Andrew G. Polson
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View article: Supplementary Table 2 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Table 2 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
Supplemental Table S2: Results of a gene set enrichment analysis comparing baseline NK cells to NK cells 24 hours after T cell-dependent bispecific (TDB) treatment.
View article: Supplementary Figure 4 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figure 4 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
Cytokines produced during TDB-mediated killing impact the NK-cell transcriptome and their function.
View article: Supplementary Figure 3 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figure 3 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
NK cells exposed to TDB-treated cells have increased cytolytic function.
View article: Supplementary Figure 1 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figure 1 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
Gating strategy and time course of activation for circulating NK cells after Mosunetuzumab treatment.
View article: Data from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Data from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
T cell–retargeting therapies have transformed the therapeutic landscape for hematologic diseases. T cell–dependent bispecific antibodies (TDB) function as conditional agonists that induce a polyclonal T-cell response, resulting in target c…
View article: Supplementary Table 1 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Table 1 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
Supplemental Table S1: Results of a differential gene expression analysis comparing baseline NK cells to NK cells 24 hours after T cell-dependent bispecific (TDB) treatment.
View article: Supplementary Figure 6 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figure 6 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
In vivo CD20-TDB induces systemic cytokine release.
View article: Supplementary Figures and Legends from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figures and Legends from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
Supplementary Figures and Legends
View article: Supplementary Table 1 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Table 1 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
Supplemental Table S1: Results of a differential gene expression analysis comparing baseline NK cells to NK cells 24 hours after T cell-dependent bispecific (TDB) treatment.
View article: Supplementary Figure 4 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figure 4 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
Cytokines produced during TDB-mediated killing impact the NK-cell transcriptome and their function.
View article: Supplementary Figures and Legends from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figures and Legends from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
Supplementary Figures and Legends
View article: Supplementary Figure 2 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figure 2 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
NK-cell activation by TDB-induced killing increases expression of cytolytic genes.
View article: Supplementary Figure 5 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figure 5 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
Cytokines produced during TDB-mediated killing alters surface protein expression on macrophages.
View article: Supplementary Figure 2 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figure 2 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
NK-cell activation by TDB-induced killing increases expression of cytolytic genes.
View article: Supplementary Figure 6 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figure 6 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
In vivo CD20-TDB induces systemic cytokine release.
View article: Supplementary Figure 3 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figure 3 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
NK cells exposed to TDB-treated cells have increased cytolytic function.
View article: Supplementary Figure 1 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figure 1 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
Gating strategy and time course of activation for circulating NK cells after Mosunetuzumab treatment.
View article: Data from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Data from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
T cell–retargeting therapies have transformed the therapeutic landscape for hematologic diseases. T cell–dependent bispecific antibodies (TDB) function as conditional agonists that induce a polyclonal T-cell response, resulting in target c…
View article: Supplementary Table 2 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Table 2 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
Supplemental Table S2: Results of a gene set enrichment analysis comparing baseline NK cells to NK cells 24 hours after T cell-dependent bispecific (TDB) treatment.
View article: Supplementary Figure 5 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing
Supplementary Figure 5 from T cell–Dependent Bispecific Therapy Enhances Innate Immune Activation and Antibody-Mediated Killing Open
Cytokines produced during TDB-mediated killing alters surface protein expression on macrophages.
