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human mesothelin duoset elisa  (R&D Systems)


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    R&D Systems human mesothelin duoset elisa
    A) Schematic of dual-targeting Meso-FAP CAR TEAM T cells engineered to co-target PDAC tumor cells, through a <t>mesothelin-targeting</t> CAR, and tumor-associated CAFs, through a secreted FAP-targeting TEAM molecule. The secreted FAP TEAM molecule can redirect the cytotoxicity of both meso-CAR-T cells as well as CAR-negative bystander T cells that are present in the tumor microenvironment 8 . Created in BioRender.com . Escobar, Giulia. https://app.biorender.com/illustrations/66eeece9f2d42f9534e90be7?slideId=be6d217b-9bf9–4f4e-8420-dc13e4db9d9bB ). Schematic of the experimental design. Mice are implanted with subcutaneous AsPC-1 tumors cells and then adoptively transferred with meso-CAR-T cells (3e6) or UTD T cells by intravenous injection at 14 days post tumor challenge. C) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated as shown in B (n=6 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 74%). D) Survival curve of mice treated as shown in B. Mantel-Cox test. E) Schematic of the experimental design. Mice are injected intraperitoneally with AsPC-1 tumor cells and allowed to form peritoneal tumors. 7 days post tumor challenge, mice were adoptively transferred with meso-CAR-T cells (2e6) or UTD T cells by intravenous or intraperitoneal injections. F) Tumor growth kinetic (flux, photons/s, mean ± SEM) as measured by bioluminescence imaging (BLI) in mice treated as shown in E (n=6–7 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 91%). G) Tumor burden in each individual mouse from F as measured by BLI. H) Absolute numbers (mean ± SEM) of meso-CAR-T cells in the blood of AsPC-1 tumor-bearing mice from F, treated as indicated and as shown in E. Two-way ANOVA. I) Proportion of CD4 and CD8 T cells within CAR-T cells in the blood of mice in F, at day15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. J) Phenotype of CD4-positive and CD8-positive CAR-T cells in the peripheral blood of tumor-bearing mice from F, at day 15 following CAR-T cell adoptive transfer by intraperitoneal or intravenous injection. T stem cell memory cells (TSCM, CD45RA+CCR7+CD95+), central memory (CM, CD45RA-CCR7+), effector memory (CD45RA-CCR7-) and terminally differentiated effector memory (TEMRA, CD45RA+CCR7-) T cells. Unpaired Student’s t test. K) Expression of PD-1, TIM3 and CD39 markers (frequency, mean ± SEM) on the surface of CD4-positive and CD8-positive CAR-T cells in the blood of mice from F, at day 15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. **p<0.01, ***p<0.001, ****p<0.0001.
    Human Mesothelin Duoset Elisa, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+mesothelin+duoset+elisa/pmc12720996-144-9-13?v=R%26D+Systems
    Average 93 stars, based on 6 article reviews
    human mesothelin duoset elisa - by Bioz Stars, 2026-08
    93/100 stars

    Images

    1) Product Images from "Ibrutinib and PD-1 blockade potentiate mesothelin-targeting CAR-T cell therapy in preclinical models of pancreatic cancer"

    Article Title: Ibrutinib and PD-1 blockade potentiate mesothelin-targeting CAR-T cell therapy in preclinical models of pancreatic cancer

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    doi: 10.1158/1078-0432.CCR-25-2907

