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anti psma ab (MedChemExpress)

Name: anti psma ab
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Rating: 94 (15 reviews)

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MedChemExpress anti psma ab

Evaluation of the cytotoxic activity of NK cells treated with <t>anti-PSMA</t> Ab in vitro . (A, B) The killing rates of NK cells against 22RV1 cells (PSMA strongly positive) in the NK, NK + IgG (10 μg/mL), NK + anti-PSMA Ab (5, 10, 20 μg/mL) treatment groups measured using the Cell Counting Kit-8 (CCK-8) assay at 2 and 6 h after co-culturing (n = 3). E/T = 0.5:1 (A) , 1:1 (B) , respectively; (C, D) The killing rates of NK cells against PC3 cells (PSMA negative) in the NK, NK + IgG (10 μg/mL), NK + anti-PSMA Ab (5, 10, 20 μg/mL) treatment groups measured using the CCK-8 assay at 2 and 6 h after co-culturing (n = 3). E/T = 0.5:1 (C) , 1:1 (D) , respectively; (E, F) The killing rates of NK cells against RWPE-1 cells (PSMA moderately positive) in the NK, NK + IgG (10 μg/mL), NK + anti-PSMA Ab (5, 10, 20 μg/mL) treatment groups measured using the CCK-8 assay at 2 and 6 h after co-culturing (n = 3). E/T = 0.5:1 (E) , 1:1 (F) , respectively; (G) PSA levels in the culture supernatant of NK cells co-cultured with 22RV1 cells in the control and treatment groups, including NK, NK + IgG, and NK + anti-PSMA Ab (10 μg/mL), measured via ELISA at 2, 6, 12, and 24 h after co-culturing (n = 3); (H) Representative flow cytometry plots and summary data (n = 3) of the MFI for CD107a expression in NK cells co-cultured with 22RV1 cells in the presence of anti-PSMA Ab (10 μg/mL) or IgG control (10 μg/mL). CD107a expression in NK cells was set as a negative control. Degranulation of NK cells was induced upon interaction with 22RV1 cells at a 1:1 ratio with anti-PSMA Ab or IgG for 6 h at 37 °C, the GolgiStop protein transport inhibitor was added during the final 2 h of the culture and NK cells were collected for cytometry measurement; (I, J) Comparison of supernatant perforin (I) and granzyme B (J) levels among NK cells co-cultured with 22RV1 cells and their counterparts co-cultured with 22RV1 cells in the presence of IgG control (10 μg/mL) or anti-PSMA Ab (10 μg/mL) at E:T of 1:1 after 6h coculture (n = 3). NK cells alone were set as negative control; (K, L) Comparison of IFN-γ (K) and TNF-α (L) levels among NK cells co-cultured with 22RV1 cells and their counterparts co-cultured with 22RV1 cells in the presence of IgG control (10 μg/mL) or anti-PSMA Ab (10 μg/mL) at E:T of 1:1 after 6h co-culture (n=3). NK cells alone were set as negative control; Data expressed as means ± SD were plotted, and ANOVA followed by a Tukey’s post hoc test was used to compare three or more groups (A–L) . *p < 0.05; ns, not significant. anti-PSMA Ab, anti-prostate-specific membrane antigen antibody; PSA, prostate-specific antigen; ELISA, enzyme-linked immunosorbent assay; IFN-γ, interferon-γ; TNF-α, tumor necrosis factor-α; E:T, effector-to-target ratio.

Anti Psma Ab, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Combined treatment with anti-PSMA antibody and human peripheral blood-derived NK cells for castration-resistant prostate cancer"

Article Title: Combined treatment with anti-PSMA antibody and human peripheral blood-derived NK cells for castration-resistant prostate cancer

Journal: Frontiers in Immunology

doi: 10.3389/fimmu.2025.1572676

Evaluation of the cytotoxic activity of NK cells treated with anti-PSMA Ab in vitro . (A, B) The killing rates of NK cells against 22RV1 cells (PSMA strongly positive) in the NK, NK + IgG (10 μg/mL), NK + anti-PSMA Ab (5, 10, 20 μg/mL) treatment groups measured using the Cell Counting Kit-8 (CCK-8) assay at 2 and 6 h after co-culturing (n = 3). E/T = 0.5:1 (A) , 1:1 (B) , respectively; (C, D) The killing rates of NK cells against PC3 cells (PSMA negative) in the NK, NK + IgG (10 μg/mL), NK + anti-PSMA Ab (5, 10, 20 μg/mL) treatment groups measured using the CCK-8 assay at 2 and 6 h after co-culturing (n = 3). E/T = 0.5:1 (C) , 1:1 (D) , respectively; (E, F) The killing rates of NK cells against RWPE-1 cells (PSMA moderately positive) in the NK, NK + IgG (10 μg/mL), NK + anti-PSMA Ab (5, 10, 20 μg/mL) treatment groups measured using the CCK-8 assay at 2 and 6 h after co-culturing (n = 3). E/T = 0.5:1 (E) , 1:1 (F) , respectively; (G) PSA levels in the culture supernatant of NK cells co-cultured with 22RV1 cells in the control and treatment groups, including NK, NK + IgG, and NK + anti-PSMA Ab (10 μg/mL), measured via ELISA at 2, 6, 12, and 24 h after co-culturing (n = 3); (H) Representative flow cytometry plots and summary data (n = 3) of the MFI for CD107a expression in NK cells co-cultured with 22RV1 cells in the presence of anti-PSMA Ab (10 μg/mL) or IgG control (10 μg/mL). CD107a expression in NK cells was set as a negative control. Degranulation of NK cells was induced upon interaction with 22RV1 cells at a 1:1 ratio with anti-PSMA Ab or IgG for 6 h at 37 °C, the GolgiStop protein transport inhibitor was added during the final 2 h of the culture and NK cells were collected for cytometry measurement; (I, J) Comparison of supernatant perforin (I) and granzyme B (J) levels among NK cells co-cultured with 22RV1 cells and their counterparts co-cultured with 22RV1 cells in the presence of IgG control (10 μg/mL) or anti-PSMA Ab (10 μg/mL) at E:T of 1:1 after 6h coculture (n = 3). NK cells alone were set as negative control; (K, L) Comparison of IFN-γ (K) and TNF-α (L) levels among NK cells co-cultured with 22RV1 cells and their counterparts co-cultured with 22RV1 cells in the presence of IgG control (10 μg/mL) or anti-PSMA Ab (10 μg/mL) at E:T of 1:1 after 6h co-culture (n=3). NK cells alone were set as negative control; Data expressed as means ± SD were plotted, and ANOVA followed by a Tukey’s post hoc test was used to compare three or more groups (A–L) . *p < 0.05; ns, not significant. anti-PSMA Ab, anti-prostate-specific membrane antigen antibody; PSA, prostate-specific antigen; ELISA, enzyme-linked immunosorbent assay; IFN-γ, interferon-γ; TNF-α, tumor necrosis factor-α; E:T, effector-to-target ratio.

