of 51 patients (35%) developed HAMA following RIT (range of ultimate maximum titers, 6.6–1,802 μg/ml). Using the time dependent Cox proportional hazards model, maximum HAMA titers were associated with survival (P=0.02). HAMA continued to be significant for survival in multivariate analyses that included known risk factors. In Landmark analysis of 39 patients that survived at least 16 weeks, median survival of patients with HAMA less than 5 μg/ml was 61 versus 103 weeks for patients with HAMA equal or greater than 5 μg/ml at 16 weeks (P=0.02). The median survival of the five patients with highest maximum HAMA titers was 244 weeks. At 16 weeks, there was an inverse correlation between the maximum HAMA titer and the number of previous chemotherapies (P<0.003). Absolute lymphocyte counts prior to 131I-Lym-1 treatment for patients that seroconverted were higher than those for patients that did not seroconvert (P=0.01). Conclusions: Patients with B-cell malignancies that developed high HAMA titers had longer survival that was not explained by risk factors or histologic grade, suggesting the importance of the immune system.

Gail F Seelig - One of the best experts on this subject based on the ideXlab platform.

  • development of a receptor peptide antagonist to human γ interferon and characterization of its ligand bound conformation using transferred nuclear overhauser effect spectroscopy
    Journal of Biological Chemistry, 1995
    Co-Authors: Gail F Seelig, Winifred W Prosise, Julio C Hawkins, Mary M
    Abstract:

    Abstract Polyclonal anti-idiotypic antibody raised to a synthetic discontinuous peptide derived from the human -interferon (huIFN-) sequence recognizes soluble human -interferon receptor (Seelig, G. F., Prosise, W. W., and Taremi, S. S. (1994) J. Biol. Chem. 269, 358-363). We sought to use this reagent to identify a ligand-binding domain within IFN--receptor. To do this, the neutralizing anti-idiotypic antibody was used to probe overlapping linear peptide octamers of the extracellular domain of the huIFN- receptor. A 22-amino-acid residue receptor segment 120-141 identified by the antibody was synthesized. CD and NMR analysis indicates that peptide 120-141 has no apparent secondary structure in water or in water containing 50% trifluoroethanol. The synthetic receptor peptide inhibited huIFN- induced expression of HLA/DR Antigen on Colo 205 cells with an approximate ICof 35 μ M. Immobilized peptide specifically bound recombinant huIFN- but did not bind human granulocyte-macrophage colony-stimulating factor on a microtiter plate in a direct binding enzyme-linked immunosorbent assay. The binding results are supported by two-dimensional transferred nuclear Over-hauser effect (TRNOE) NMR data obtained on the peptide in the presence of recombinant huIFN-. Characterization of the conformation of the bound peptide by TRNOE suggests that this peptide assumes a distinct conformation. Intramolecular interactions within the bound peptide were detected at two non-contiguous regions and at a third region comprising a β-turn formed by the sequence DIRK. We believe that this represents the structure of the receptor within the ligand-binding domain.

  • development of a receptor peptide antagonist to human interferon and characterization of its ligand bound conformation using transferred nuclear overhauser effect spectroscopy
    Journal of Biological Chemistry, 1995
    Co-Authors: Gail F Seelig, Winifred W Prosise, Julio C Hawkins, Mary M
    Abstract:

    Abstract Polyclonal anti-idiotypic antibody raised to a synthetic discontinuous peptide derived from the human -interferon (huIFN-) sequence recognizes soluble human -interferon receptor (Seelig, G. F., Prosise, W. W., and Taremi, S. S. (1994) J. Biol. Chem. 269, 358-363). We sought to use this reagent to identify a ligand-binding domain within IFN--receptor. To do this, the neutralizing anti-idiotypic antibody was used to probe overlapping linear peptide octamers of the extracellular domain of the huIFN- receptor. A 22-amino-acid residue receptor segment 120-141 identified by the antibody was synthesized. CD and NMR analysis indicates that peptide 120-141 has no apparent secondary structure in water or in water containing 50% trifluoroethanol. The synthetic receptor peptide inhibited huIFN- induced expression of HLA/DR Antigen on Colo 205 cells with an approximate ICof 35 μ M. Immobilized peptide specifically bound recombinant huIFN- but did not bind human granulocyte-macrophage colony-stimulating factor on a microtiter plate in a direct binding enzyme-linked immunosorbent assay. The binding results are supported by two-dimensional transferred nuclear Over-hauser effect (TRNOE) NMR data obtained on the peptide in the presence of recombinant huIFN-. Characterization of the conformation of the bound peptide by TRNOE suggests that this peptide assumes a distinct conformation. Intramolecular interactions within the bound peptide were detected at two non-contiguous regions and at a third region comprising a β-turn formed by the sequence DIRK. We believe that this represents the structure of the receptor within the ligand-binding domain.