    A) Schematic of dual-targeting Meso-FAP CAR TEAM T cells engineered to co-target PDAC tumor cells, through a mesothelin-targeting CAR, and tumor-associated CAFs, through a secreted FAP-targeting TEAM molecule. The secreted FAP TEAM molecule can redirect the cytotoxicity of both meso-CAR-T cells as well as CAR-negative bystander T cells that are present in the tumor microenvironment 8 . Created in BioRender.com . Escobar, Giulia. https://app.biorender.com/illustrations/66eeece9f2d42f9534e90be7?slideId=be6d217b-9bf9–4f4e-8420-dc13e4db9d9bB ). Schematic of the experimental design. Mice are implanted with subcutaneous AsPC-1 tumors cells and then adoptively transferred with meso-CAR-T cells (3e6) or UTD T cells by intravenous injection at 14 days post tumor challenge. C) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated as shown in B (n=6 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 74%). D) Survival curve of mice treated as shown in B. Mantel-Cox test. E) Schematic of the experimental design. Mice are injected intraperitoneally with AsPC-1 tumor cells and allowed to form peritoneal tumors. 7 days post tumor challenge, mice were adoptively transferred with meso-CAR-T cells (2e6) or UTD T cells by intravenous or intraperitoneal injections. F) Tumor growth kinetic (flux, photons/s, mean ± SEM) as measured by bioluminescence imaging (BLI) in mice treated as shown in E (n=6–7 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 91%). G) Tumor burden in each individual mouse from F as measured by BLI. H) Absolute numbers (mean ± SEM) of meso-CAR-T cells in the blood of AsPC-1 tumor-bearing mice from F, treated as indicated and as shown in E. Two-way ANOVA. I) Proportion of CD4 and CD8 T cells within CAR-T cells in the blood of mice in F, at day15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. J) Phenotype of CD4-positive and CD8-positive CAR-T cells in the peripheral blood of tumor-bearing mice from F, at day 15 following CAR-T cell adoptive transfer by intraperitoneal or intravenous injection. T stem cell memory cells (TSCM, CD45RA+CCR7+CD95+), central memory (CM, CD45RA-CCR7+), effector memory (CD45RA-CCR7-) and terminally differentiated effector memory (TEMRA, CD45RA+CCR7-) T cells. Unpaired Student’s t test. K) Expression of PD-1, TIM3 and CD39 markers (frequency, mean ± SEM) on the surface of CD4-positive and CD8-positive CAR-T cells in the blood of mice from F, at day 15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. **p<0.01, ***p<0.001, ****p<0.0001.
    Figure Legend Snippet: A) Schematic of dual-targeting Meso-FAP CAR TEAM T cells engineered to co-target PDAC tumor cells, through a mesothelin-targeting CAR, and tumor-associated CAFs, through a secreted FAP-targeting TEAM molecule. The secreted FAP TEAM molecule can redirect the cytotoxicity of both meso-CAR-T cells as well as CAR-negative bystander T cells that are present in the tumor microenvironment 8 . Created in BioRender.com . Escobar, Giulia. https://app.biorender.com/illustrations/66eeece9f2d42f9534e90be7?slideId=be6d217b-9bf9–4f4e-8420-dc13e4db9d9bB ). Schematic of the experimental design. Mice are implanted with subcutaneous AsPC-1 tumors cells and then adoptively transferred with meso-CAR-T cells (3e6) or UTD T cells by intravenous injection at 14 days post tumor challenge. C) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated as shown in B (n=6 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 74%). D) Survival curve of mice treated as shown in B. Mantel-Cox test. E) Schematic of the experimental design. Mice are injected intraperitoneally with AsPC-1 tumor cells and allowed to form peritoneal tumors. 7 days post tumor challenge, mice were adoptively transferred with meso-CAR-T cells (2e6) or UTD T cells by intravenous or intraperitoneal injections. F) Tumor growth kinetic (flux, photons/s, mean ± SEM) as measured by bioluminescence imaging (BLI) in mice treated as shown in E (n=6–7 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 91%). G) Tumor burden in each individual mouse from F as measured by BLI. H) Absolute numbers (mean ± SEM) of meso-CAR-T cells in the blood of AsPC-1 tumor-bearing mice from F, treated as indicated and as shown in E. Two-way ANOVA. I) Proportion of CD4 and CD8 T cells within CAR-T cells in the blood of mice in F, at day15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. J) Phenotype of CD4-positive and CD8-positive CAR-T cells in the peripheral blood of tumor-bearing mice from F, at day 15 following CAR-T cell adoptive transfer by intraperitoneal or intravenous injection. T stem cell memory cells (TSCM, CD45RA+CCR7+CD95+), central memory (CM, CD45RA-CCR7+), effector memory (CD45RA-CCR7-) and terminally differentiated effector memory (TEMRA, CD45RA+CCR7-) T cells. Unpaired Student’s t test. K) Expression of PD-1, TIM3 and CD39 markers (frequency, mean ± SEM) on the surface of CD4-positive and CD8-positive CAR-T cells in the blood of mice from F, at day 15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. **p<0.01, ***p<0.001, ****p<0.0001.