Figure Legend Snippet: Evaluation of the cytotoxic activity of NK cells treated with anti-PSMA Ab in vitro . (A, B) The killing rates of NK cells against 22RV1 cells (PSMA strongly positive) in the NK, NK + IgG (10 μg/mL), NK + anti-PSMA Ab (5, 10, 20 μg/mL) treatment groups measured using the Cell Counting Kit-8 (CCK-8) assay at 2 and 6 h after co-culturing (n = 3). E/T = 0.5:1 (A) , 1:1 (B) , respectively; (C, D) The killing rates of NK cells against PC3 cells (PSMA negative) in the NK, NK + IgG (10 μg/mL), NK + anti-PSMA Ab (5, 10, 20 μg/mL) treatment groups measured using the CCK-8 assay at 2 and 6 h after co-culturing (n = 3). E/T = 0.5:1 (C) , 1:1 (D) , respectively; (E, F) The killing rates of NK cells against RWPE-1 cells (PSMA moderately positive) in the NK, NK + IgG (10 μg/mL), NK + anti-PSMA Ab (5, 10, 20 μg/mL) treatment groups measured using the CCK-8 assay at 2 and 6 h after co-culturing (n = 3). E/T = 0.5:1 (E) , 1:1 (F) , respectively; (G) PSA levels in the culture supernatant of NK cells co-cultured with 22RV1 cells in the control and treatment groups, including NK, NK + IgG, and NK + anti-PSMA Ab (10 μg/mL), measured via ELISA at 2, 6, 12, and 24 h after co-culturing (n = 3); (H) Representative flow cytometry plots and summary data (n = 3) of the MFI for CD107a expression in NK cells co-cultured with 22RV1 cells in the presence of anti-PSMA Ab (10 μg/mL) or IgG control (10 μg/mL). CD107a expression in NK cells was set as a negative control. Degranulation of NK cells was induced upon interaction with 22RV1 cells at a 1:1 ratio with anti-PSMA Ab or IgG for 6 h at 37 °C, the GolgiStop protein transport inhibitor was added during the final 2 h of the culture and NK cells were collected for cytometry measurement; (I, J) Comparison of supernatant perforin (I) and granzyme B (J) levels among NK cells co-cultured with 22RV1 cells and their counterparts co-cultured with 22RV1 cells in the presence of IgG control (10 μg/mL) or anti-PSMA Ab (10 μg/mL) at E:T of 1:1 after 6h coculture (n = 3). NK cells alone were set as negative control; (K, L) Comparison of IFN-γ (K) and TNF-α (L) levels among NK cells co-cultured with 22RV1 cells and their counterparts co-cultured with 22RV1 cells in the presence of IgG control (10 μg/mL) or anti-PSMA Ab (10 μg/mL) at E:T of 1:1 after 6h co-culture (n=3). NK cells alone were set as negative control; Data expressed as means ± SD were plotted, and ANOVA followed by a Tukey’s post hoc test was used to compare three or more groups (A–L) . *p < 0.05; ns, not significant. anti-PSMA Ab, anti-prostate-specific membrane antigen antibody; PSA, prostate-specific antigen; ELISA, enzyme-linked immunosorbent assay; IFN-γ, interferon-γ; TNF-α, tumor necrosis factor-α; E:T, effector-to-target ratio.

Techniques Used: Activity Assay, In Vitro, Cell Counting, CCK-8 Assay, Cell Culture, Control, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Expressing, Negative Control, Cytometry, Comparison, Co-Culture Assay, Membrane

Development of PDO PCa models and cytotoxicity of combined treatment with anti-PSMA antibody and human peripheral blood-derived NK cells against the PDO. (A) Representative hematoxylin-and-eosin images of PCa tissue-derived organoid derived from PCa specimens (scale bar 200 μm). The left image was the panorama, and the right four images were local magnifications part by part (a→a’, b→b’, c→c’, d→d’); (B) Representative PSMA immunohistochemistry images of PCa tissue-derived organoid derived from PCa specimens (scale bar 200 μm). The left image was the panorama, and the right four images were local magnifications part by part (a→a’, b→b’, c→c’, d→d’); (C) Representative bright-field image of coculture of NK cells with PCa tissue-derived organoid in the presence of IgG or the constructed anti-PSMA antibody after 2 h and 6h coculture, PDOs alone were set as controls (n = 3); (D) Cytotoxicity of NK cells with IgG or anti-PSMA antibody (10 μg/mL) against PCa tissue-derived organoid at E/T ratio of 5:1 after 2 h and 6h coculture measured using LDH assay (n = 3); (E) IFN-γ levels of the supernatant after the NK cells were co-cultured with PCa tissue-derived organoid at E/T ratio of 5:1 after 2 h and 6h coculture measured using ELISA (n = 3). Data are shown as mean ± SD. Statistical significance was determined using an unpaired t-test (D, E) . *p < 0.05; ns, not significant. PDO, patient-derived organoid; PCa, prostate cancer; PSMA, prostate-specific membrane antigen; IgG, immunoglobulin G; E/T, effector-to-target ratio; LDH, lactate dehydrogenase; IFN-γ, interferon-gamma; ELISA, enzyme-linked immunosorbent assay.

Figure Legend Snippet: Development of PDO PCa models and cytotoxicity of combined treatment with anti-PSMA antibody and human peripheral blood-derived NK cells against the PDO. (A) Representative hematoxylin-and-eosin images of PCa tissue-derived organoid derived from PCa specimens (scale bar 200 μm). The left image was the panorama, and the right four images were local magnifications part by part (a→a’, b→b’, c→c’, d→d’); (B) Representative PSMA immunohistochemistry images of PCa tissue-derived organoid derived from PCa specimens (scale bar 200 μm). The left image was the panorama, and the right four images were local magnifications part by part (a→a’, b→b’, c→c’, d→d’); (C) Representative bright-field image of coculture of NK cells with PCa tissue-derived organoid in the presence of IgG or the constructed anti-PSMA antibody after 2 h and 6h coculture, PDOs alone were set as controls (n = 3); (D) Cytotoxicity of NK cells with IgG or anti-PSMA antibody (10 μg/mL) against PCa tissue-derived organoid at E/T ratio of 5:1 after 2 h and 6h coculture measured using LDH assay (n = 3); (E) IFN-γ levels of the supernatant after the NK cells were co-cultured with PCa tissue-derived organoid at E/T ratio of 5:1 after 2 h and 6h coculture measured using ELISA (n = 3). Data are shown as mean ± SD. Statistical significance was determined using an unpaired t-test (D, E) . *p < 0.05; ns, not significant. PDO, patient-derived organoid; PCa, prostate cancer; PSMA, prostate-specific membrane antigen; IgG, immunoglobulin G; E/T, effector-to-target ratio; LDH, lactate dehydrogenase; IFN-γ, interferon-gamma; ELISA, enzyme-linked immunosorbent assay.