Desiree S Goldstein - One of the best experts on this subject based on the ideXlab platform.

  • survival benefit associated with human anti mouse antibody hama in patients with b cell malignancies
    Cancer Immunology Immunotherapy, 2006
    Co-Authors: Ignacio Azinovic, Gary R. Mirick, Bonnie M. Bradt, Gerald L. Denardo, Kathleen R Lamborn, Desiree S Goldstein, Sally J. Denardo
    Abstract:

    Background: About one-third of patients with relapsed B-cell malignancies develop human anti-mouse antibody (HAMA) following mouse antibody treatment. The purpose of this study was to assess the relationship between HAMA and survival in patients given a mouse anti-lymphoma monoclonal antibody (mAb), Lym-1, directed against a unique epitope of HLA-DR Antigen that is up-regulated on malignant B-cells. Methods: ELISA was used to quantify HAMA in 51 patients with B-cell malignancies treated with iodine-131 (131I) labeled Lym-1. Sera were collected prior to and following radioimmunotherapy (RIT) with 131I-Lym-1 until documented to be HAMA negative or throughout lifetime. Univariate, then multivariate analyses including other risk factors, were used to analyze the relationship of HAMA to survival. The relationships of HAMA to prior chemotherapies and to absolute lymphocyte counts prior to RIT were also assessed. Results: Eighteen of 51 patients (35%) developed HAMA following RIT (range of ultimate maximum titers, 6.6–1,802 μg/ml). Using the time dependent Cox proportional hazards model, maximum HAMA titers were associated with survival (P=0.02). HAMA continued to be significant for survival in multivariate analyses that included known risk factors. In Landmark analysis of 39 patients that survived at least 16 weeks, median survival of patients with HAMA less than 5 μg/ml was 61 versus 103 weeks for patients with HAMA equal or greater than 5 μg/ml at 16 weeks (P=0.02). The median survival of the five patients with highest maximum HAMA titers was 244 weeks. At 16 weeks, there was an inverse correlation between the maximum HAMA titer and the number of previous chemotherapies (P<0.003). Absolute lymphocyte counts prior to 131I-Lym-1 treatment for patients that seroconverted were higher than those for patients that did not seroconvert (P=0.01). Conclusions: Patients with B-cell malignancies that developed high HAMA titers had longer survival that was not explained by risk factors or histologic grade, suggesting the importance of the immune system.

  • survival benefit associated with human anti mouse antibody hama in patients with b cell malignancies
    Cancer Immunology Immunotherapy, 2006
    Co-Authors: Ignacio Azinovic, Gary R. Mirick, Bonnie M. Bradt, Gerald L. Denardo, Kathleen R Lamborn, Desiree S Goldstein, Sally J. Denardo
    Abstract:

    Background: About one-third of patients with relapsed B-cell malignancies develop human anti-mouse antibody (HAMA) following mouse antibody treatment. The purpose of this study was to assess the relationship between HAMA and survival in patients given a mouse anti-lymphoma monoclonal antibody (mAb), Lym-1, directed against a unique epitope of HLA-DR Antigen that is up-regulated on malignant B-cells. Methods: ELISA was used to quantify HAMA in 51 patients with B-cell malignancies treated with iodine-131 (131I) labeled Lym-1. Sera were collected prior to and following radioimmunotherapy (RIT) with 131I-Lym-1 until documented to be HAMA negative or throughout lifetime. Univariate, then multivariate analyses including other risk factors, were used to analyze the relationship of HAMA to survival. The relationships of HAMA to prior chemotherapies and to absolute lymphocyte counts prior to RIT were also assessed. Results: Eighteen of 51 patients (35%) developed HAMA following RIT (range of ultimate maximum titers, 6.6–1,802 μg/ml). Using the time dependent Cox proportional hazards model, maximum HAMA titers were associated with survival (P=0.02). HAMA continued to be significant for survival in multivariate analyses that included known risk factors. In Landmark analysis of 39 patients that survived at least 16 weeks, median survival of patients with HAMA less than 5 μg/ml was 61 versus 103 weeks for patients with HAMA equal or greater than 5 μg/ml at 16 weeks (P=0.02). The median survival of the five patients with highest maximum HAMA titers was 244 weeks. At 16 weeks, there was an inverse correlation between the maximum HAMA titer and the number of previous chemotherapies (P<0.003). Absolute lymphocyte counts prior to 131I-Lym-1 treatment for patients that seroconverted were higher than those for patients that did not seroconvert (P=0.01). Conclusions: Patients with B-cell malignancies that developed high HAMA titers had longer survival that was not explained by risk factors or histologic grade, suggesting the importance of the immune system.