    Techniques Used: Injection, Transduction, Imaging, Adoptive Transfer Assay, Expressing

    A) Representative histograms of ADAM-10 and ADAM-17 expression in the indicated pancreatic cancer cell lines as measured by flow cytometry. B) Representative flow histograms of mesothelin expression in the indicated pancreatic cancer cell lines. C-E) Representative flow histograms (C) and quantification (C-E; mean ± SEM; frequency and mean fluorescence intensity, MFI) of mesothelin expression in AsPC-1, CAPAN-2 and BxPC-3 tumor cells either left untreated (DMSO) or treated with the indicated concentrations of aderbasib for 72 hours. Mesothelin knock-out (Meso-KO) AsPC-1 tumor cells are included as a negative control. Shown is one of two independent experiments per tumor cell line. One-way ANOVA with Dunnett’s multiple comparison test, vs DMSO-treated condition. F) Quantification (mean ± SEM) of soluble mesothelin by ELISA in the culture supernatant of the indicated pancreatic tumor cell lines treated for 72 hours with increasing concentrations of aderbasib. Meso-KO AsPC-1 cells are included as a negative control. One-way ANOVA with Dunnett’s multiple comparison test, vs DMSO-treated condition. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.
    Figure Legend Snippet: A) Representative histograms of ADAM-10 and ADAM-17 expression in the indicated pancreatic cancer cell lines as measured by flow cytometry. B) Representative flow histograms of mesothelin expression in the indicated pancreatic cancer cell lines. C-E) Representative flow histograms (C) and quantification (C-E; mean ± SEM; frequency and mean fluorescence intensity, MFI) of mesothelin expression in AsPC-1, CAPAN-2 and BxPC-3 tumor cells either left untreated (DMSO) or treated with the indicated concentrations of aderbasib for 72 hours. Mesothelin knock-out (Meso-KO) AsPC-1 tumor cells are included as a negative control. Shown is one of two independent experiments per tumor cell line. One-way ANOVA with Dunnett’s multiple comparison test, vs DMSO-treated condition. F) Quantification (mean ± SEM) of soluble mesothelin by ELISA in the culture supernatant of the indicated pancreatic tumor cell lines treated for 72 hours with increasing concentrations of aderbasib. Meso-KO AsPC-1 cells are included as a negative control. One-way ANOVA with Dunnett’s multiple comparison test, vs DMSO-treated condition. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

    Techniques Used: Expressing, In Vitro, Flow Cytometry, Fluorescence, Knock-Out, Negative Control, Comparison, Enzyme-linked Immunosorbent Assay