Techniques Used: Derivative Assay, Immunohistochemistry, Construct, Lactate Dehydrogenase Assay, Cell Culture, Enzyme-linked Immunosorbent Assay, Membrane

Anti-tumor effect of NK cells against CRPC in combination with anti-PSMA Ab in a subcutaneous tumor model in vivo . (A) Experimental protocol for the CRPC model used in (B–I) : mice were injected with PBS, anti-PSMA Ab or isotype-matched control mAb (10 mg/mg) intraperitoneally (i.p.) on days 10, 18 and injected with NK cells (1 × 10 7 ) intravenously (i.v.) on days 11, 15, 19, and 23 after injections of 2 × 10 6 22RV1 cancer cells subcutaneously (s.c.) on day 0 (n = 6 per group); (B) Tumor volumes at various times (horizontal axis) after tumor inoculation in the control, NK, NK + IgG, and NK + anti-PSMA Ab groups. Tumor volumes were calculated according to the formula L × W 2 /2, where L and W represent the longest and shortest diameters measured using a caliper, respectively (n = 6 per group); (C) Body weights in the control and treatment groups over the whole treatment course (n = 6 per group); (D) Serum PSA levels of mice in the control, NK, NK + IgG, and anti-PSMA Ab groups (n = 6 per group) on days 10, 16, 22, and 28; (E) Images of tumors in mice 28 days after tumor inoculation (n = 5–6 in each group); (F) Tumor weights corresponding to each group when harvested on day 28 (n = 5–6 in each group); (G) HE examination of tumor specimen in the control and treatment groups on day 28 (n = 5–6 in each group); (H) Serum IL-6 levels in the control and treatment groups on day 28; (I) Cumulative Kaplan–Meier survival curves for mice (n = 6 per group) after tumor implantation. Data expressed as the means ± SD were plotted, and ANOVA followed by a Tukey’s post hoc test was used for multiple group comparisons (B-D, F, H) . The Kaplan–Meier method was used to estimate survival functions, and the log-rank test was used for group comparisons (I) . *p < 0.05; ns, not significant. CRPC, castration-resistant prostate cancer; PSMA, prostate-specific membrane antigen; Ab, antibody; PSA, prostate-specific antigen; IL-6, interleukin-6.

Figure Legend Snippet: Anti-tumor effect of NK cells against CRPC in combination with anti-PSMA Ab in a subcutaneous tumor model in vivo . (A) Experimental protocol for the CRPC model used in (B–I) : mice were injected with PBS, anti-PSMA Ab or isotype-matched control mAb (10 mg/mg) intraperitoneally (i.p.) on days 10, 18 and injected with NK cells (1 × 10 7 ) intravenously (i.v.) on days 11, 15, 19, and 23 after injections of 2 × 10 6 22RV1 cancer cells subcutaneously (s.c.) on day 0 (n = 6 per group); (B) Tumor volumes at various times (horizontal axis) after tumor inoculation in the control, NK, NK + IgG, and NK + anti-PSMA Ab groups. Tumor volumes were calculated according to the formula L × W 2 /2, where L and W represent the longest and shortest diameters measured using a caliper, respectively (n = 6 per group); (C) Body weights in the control and treatment groups over the whole treatment course (n = 6 per group); (D) Serum PSA levels of mice in the control, NK, NK + IgG, and anti-PSMA Ab groups (n = 6 per group) on days 10, 16, 22, and 28; (E) Images of tumors in mice 28 days after tumor inoculation (n = 5–6 in each group); (F) Tumor weights corresponding to each group when harvested on day 28 (n = 5–6 in each group); (G) HE examination of tumor specimen in the control and treatment groups on day 28 (n = 5–6 in each group); (H) Serum IL-6 levels in the control and treatment groups on day 28; (I) Cumulative Kaplan–Meier survival curves for mice (n = 6 per group) after tumor implantation. Data expressed as the means ± SD were plotted, and ANOVA followed by a Tukey’s post hoc test was used for multiple group comparisons (B-D, F, H) . The Kaplan–Meier method was used to estimate survival functions, and the log-rank test was used for group comparisons (I) . *p < 0.05; ns, not significant. CRPC, castration-resistant prostate cancer; PSMA, prostate-specific membrane antigen; Ab, antibody; PSA, prostate-specific antigen; IL-6, interleukin-6.

Techniques Used: In Vivo, Injection, Control, Tumor Implantation, Membrane

Image Search Results

Journal: Frontiers in Immunology

Article Title: Combined treatment with anti-PSMA antibody and human peripheral blood-derived NK cells for castration-resistant prostate cancer

doi: 10.3389/fimmu.2025.1572676

Figure Lengend Snippet: Evaluation of the cytotoxic activity of NK cells treated with anti-PSMA Ab in vitro . (A, B) The killing rates of NK cells against 22RV1 cells (PSMA strongly positive) in the NK, NK + IgG (10 μg/mL), NK + anti-PSMA Ab (5, 10, 20 μg/mL) treatment groups measured using the Cell Counting Kit-8 (CCK-8) assay at 2 and 6 h after co-culturing (n = 3). E/T = 0.5:1 (A) , 1:1 (B) , respectively; (C, D) The killing rates of NK cells against PC3 cells (PSMA negative) in the NK, NK + IgG (10 μg/mL), NK + anti-PSMA Ab (5, 10, 20 μg/mL) treatment groups measured using the CCK-8 assay at 2 and 6 h after co-culturing (n = 3). E/T = 0.5:1 (C) , 1:1 (D) , respectively; (E, F) The killing rates of NK cells against RWPE-1 cells (PSMA moderately positive) in the NK, NK + IgG (10 μg/mL), NK + anti-PSMA Ab (5, 10, 20 μg/mL) treatment groups measured using the CCK-8 assay at 2 and 6 h after co-culturing (n = 3). E/T = 0.5:1 (E) , 1:1 (F) , respectively; (G) PSA levels in the culture supernatant of NK cells co-cultured with 22RV1 cells in the control and treatment groups, including NK, NK + IgG, and NK + anti-PSMA Ab (10 μg/mL), measured via ELISA at 2, 6, 12, and 24 h after co-culturing (n = 3); (H) Representative flow cytometry plots and summary data (n = 3) of the MFI for CD107a expression in NK cells co-cultured with 22RV1 cells in the presence of anti-PSMA Ab (10 μg/mL) or IgG control (10 μg/mL). CD107a expression in NK cells was set as a negative control. Degranulation of NK cells was induced upon interaction with 22RV1 cells at a 1:1 ratio with anti-PSMA Ab or IgG for 6 h at 37 °C, the GolgiStop protein transport inhibitor was added during the final 2 h of the culture and NK cells were collected for cytometry measurement; (I, J) Comparison of supernatant perforin (I) and granzyme B (J) levels among NK cells co-cultured with 22RV1 cells and their counterparts co-cultured with 22RV1 cells in the presence of IgG control (10 μg/mL) or anti-PSMA Ab (10 μg/mL) at E:T of 1:1 after 6h coculture (n = 3). NK cells alone were set as negative control; (K, L) Comparison of IFN-γ (K) and TNF-α (L) levels among NK cells co-cultured with 22RV1 cells and their counterparts co-cultured with 22RV1 cells in the presence of IgG control (10 μg/mL) or anti-PSMA Ab (10 μg/mL) at E:T of 1:1 after 6h co-culture (n=3). NK cells alone were set as negative control; Data expressed as means ± SD were plotted, and ANOVA followed by a Tukey’s post hoc test was used to compare three or more groups (A–L) . *p < 0.05; ns, not significant. anti-PSMA Ab, anti-prostate-specific membrane antigen antibody; PSA, prostate-specific antigen; ELISA, enzyme-linked immunosorbent assay; IFN-γ, interferon-γ; TNF-α, tumor necrosis factor-α; E:T, effector-to-target ratio.