View article: Loss of CD20 expression as a mechanism of resistance to mosunetuzumab in relapsed/refractory B-cell lymphomas
Loss of CD20 expression as a mechanism of resistance to mosunetuzumab in relapsed/refractory B-cell lymphomas Open
CD20 is an established therapeutic target in B-cell malignancies. The CD20 × CD3 bispecific antibody mosunetuzumab has significant efficacy in B-cell non-Hodgkin lymphomas (NHLs). Because target antigen loss is a recognized mechanism of re…
View article: Supplementary Data from An Anti–CD22-<i>seco</i>-CBI-Dimer Antibody–Drug Conjugate (ADC) for the Treatment of Non-Hodgkin Lymphoma That Provides a Longer Duration of Response than Auristatin-Based ADCs in Preclinical Models
Supplementary Data from An Anti–CD22-<i>seco</i>-CBI-Dimer Antibody–Drug Conjugate (ADC) for the Treatment of Non-Hodgkin Lymphoma That Provides a Longer Duration of Response than Auristatin-Based ADCs in Preclinical Models Open
Supplementary Data
View article: Data from An Anti–CD22-<i>seco</i>-CBI-Dimer Antibody–Drug Conjugate (ADC) for the Treatment of Non-Hodgkin Lymphoma That Provides a Longer Duration of Response than Auristatin-Based ADCs in Preclinical Models
Data from An Anti–CD22-<i>seco</i>-CBI-Dimer Antibody–Drug Conjugate (ADC) for the Treatment of Non-Hodgkin Lymphoma That Provides a Longer Duration of Response than Auristatin-Based ADCs in Preclinical Models Open
We are interested in developing a second generation of antibody–drug conjugates (ADCs) for the treatment of non-Hodgkin lymphoma (NHL) that could provide a longer duration of response and be more effective in indolent NHL than the microtub…
View article: Supplementary Figure 4 from FcRL5 as a Target of Antibody–Drug Conjugates for the Treatment of Multiple Myeloma
Supplementary Figure 4 from FcRL5 as a Target of Antibody–Drug Conjugates for the Treatment of Multiple Myeloma Open
PDF file - 48KB, In vivo efficacy of anti-FcRL5-MC-vc-PAB-MMAE in combination with lenalidomide
View article: Data from Calicheamicin Antibody–Drug Conjugates with Improved Properties
Data from Calicheamicin Antibody–Drug Conjugates with Improved Properties Open
Calicheamicin antibody–drug conjugates (ADCs) are effective therapeutics for leukemias with two recently approved in the United States: Mylotarg (gemtuzumab ozogamicin) targeting CD33 for acute myeloid leukemia and Besponsa (inotuzumab ozo…
View article: Supplementary Figure 1 from DCDT2980S, an Anti-CD22-Monomethyl Auristatin E Antibody–Drug Conjugate, Is a Potential Treatment for Non-Hodgkin Lymphoma
Supplementary Figure 1 from DCDT2980S, an Anti-CD22-Monomethyl Auristatin E Antibody–Drug Conjugate, Is a Potential Treatment for Non-Hodgkin Lymphoma Open
PDF file - 61K, Supplemental Figure 1. Human, cynomolgus monkey, and rat PBMCs were isolated from whole blood in accordance with BD Vacutainer CPT protocol. Mouse PBMCs were isolated from whole blood by ACK lysis buffer treatment to lyse…
View article: Supplementary Figure 2 from FcRL5 as a Target of Antibody–Drug Conjugates for the Treatment of Multiple Myeloma
Supplementary Figure 2 from FcRL5 as a Target of Antibody–Drug Conjugates for the Treatment of Multiple Myeloma Open
PDF file - 62KB, In vivo efficacy of anti-FcRL5-SPDB-DM4 in combination with bortezomib
View article: Supplementary Data from An Anti–CD22-<i>seco</i>-CBI-Dimer Antibody–Drug Conjugate (ADC) for the Treatment of Non-Hodgkin Lymphoma That Provides a Longer Duration of Response than Auristatin-Based ADCs in Preclinical Models
Supplementary Data from An Anti–CD22-<i>seco</i>-CBI-Dimer Antibody–Drug Conjugate (ADC) for the Treatment of Non-Hodgkin Lymphoma That Provides a Longer Duration of Response than Auristatin-Based ADCs in Preclinical Models Open
Supplementary Data
View article: Data from DCDT2980S, an Anti-CD22-Monomethyl Auristatin E Antibody–Drug Conjugate, Is a Potential Treatment for Non-Hodgkin Lymphoma
Data from DCDT2980S, an Anti-CD22-Monomethyl Auristatin E Antibody–Drug Conjugate, Is a Potential Treatment for Non-Hodgkin Lymphoma Open
Antibody–drug conjugates (ADC), potent cytotoxic drugs linked to antibodies via chemical linkers, allow specific targeting of drugs to neoplastic cells. We have used this technology to develop the ADC DCDT2980S that targets CD22, an antige…
View article: Data from Intratumoral Payload Concentration Correlates with the Activity of Antibody–Drug Conjugates
Data from Intratumoral Payload Concentration Correlates with the Activity of Antibody–Drug Conjugates Open
Antibody–drug conjugates (ADC) have become important scaffolds for targeted cancer therapies. However, ADC exposure–response correlation is not well characterized. We demonstrated that intratumor payload exposures correlated well with the …