    A) Fold change over timepoint 0 of the green area (mean ± SEM) of GFP-positive pancreatic tumor cells cultured alone or together with untransduced T cells (UTD) or meso-CAR-T cells in the absence (DMSO) or presence of 5uM aderbasib. Healthy donor (HD) 105 was used to manufacture meso-CAR-T cells. Two-way ANOVA is calculated between the meso-CAR + DMSO and the meso-CAR + aderbasib groups and between the UTD + DMSO and UTD + aderbasib groups. B) Schematic of the experimental design. AsPC-1-tumor bearing mice received aderbasib treatment by oral gavage (60mg/kg) starting 3 days prior and up to 14 days post adoptive transfer of 3e6 meso-CAR-T cells. C) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated with UTD T cells or 3e6 meso-CAR-T cells either as monotherapy or in combination with aderbasib (treatment window is indicated by the lilac square. n=6 mice per group). HD53 was used to manufacture meso-CAR-T cells (transduction: 66%, viability at infusion: >80%). Two-way ANOVA. D) Absolute numbers (mean ± SEM) of meso-CAR-T cells in the blood of AsPC-1 tumor-bearing mice treated as indicated and as shown in B. E) Schematic of the experimental design. AsPC-1 tumor-bearing mice received aderbasib treatment by oral gavage (60mg/kg) starting 4 days post CAR-T cell transfer (1.5e6 cells) and up to day 25. F) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated with UTD T cells or 1.5e6 meso-CAR-T cells either as monotherapy or in combination with aderbasib (treatment window is indicated by the lilac square; n=4–6 mice per group). Two-way ANOVA. HD207 was used to generate meso-CAR-T cells (transduction: 68%, viability at infusion: >80%). G) Representative flow histograms and quantification (frequency and MFI, mean ± SEM) of mesothelin expression in AsPC-1 (GFP+) tumors harvested at day 28 from mice treated with UTD T cells alone or in combination with aderbasib from F. Statistical significance was determined using unpaired Student’s t test. *p<0.05, **p<0.01, ****p<0.0001.
    Figure Legend Snippet: A) Fold change over timepoint 0 of the green area (mean ± SEM) of GFP-positive pancreatic tumor cells cultured alone or together with untransduced T cells (UTD) or meso-CAR-T cells in the absence (DMSO) or presence of 5uM aderbasib. Healthy donor (HD) 105 was used to manufacture meso-CAR-T cells. Two-way ANOVA is calculated between the meso-CAR + DMSO and the meso-CAR + aderbasib groups and between the UTD + DMSO and UTD + aderbasib groups. B) Schematic of the experimental design. AsPC-1-tumor bearing mice received aderbasib treatment by oral gavage (60mg/kg) starting 3 days prior and up to 14 days post adoptive transfer of 3e6 meso-CAR-T cells. C) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated with UTD T cells or 3e6 meso-CAR-T cells either as monotherapy or in combination with aderbasib (treatment window is indicated by the lilac square. n=6 mice per group). HD53 was used to manufacture meso-CAR-T cells (transduction: 66%, viability at infusion: >80%). Two-way ANOVA. D) Absolute numbers (mean ± SEM) of meso-CAR-T cells in the blood of AsPC-1 tumor-bearing mice treated as indicated and as shown in B. E) Schematic of the experimental design. AsPC-1 tumor-bearing mice received aderbasib treatment by oral gavage (60mg/kg) starting 4 days post CAR-T cell transfer (1.5e6 cells) and up to day 25. F) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated with UTD T cells or 1.5e6 meso-CAR-T cells either as monotherapy or in combination with aderbasib (treatment window is indicated by the lilac square; n=4–6 mice per group). Two-way ANOVA. HD207 was used to generate meso-CAR-T cells (transduction: 68%, viability at infusion: >80%). G) Representative flow histograms and quantification (frequency and MFI, mean ± SEM) of mesothelin expression in AsPC-1 (GFP+) tumors harvested at day 28 from mice treated with UTD T cells alone or in combination with aderbasib from F. Statistical significance was determined using unpaired Student’s t test. *p<0.05, **p<0.01, ****p<0.0001.

    Techniques Used: In Vitro, In Vivo, Cell Culture, Adoptive Transfer Assay, Transduction, Expressing