Article Snippet: Anti-PSMA Ab (10 mg/kg), IgG1 isotype (Med Chem Express, HY-P99001; 10 mg/kg), or PBS were administered intraperitoneally on days 10 and 18 after tumor inoculation.

Techniques: Activity Assay, In Vitro, Cell Counting, CCK-8 Assay, Cell Culture, Control, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Expressing, Negative Control, Cytometry, Comparison, Co-Culture Assay, Membrane

Journal: Frontiers in Immunology

Article Title: Combined treatment with anti-PSMA antibody and human peripheral blood-derived NK cells for castration-resistant prostate cancer

doi: 10.3389/fimmu.2025.1572676

Figure Lengend Snippet: Development of PDO PCa models and cytotoxicity of combined treatment with anti-PSMA antibody and human peripheral blood-derived NK cells against the PDO. (A) Representative hematoxylin-and-eosin images of PCa tissue-derived organoid derived from PCa specimens (scale bar 200 μm). The left image was the panorama, and the right four images were local magnifications part by part (a→a’, b→b’, c→c’, d→d’); (B) Representative PSMA immunohistochemistry images of PCa tissue-derived organoid derived from PCa specimens (scale bar 200 μm). The left image was the panorama, and the right four images were local magnifications part by part (a→a’, b→b’, c→c’, d→d’); (C) Representative bright-field image of coculture of NK cells with PCa tissue-derived organoid in the presence of IgG or the constructed anti-PSMA antibody after 2 h and 6h coculture, PDOs alone were set as controls (n = 3); (D) Cytotoxicity of NK cells with IgG or anti-PSMA antibody (10 μg/mL) against PCa tissue-derived organoid at E/T ratio of 5:1 after 2 h and 6h coculture measured using LDH assay (n = 3); (E) IFN-γ levels of the supernatant after the NK cells were co-cultured with PCa tissue-derived organoid at E/T ratio of 5:1 after 2 h and 6h coculture measured using ELISA (n = 3). Data are shown as mean ± SD. Statistical significance was determined using an unpaired t-test (D, E) . *p < 0.05; ns, not significant. PDO, patient-derived organoid; PCa, prostate cancer; PSMA, prostate-specific membrane antigen; IgG, immunoglobulin G; E/T, effector-to-target ratio; LDH, lactate dehydrogenase; IFN-γ, interferon-gamma; ELISA, enzyme-linked immunosorbent assay.

Article Snippet: Anti-PSMA Ab (10 mg/kg), IgG1 isotype (Med Chem Express, HY-P99001; 10 mg/kg), or PBS were administered intraperitoneally on days 10 and 18 after tumor inoculation.

Techniques: Derivative Assay, Immunohistochemistry, Construct, Lactate Dehydrogenase Assay, Cell Culture, Enzyme-linked Immunosorbent Assay, Membrane

Journal: Frontiers in Immunology

Article Title: Combined treatment with anti-PSMA antibody and human peripheral blood-derived NK cells for castration-resistant prostate cancer

doi: 10.3389/fimmu.2025.1572676

Figure Lengend Snippet: Anti-tumor effect of NK cells against CRPC in combination with anti-PSMA Ab in a subcutaneous tumor model in vivo . (A) Experimental protocol for the CRPC model used in (B–I) : mice were injected with PBS, anti-PSMA Ab or isotype-matched control mAb (10 mg/mg) intraperitoneally (i.p.) on days 10, 18 and injected with NK cells (1 × 10 7 ) intravenously (i.v.) on days 11, 15, 19, and 23 after injections of 2 × 10 6 22RV1 cancer cells subcutaneously (s.c.) on day 0 (n = 6 per group); (B) Tumor volumes at various times (horizontal axis) after tumor inoculation in the control, NK, NK + IgG, and NK + anti-PSMA Ab groups. Tumor volumes were calculated according to the formula L × W 2 /2, where L and W represent the longest and shortest diameters measured using a caliper, respectively (n = 6 per group); (C) Body weights in the control and treatment groups over the whole treatment course (n = 6 per group); (D) Serum PSA levels of mice in the control, NK, NK + IgG, and anti-PSMA Ab groups (n = 6 per group) on days 10, 16, 22, and 28; (E) Images of tumors in mice 28 days after tumor inoculation (n = 5–6 in each group); (F) Tumor weights corresponding to each group when harvested on day 28 (n = 5–6 in each group); (G) HE examination of tumor specimen in the control and treatment groups on day 28 (n = 5–6 in each group); (H) Serum IL-6 levels in the control and treatment groups on day 28; (I) Cumulative Kaplan–Meier survival curves for mice (n = 6 per group) after tumor implantation. Data expressed as the means ± SD were plotted, and ANOVA followed by a Tukey’s post hoc test was used for multiple group comparisons (B-D, F, H) . The Kaplan–Meier method was used to estimate survival functions, and the log-rank test was used for group comparisons (I) . *p < 0.05; ns, not significant. CRPC, castration-resistant prostate cancer; PSMA, prostate-specific membrane antigen; Ab, antibody; PSA, prostate-specific antigen; IL-6, interleukin-6.

Article Snippet: Anti-PSMA Ab (10 mg/kg), IgG1 isotype (Med Chem Express, HY-P99001; 10 mg/kg), or PBS were administered intraperitoneally on days 10 and 18 after tumor inoculation.

Techniques: In Vivo, Injection, Control, Tumor Implantation, Membrane

Development of murine prostate cancer lines expressing hPSMA or hEGFR and their detection by PSMA Ab3.9 or Cetuximab. a Amino acid sequence of wild-type (WT) hPSMA and its NΔ9 variant lacking the MWNLL internalization domain. b Flow cytometry analysis of surface hPSMA on indicated Myc-CaP (MC) lines using commercial hPSMA-APC Ab. c Comparison of surface hPSMA expression in human LNCaP cells and MC/hPSMA(NΔ9) cells. d Detection of surface hPSMA by PSMA Ab3.9, in conjunction with goat anti-murine IgG-PE secondary Ab, on MC/hPSMA(NΔ9) cells. e Detection of surface hEGFR on MC/hEGFR cells and LNCaP cells using hEGFR-Alexa-647 Ab. f Detection of hEGFR on MC/hEGFR cells using Cetuximab, with rat anti-human IgG-PE. These data are each from a single assessment

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: PSMA antibody, humanized PSMA.CAR10.3, or Cetuximab increases prostate cancer localization of NF-κB p50-deficient immature myeloid cells (p50-IMC) and phagocytosis by their macrophage progeny

doi: 10.1007/s00262-024-03939-4

Figure Lengend Snippet: Development of murine prostate cancer lines expressing hPSMA or hEGFR and their detection by PSMA Ab3.9 or Cetuximab. a Amino acid sequence of wild-type (WT) hPSMA and its NΔ9 variant lacking the MWNLL internalization domain. b Flow cytometry analysis of surface hPSMA on indicated Myc-CaP (MC) lines using commercial hPSMA-APC Ab. c Comparison of surface hPSMA expression in human LNCaP cells and MC/hPSMA(NΔ9) cells. d Detection of surface hPSMA by PSMA Ab3.9, in conjunction with goat anti-murine IgG-PE secondary Ab, on MC/hPSMA(NΔ9) cells. e Detection of surface hEGFR on MC/hEGFR cells and LNCaP cells using hEGFR-Alexa-647 Ab. f Detection of hEGFR on MC/hEGFR cells using Cetuximab, with rat anti-human IgG-PE. These data are each from a single assessment

Article Snippet: Total cellular proteins in Laemmli sample buffer were subjected to Western blotting using anti-murine/human PSMA Ab (#12815, Cell Signaling Technology, Danvers, MA, USA) and β -actin Ab (AC-15, Sigma) as described [ ].

Techniques: Expressing, Sequencing, Variant Assay, Flow Cytometry, Comparison

PSMA antibody increases phagocytosis of hPSMA-expressing prostate cancer cells. a Diagram of the Fc domain of an Ab bound to a macrophage via the Fc receptor (FcR). b Lineage-negative (Lin − ) WT or p50 −/− murine bone marrow (mBM) cells were expanded, differentiated to macrophages using M-CSF, M1- or M2-polarized using IFNγ or IL-4, and co-cultured for 3 h with CFSE-labeled MC/PSMA(NΔ9) that had been incubated with PSMA Ab3.9 or isotype IgG control, as diagrammed. c Representative flow cytometry data, previously gating on CD11b + cells. d Results of three experiments (one repetition per experiment) evaluating CFSE + cells as a percentage of CD11b + macrophages. (mean, SD) * p < .05, ** p < .01. e CFSE-labeled macrophages (green) were co-cultured with pHRodo, Red SE-labeled MC/PSMA(NΔ9) cells and PSMA Ab3.9, followed by microscopy (bright field, red, and green channels). Phagocytosed cancer cells are indicated by white arrows

Journal: Cancer Immunology, Immunotherapy : CII

doi: 10.1007/s00262-024-03939-4

Figure Lengend Snippet: PSMA antibody increases phagocytosis of hPSMA-expressing prostate cancer cells. a Diagram of the Fc domain of an Ab bound to a macrophage via the Fc receptor (FcR). b Lineage-negative (Lin − ) WT or p50 −/− murine bone marrow (mBM) cells were expanded, differentiated to macrophages using M-CSF, M1- or M2-polarized using IFNγ or IL-4, and co-cultured for 3 h with CFSE-labeled MC/PSMA(NΔ9) that had been incubated with PSMA Ab3.9 or isotype IgG control, as diagrammed. c Representative flow cytometry data, previously gating on CD11b + cells. d Results of three experiments (one repetition per experiment) evaluating CFSE + cells as a percentage of CD11b + macrophages. (mean, SD) * p < .05, ** p < .01. e CFSE-labeled macrophages (green) were co-cultured with pHRodo, Red SE-labeled MC/PSMA(NΔ9) cells and PSMA Ab3.9, followed by microscopy (bright field, red, and green channels). Phagocytosed cancer cells are indicated by white arrows

Techniques: Expressing, Cell Culture, Labeling, Incubation, Control, Flow Cytometry, Microscopy

Development of a fully humanized PSMA.CAR10.3. Diagram of PSMA.CAR10.3, containing a leader sequence from human IgG1, an scFv domain derived from PSMA Ab10.3 by connecting its V H and V L domains with a linker peptide, spacer and trans-membrane (TM) domains from human CD8 (hCD8), and the intracellular (IC) signaling domain from human CD3ζ (hCD3ζ). PSMA Ab10.3 was developed from mice harboring only human immunoglobulin genes. The amino acid sequences of the PSMA.CAR10.3 domains are also shown

Journal: Cancer Immunology, Immunotherapy : CII

doi: 10.1007/s00262-024-03939-4

Figure Lengend Snippet: Development of a fully humanized PSMA.CAR10.3. Diagram of PSMA.CAR10.3, containing a leader sequence from human IgG1, an scFv domain derived from PSMA Ab10.3 by connecting its V H and V L domains with a linker peptide, spacer and trans-membrane (TM) domains from human CD8 (hCD8), and the intracellular (IC) signaling domain from human CD3ζ (hCD3ζ). PSMA Ab10.3 was developed from mice harboring only human immunoglobulin genes. The amino acid sequences of the PSMA.CAR10.3 domains are also shown

Techniques: Sequencing, Derivative Assay, Membrane

PSMA.CAR10.3 increases phagocytosis of hPSMA-expressing prostate cancer cells. a Diagram of a CAR expressed on a macrophage. b WT or p50 −/− Lin − murine bone marrow cells were expanded and transduced with vector or PSMA.CAR10.3, differentiated to macrophages, M1- or M2-polarized, and co-cultured with CFSE-labeled MC/PSMA(NΔ9) cells, as diagrammed. c Flow cytometry of vector- and PSMA.CAR10.3-transduced IMC, after puromycin-selection, using hPSMA-biotin and SA-APC. d Representative flow cytometry showing phagocytosis by vector versus CAR-expressing macrophages, previously gating on CD11b + cells. e Results of three experiments (one repetition per experiment) evaluating CFSE + cells as a percentage of CD11b + macrophages (mean, SD). * p < .05, ** p < .01, *** p < .001. f CFSE-labeled macrophages expressing PSMA.CAR10.3 (green) were combined with pHRodo, Red SE-labeled MC/PSMA(NΔ9) cells, followed by microscopy (bright field, red, and green channels). Phagocytosed cancer cells are indicated by white arrows

Journal: Cancer Immunology, Immunotherapy : CII

doi: 10.1007/s00262-024-03939-4

Figure Lengend Snippet: PSMA.CAR10.3 increases phagocytosis of hPSMA-expressing prostate cancer cells. a Diagram of a CAR expressed on a macrophage. b WT or p50 −/− Lin − murine bone marrow cells were expanded and transduced with vector or PSMA.CAR10.3, differentiated to macrophages, M1- or M2-polarized, and co-cultured with CFSE-labeled MC/PSMA(NΔ9) cells, as diagrammed. c Flow cytometry of vector- and PSMA.CAR10.3-transduced IMC, after puromycin-selection, using hPSMA-biotin and SA-APC. d Representative flow cytometry showing phagocytosis by vector versus CAR-expressing macrophages, previously gating on CD11b + cells. e Results of three experiments (one repetition per experiment) evaluating CFSE + cells as a percentage of CD11b + macrophages (mean, SD). * p < .05, ** p < .01, *** p < .001. f CFSE-labeled macrophages expressing PSMA.CAR10.3 (green) were combined with pHRodo, Red SE-labeled MC/PSMA(NΔ9) cells, followed by microscopy (bright field, red, and green channels). Phagocytosed cancer cells are indicated by white arrows

Techniques: Expressing, Transduction, Plasmid Preparation, Cell Culture, Labeling, Flow Cytometry, Selection, Microscopy

PSMA antibody increases p50-IMC localization to hPSMA-expressing prostate cancer tumors when given after 5-FU. a Lin − p50 −/− murine bone marrow cells were expanded, cultured with M-CSF for one day to obtain p50-IMC, CFSE-labeled, incubated with 100 μg PSMA antibody or isotype IgG control for one hour on ice, and injected into NSG mice bearing subcutaneous tumors derived from MC/CaP-hPSMA(NΔ9) cells in Matrigel, with or without 5-FU (112.5 mg/kg i.p.) given to the mice five days prior to cell injection, followed by tumor flow cytometry at 24 h, as diagrammed. b Representative CFSE/CD11b flow cytometry. c Tumor weight, total tumor CD11b + CSFE + cells, and CD11b + CSFE + cells per mg of tumor in mice that did not receive 5-FU (mean, SE; n = 4 per group, from one experiment). d Tumor weight, total tumor CD11b + CSFE + cells, and CD11b + CSFE + cells per mg of tumor in mice that did receive 5-FU (mean, SD; IgG n = 9 and PSMA Ab n = 10; data are combined from two experiments). e The experiment in d was repeated with removal of excess PSMA Ab or isotype control by centrifugation, supernatant aspiration, and resuspension in HBSS prior to injection ( n = 5 per group, from one experiment). * p < 0.05, ** p < 0.01

Journal: Cancer Immunology, Immunotherapy : CII

doi: 10.1007/s00262-024-03939-4

Figure Lengend Snippet: PSMA antibody increases p50-IMC localization to hPSMA-expressing prostate cancer tumors when given after 5-FU. a Lin − p50 −/− murine bone marrow cells were expanded, cultured with M-CSF for one day to obtain p50-IMC, CFSE-labeled, incubated with 100 μg PSMA antibody or isotype IgG control for one hour on ice, and injected into NSG mice bearing subcutaneous tumors derived from MC/CaP-hPSMA(NΔ9) cells in Matrigel, with or without 5-FU (112.5 mg/kg i.p.) given to the mice five days prior to cell injection, followed by tumor flow cytometry at 24 h, as diagrammed. b Representative CFSE/CD11b flow cytometry. c Tumor weight, total tumor CD11b + CSFE + cells, and CD11b + CSFE + cells per mg of tumor in mice that did not receive 5-FU (mean, SE; n = 4 per group, from one experiment). d Tumor weight, total tumor CD11b + CSFE + cells, and CD11b + CSFE + cells per mg of tumor in mice that did receive 5-FU (mean, SD; IgG n = 9 and PSMA Ab n = 10; data are combined from two experiments). e The experiment in d was repeated with removal of excess PSMA Ab or isotype control by centrifugation, supernatant aspiration, and resuspension in HBSS prior to injection ( n = 5 per group, from one experiment). * p < 0.05, ** p < 0.01

Techniques: Expressing, Cell Culture, Labeling, Incubation, Control, Injection, Derivative Assay, Flow Cytometry, Centrifugation

PSMA.CAR10.3 increases p50-IMC localization to hPSMA-expressing prostate cancer tumors. a Lin − p50 −/− murine bone marrow cells were expanded, transduced with vector or PSMA.CAR10.3, cultured with M-CSF, CFSE-labeled, and injected into NSG mice bearing tumors derived from MC/CaP-hPSMA(NΔ9) cells, and analyzed by flow cytometry 24 h later, as diagrammed. Mice received 5-FU five days prior to p50-IMC injection. b Tumor weight, total tumor CD11b + CFSE + cells, and CD11b + CFSE + cells per mg of tumor (mean, SD; n = 4 for vector and n = 5 for PSMA.CAR10.3, from one experiment)

Journal: Cancer Immunology, Immunotherapy : CII

doi: 10.1007/s00262-024-03939-4

Figure Lengend Snippet: PSMA.CAR10.3 increases p50-IMC localization to hPSMA-expressing prostate cancer tumors. a Lin − p50 −/− murine bone marrow cells were expanded, transduced with vector or PSMA.CAR10.3, cultured with M-CSF, CFSE-labeled, and injected into NSG mice bearing tumors derived from MC/CaP-hPSMA(NΔ9) cells, and analyzed by flow cytometry 24 h later, as diagrammed. Mice received 5-FU five days prior to p50-IMC injection. b Tumor weight, total tumor CD11b + CFSE + cells, and CD11b + CFSE + cells per mg of tumor (mean, SD; n = 4 for vector and n = 5 for PSMA.CAR10.3, from one experiment)

Techniques: Expressing, Transduction, Plasmid Preparation, Cell Culture, Labeling, Injection, Derivative Assay, Flow Cytometry

Functional characterization of a bi-specific PSMA-4-1BB aptamer conjugate. (a) Sequence and computer generated secondary structure of the PSMA-4-1BB aptamer conjugate. See Methods section for full sequence. (b) Binding to PSMA-expressing CT26 tumor cells. Parental CT26 cells, CT26 cells expressing a wild-type PSMA (PSMA-CT26) or CT26 cells expressing an internalization-deficient mutant (ΔPSMA-CT26) were incubated with anti-PSMA antibody (green) or Cy3-conjugated PSMA-4-1BB aptamer conjugate (red) and analyzed by confocal microscopy (×60 magnification). Nuclei were stained with DAPI (blue) (N = 3). (c) 4-1BB costimulation. CD8+ T cells were labeled with CFSE, activated with suboptimal concentrations of anti-CD3 antibody, and incubated with anti-4-1BB antibody/isotype control IgG, unconjugated agonistic 4-1BB/costimulation-deficient mut4-1BB aptamers, or with PSMA-4-1BB /PSMA-mut4-1BB aptamer dimer conjugates. Two days later cells were analyzed by flow cytometry (N = 2). CFSE, carboxyfluorescein succinimidyl ester; PSMA, prostate specific membrane antigen.

Journal: Molecular Therapy

Article Title: Targeting 4-1BB Costimulation to Disseminated Tumor Lesions With Bi-specific Oligonucleotide Aptamers

doi: 10.1038/mt.2011.145

Figure Lengend Snippet: Functional characterization of a bi-specific PSMA-4-1BB aptamer conjugate. (a) Sequence and computer generated secondary structure of the PSMA-4-1BB aptamer conjugate. See Methods section for full sequence. (b) Binding to PSMA-expressing CT26 tumor cells. Parental CT26 cells, CT26 cells expressing a wild-type PSMA (PSMA-CT26) or CT26 cells expressing an internalization-deficient mutant (ΔPSMA-CT26) were incubated with anti-PSMA antibody (green) or Cy3-conjugated PSMA-4-1BB aptamer conjugate (red) and analyzed by confocal microscopy (×60 magnification). Nuclei were stained with DAPI (blue) (N = 3). (c) 4-1BB costimulation. CD8+ T cells were labeled with CFSE, activated with suboptimal concentrations of anti-CD3 antibody, and incubated with anti-4-1BB antibody/isotype control IgG, unconjugated agonistic 4-1BB/costimulation-deficient mut4-1BB aptamers, or with PSMA-4-1BB /PSMA-mut4-1BB aptamer dimer conjugates. Two days later cells were analyzed by flow cytometry (N = 2). CFSE, carboxyfluorescein succinimidyl ester; PSMA, prostate specific membrane antigen.

Article Snippet: Tumor cells were washed with phosphate-buffered saline and incubated with 40 nmol/l of Cy3-labeled aptamer conjugate or with 10 mg/ml anti-PSMA Ab (MBL, Woburn, MA) and Alexa Fluor 488 goat anti-mouse IgG (Molecular Pobes, Eugene, OR).

Techniques: Functional Assay, Sequencing, Generated, Binding Assay, Expressing, Mutagenesis, Incubation, Confocal Microscopy, Staining, Labeling, Control, Flow Cytometry, Membrane

Inhibition of tumor growth in mice treated with PSMA-4-1BB aptamer conjugate. (a) Subcutaneous tumor model. Mice bearing ΔPSMA-CT26 tumors, at days 3, 4, 5, and 7 mice were treated with 50 pmol of PSMA-4-1BB aptamer conjugate, 4-1BB aptamer, PSMA aptamer, mixture of 4-1BB and PSMA aptamer, or with phosphate buffered-saline (PBS), and monitored for tumor growth. Statistical analysis of average tumor size at day 20. PBS versus PSMA, 4-1BB, 4-1BB & PSMA and PSMA-4-1BB conjugate, P = 0.1567, 0.0347, 0.075, <0.0001, respectively. PSMA-4-1BB conjugate versus PSMA & 4-1BB, P = 0.0008. (N = 1). (b) Survival curves of the aptamer treated mice. Statistical analysis. PBS versus 4-1BB & PSMA or PSMA-4-1BB conjugate, P = 0.0003 and <0.0001, respectively. 4-1BB & PSMA versus PSMA-4-1BB conjugate, P < 0.0001. (N = 1). (c) Lung metastasis model. Mice were implanted with ΔPSMA-B16/F10 cells and injected with 50 pmol of PSMA-4-1BB or PSMA-mut4-1BB aptamer conjugates at days 5, 8, 11, 14. When about half of the mice in the control groups have shown signs of morbidity (circa days 25–28), mice were killed and lungs were weighed (N = 2). PSMA, prostate specific membrane antigen.

Journal: Molecular Therapy

Article Title: Targeting 4-1BB Costimulation to Disseminated Tumor Lesions With Bi-specific Oligonucleotide Aptamers

doi: 10.1038/mt.2011.145

Figure Lengend Snippet: Inhibition of tumor growth in mice treated with PSMA-4-1BB aptamer conjugate. (a) Subcutaneous tumor model. Mice bearing ΔPSMA-CT26 tumors, at days 3, 4, 5, and 7 mice were treated with 50 pmol of PSMA-4-1BB aptamer conjugate, 4-1BB aptamer, PSMA aptamer, mixture of 4-1BB and PSMA aptamer, or with phosphate buffered-saline (PBS), and monitored for tumor growth. Statistical analysis of average tumor size at day 20. PBS versus PSMA, 4-1BB, 4-1BB & PSMA and PSMA-4-1BB conjugate, P = 0.1567, 0.0347, 0.075, <0.0001, respectively. PSMA-4-1BB conjugate versus PSMA & 4-1BB, P = 0.0008. (N = 1). (b) Survival curves of the aptamer treated mice. Statistical analysis. PBS versus 4-1BB & PSMA or PSMA-4-1BB conjugate, P = 0.0003 and <0.0001, respectively. 4-1BB & PSMA versus PSMA-4-1BB conjugate, P < 0.0001. (N = 1). (c) Lung metastasis model. Mice were implanted with ΔPSMA-B16/F10 cells and injected with 50 pmol of PSMA-4-1BB or PSMA-mut4-1BB aptamer conjugates at days 5, 8, 11, 14. When about half of the mice in the control groups have shown signs of morbidity (circa days 25–28), mice were killed and lungs were weighed (N = 2). PSMA, prostate specific membrane antigen.

Techniques: Inhibition, Saline, Injection, Control, Membrane

PSMA-binding-4-1BB aptamer conjugate mediated inhibition of tumor growth is dependent on PSMA expression on the tumor cells. Balb/c were coimplanted subcutaneously with ΔPSMA-expressing (left flank) and parental (right flank) CT26 tumor cells and treated with PSMA-binding-4-1BB aptamer conjugate. (a) 15 days post-tumor inoculation 32P-labeled aptamer conjugate was injected, and 6, 24, and 48 hours later tumors were excised and 32P content determined (three mice per group). (N = 3). (b) 3 days post-tumor inoculation mice were treated with 50 pmol per injection of PSMA-4-1BB, PSMA-mut4-1BB aptamer conjugates, or unconjugated 4-1BB aptamer (five mice per group) and tumor growth monitored.(open circle) Parental CT26, (closed circle) ΔPSMA-CT26. Statistical analysis of average tumor size at day 19: ΔPSMA-CT26 versus CT26 tumor size in the PSMA-mut4-1BB treated mice, P = 0.0051, and in the PSMA-4-1BB treated mice, P = 0.0013. ΔPSMA-CT26 tumor size in the PSMA-mut4-1BB versus PSMA-4-1BB treated mice, P = 0.0007. ΔPSMA-CT26 versus CT26 tumor size in the PSMA-4-1BB treated mice at day 15 P = 0.0096, and day 17 P = 0.0076. (N = 2). PSMA, prostate specific membrane antigen.

Journal: Molecular Therapy

Article Title: Targeting 4-1BB Costimulation to Disseminated Tumor Lesions With Bi-specific Oligonucleotide Aptamers

doi: 10.1038/mt.2011.145

Figure Lengend Snippet: PSMA-binding-4-1BB aptamer conjugate mediated inhibition of tumor growth is dependent on PSMA expression on the tumor cells. Balb/c were coimplanted subcutaneously with ΔPSMA-expressing (left flank) and parental (right flank) CT26 tumor cells and treated with PSMA-binding-4-1BB aptamer conjugate. (a) 15 days post-tumor inoculation 32P-labeled aptamer conjugate was injected, and 6, 24, and 48 hours later tumors were excised and 32P content determined (three mice per group). (N = 3). (b) 3 days post-tumor inoculation mice were treated with 50 pmol per injection of PSMA-4-1BB, PSMA-mut4-1BB aptamer conjugates, or unconjugated 4-1BB aptamer (five mice per group) and tumor growth monitored.(open circle) Parental CT26, (closed circle) ΔPSMA-CT26. Statistical analysis of average tumor size at day 19: ΔPSMA-CT26 versus CT26 tumor size in the PSMA-mut4-1BB treated mice, P = 0.0051, and in the PSMA-4-1BB treated mice, P = 0.0013. ΔPSMA-CT26 tumor size in the PSMA-mut4-1BB versus PSMA-4-1BB treated mice, P = 0.0007. ΔPSMA-CT26 versus CT26 tumor size in the PSMA-4-1BB treated mice at day 15 P = 0.0096, and day 17 P = 0.0076. (N = 2). PSMA, prostate specific membrane antigen.

Techniques: Binding Assay, Inhibition, Expressing, Labeling, Injection, Membrane

PSMA-targeted 4-1BB costimulation potentiates vaccine-induced tumor immunity. Mice bearing B16.F10 tumors were treated with 25 pmol per injection of PSMA-4-1BB aptamer conjugates and/or vaccinated with GM-CSF expressing irradiated tumor cells38 at day 5 post-tumor inoculation. Lung metastasis was determined by measuring lung weight (left) and visual inspection (right) (N = 1). PSMA, prostate specific membrane antigen.

Journal: Molecular Therapy

Article Title: Targeting 4-1BB Costimulation to Disseminated Tumor Lesions With Bi-specific Oligonucleotide Aptamers

doi: 10.1038/mt.2011.145

Figure Lengend Snippet: PSMA-targeted 4-1BB costimulation potentiates vaccine-induced tumor immunity. Mice bearing B16.F10 tumors were treated with 25 pmol per injection of PSMA-4-1BB aptamer conjugates and/or vaccinated with GM-CSF expressing irradiated tumor cells38 at day 5 post-tumor inoculation. Lung metastasis was determined by measuring lung weight (left) and visual inspection (right) (N = 1). PSMA, prostate specific membrane antigen.

Techniques: Injection, Expressing, Irradiation, Membrane

PSMA- and 4-1BB-dependent intratumoral infiltration of transgenic Pmel-1 CD8 T cells in mice treated with PSMA-4-1BB aptamer conjugate. At days 11, 12, 13, and 17 B16/F10 (B16) or ΔPSMA-expressing B16/F10 (ΔPSMA-B16) tumor-bearing mice implanted with Pmel-1 CD8+ T cells were treated with PSMA-4-1BB or PSMA-binding-mut4-1BB aptamer conjugate (50 pmol per injection) or with PBS. At day 21 mice were killed, tumor isolated, and the number of tumor-infiltrating Pmel-1 cell was determined by flow cytometry. Where indicated, anti-4-1BB or isotype antibody was injected intratumorally immediately after aptamer injection. N = 2. PSMA, prostate specific membrane antigen.

Journal: Molecular Therapy

Article Title: Targeting 4-1BB Costimulation to Disseminated Tumor Lesions With Bi-specific Oligonucleotide Aptamers

doi: 10.1038/mt.2011.145

Figure Lengend Snippet: PSMA- and 4-1BB-dependent intratumoral infiltration of transgenic Pmel-1 CD8 T cells in mice treated with PSMA-4-1BB aptamer conjugate. At days 11, 12, 13, and 17 B16/F10 (B16) or ΔPSMA-expressing B16/F10 (ΔPSMA-B16) tumor-bearing mice implanted with Pmel-1 CD8+ T cells were treated with PSMA-4-1BB or PSMA-binding-mut4-1BB aptamer conjugate (50 pmol per injection) or with PBS. At day 21 mice were killed, tumor isolated, and the number of tumor-infiltrating Pmel-1 cell was determined by flow cytometry. Where indicated, anti-4-1BB or isotype antibody was injected intratumorally immediately after aptamer injection. N = 2. PSMA, prostate specific membrane antigen.

Techniques: Transgenic Assay, Expressing, Binding Assay, Injection, Isolation, Flow Cytometry, Membrane

Therapeutic index of costimulatory 4-1BB ligands. (a) Comparative analysis of the tumor inhibitory capacity of PSMA-4-1BB aptamer conjugate, free 4-1BB aptamer and 4-1BB antibody. ΔPSMA-CT26 tumor-bearing mice were treated with PBS (open circle), 50 (closed triangle) or 500 (open triangle) pmol per injection of anti-4-1BB antibody, 50 (closed square) or 500 (open square) pmol per injection of unconjugated 4-1BB aptamer, or 50 pmol per injection of PSMA-binding-4-1BB aptamer conjugates (closed circle), starting at day 3 post-tumor implantation (10 mice per group). Data were separated into two panels for clarity purposes. Left panel compares the 4-1BB antibody to the unconjugated 4-1BB aptamer and the right panel compares the unconjugated to the PSMA-conjugated 4-1BB aptamer. (N = 1). (b) Evaluation of nonspecific immune stimulatory effects in mice treated with therapeutic doses of 4-1BB ligands. Balb/c mice were injected with 4-1BB antibody (500 pmol per injection), unconjugated 4-1BB aptamer (500 pmol per injection), PSMA-4-1-BB aptamer conjugate (50 pmol per injection), or PBS at days 1, 2, 3, 5. Two weeks after the last injection mice were killed, the spleen and the two inguinal lymph nodes were weighed and percentage of CD8 T cells in spleen and liver was determined by flow cytometry. (N = 2). PSMA, prostate specific membrane antigen.

Journal: Molecular Therapy

Article Title: Targeting 4-1BB Costimulation to Disseminated Tumor Lesions With Bi-specific Oligonucleotide Aptamers

doi: 10.1038/mt.2011.145

Figure Lengend Snippet: Therapeutic index of costimulatory 4-1BB ligands. (a) Comparative analysis of the tumor inhibitory capacity of PSMA-4-1BB aptamer conjugate, free 4-1BB aptamer and 4-1BB antibody. ΔPSMA-CT26 tumor-bearing mice were treated with PBS (open circle), 50 (closed triangle) or 500 (open triangle) pmol per injection of anti-4-1BB antibody, 50 (closed square) or 500 (open square) pmol per injection of unconjugated 4-1BB aptamer, or 50 pmol per injection of PSMA-binding-4-1BB aptamer conjugates (closed circle), starting at day 3 post-tumor implantation (10 mice per group). Data were separated into two panels for clarity purposes. Left panel compares the 4-1BB antibody to the unconjugated 4-1BB aptamer and the right panel compares the unconjugated to the PSMA-conjugated 4-1BB aptamer. (N = 1). (b) Evaluation of nonspecific immune stimulatory effects in mice treated with therapeutic doses of 4-1BB ligands. Balb/c mice were injected with 4-1BB antibody (500 pmol per injection), unconjugated 4-1BB aptamer (500 pmol per injection), PSMA-4-1-BB aptamer conjugate (50 pmol per injection), or PBS at days 1, 2, 3, 5. Two weeks after the last injection mice were killed, the spleen and the two inguinal lymph nodes were weighed and percentage of CD8 T cells in spleen and liver was determined by flow cytometry. (N = 2). PSMA, prostate specific membrane antigen.

Techniques: Injection, Binding Assay, Tumor Implantation, Flow Cytometry, Membrane

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