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    R&D Systems immunosorbent assays elisa
    A) Schematic of dual-targeting Meso-FAP CAR TEAM T cells engineered to co-target PDAC tumor cells, through a <t>mesothelin-targeting</t> CAR, and tumor-associated CAFs, through a secreted FAP-targeting TEAM molecule. The secreted FAP TEAM molecule can redirect the cytotoxicity of both meso-CAR-T cells as well as CAR-negative bystander T cells that are present in the tumor microenvironment 8 . Created in BioRender.com . Escobar, Giulia. https://app.biorender.com/illustrations/66eeece9f2d42f9534e90be7?slideId=be6d217b-9bf9–4f4e-8420-dc13e4db9d9bB ). Schematic of the experimental design. Mice are implanted with subcutaneous AsPC-1 tumors cells and then adoptively transferred with meso-CAR-T cells (3e6) or UTD T cells by intravenous injection at 14 days post tumor challenge. C) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated as shown in B (n=6 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 74%). D) Survival curve of mice treated as shown in B. Mantel-Cox test. E) Schematic of the experimental design. Mice are injected intraperitoneally with AsPC-1 tumor cells and allowed to form peritoneal tumors. 7 days post tumor challenge, mice were adoptively transferred with meso-CAR-T cells (2e6) or UTD T cells by intravenous or intraperitoneal injections. F) Tumor growth kinetic (flux, photons/s, mean ± SEM) as measured by bioluminescence imaging (BLI) in mice treated as shown in E (n=6–7 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 91%). G) Tumor burden in each individual mouse from F as measured by BLI. H) Absolute numbers (mean ± SEM) of meso-CAR-T cells in the blood of AsPC-1 tumor-bearing mice from F, treated as indicated and as shown in E. Two-way ANOVA. I) Proportion of CD4 and CD8 T cells within CAR-T cells in the blood of mice in F, at day15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. J) Phenotype of CD4-positive and CD8-positive CAR-T cells in the peripheral blood of tumor-bearing mice from F, at day 15 following CAR-T cell adoptive transfer by intraperitoneal or intravenous injection. T stem cell memory cells (TSCM, CD45RA+CCR7+CD95+), central memory (CM, CD45RA-CCR7+), effector memory (CD45RA-CCR7-) and terminally differentiated effector memory (TEMRA, CD45RA+CCR7-) T cells. Unpaired Student’s t test. K) Expression of PD-1, TIM3 and CD39 markers (frequency, mean ± SEM) on the surface of CD4-positive and CD8-positive CAR-T cells in the blood of mice from F, at day 15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. **p<0.01, ***p<0.001, ****p<0.0001.
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    human mesothelin propeptide mpf duoset elisa  (R&D Systems)
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    R&D Systems human mesothelin propeptide mpf duoset elisa
    A) Schematic of dual-targeting Meso-FAP CAR TEAM T cells engineered to co-target PDAC tumor cells, through a <t>mesothelin-targeting</t> CAR, and tumor-associated CAFs, through a secreted FAP-targeting TEAM molecule. The secreted FAP TEAM molecule can redirect the cytotoxicity of both meso-CAR-T cells as well as CAR-negative bystander T cells that are present in the tumor microenvironment 8 . Created in BioRender.com . Escobar, Giulia. https://app.biorender.com/illustrations/66eeece9f2d42f9534e90be7?slideId=be6d217b-9bf9–4f4e-8420-dc13e4db9d9bB ). Schematic of the experimental design. Mice are implanted with subcutaneous AsPC-1 tumors cells and then adoptively transferred with meso-CAR-T cells (3e6) or UTD T cells by intravenous injection at 14 days post tumor challenge. C) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated as shown in B (n=6 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 74%). D) Survival curve of mice treated as shown in B. Mantel-Cox test. E) Schematic of the experimental design. Mice are injected intraperitoneally with AsPC-1 tumor cells and allowed to form peritoneal tumors. 7 days post tumor challenge, mice were adoptively transferred with meso-CAR-T cells (2e6) or UTD T cells by intravenous or intraperitoneal injections. F) Tumor growth kinetic (flux, photons/s, mean ± SEM) as measured by bioluminescence imaging (BLI) in mice treated as shown in E (n=6–7 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 91%). G) Tumor burden in each individual mouse from F as measured by BLI. H) Absolute numbers (mean ± SEM) of meso-CAR-T cells in the blood of AsPC-1 tumor-bearing mice from F, treated as indicated and as shown in E. Two-way ANOVA. I) Proportion of CD4 and CD8 T cells within CAR-T cells in the blood of mice in F, at day15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. J) Phenotype of CD4-positive and CD8-positive CAR-T cells in the peripheral blood of tumor-bearing mice from F, at day 15 following CAR-T cell adoptive transfer by intraperitoneal or intravenous injection. T stem cell memory cells (TSCM, CD45RA+CCR7+CD95+), central memory (CM, CD45RA-CCR7+), effector memory (CD45RA-CCR7-) and terminally differentiated effector memory (TEMRA, CD45RA+CCR7-) T cells. Unpaired Student’s t test. K) Expression of PD-1, TIM3 and CD39 markers (frequency, mean ± SEM) on the surface of CD4-positive and CD8-positive CAR-T cells in the blood of mice from F, at day 15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. **p<0.01, ***p<0.001, ****p<0.0001.
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    dy3265  (R&D Systems)
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    R&D Systems dy3265
    A) Schematic of dual-targeting Meso-FAP CAR TEAM T cells engineered to co-target PDAC tumor cells, through a <t>mesothelin-targeting</t> CAR, and tumor-associated CAFs, through a secreted FAP-targeting TEAM molecule. The secreted FAP TEAM molecule can redirect the cytotoxicity of both meso-CAR-T cells as well as CAR-negative bystander T cells that are present in the tumor microenvironment 8 . Created in BioRender.com . Escobar, Giulia. https://app.biorender.com/illustrations/66eeece9f2d42f9534e90be7?slideId=be6d217b-9bf9–4f4e-8420-dc13e4db9d9bB ). Schematic of the experimental design. Mice are implanted with subcutaneous AsPC-1 tumors cells and then adoptively transferred with meso-CAR-T cells (3e6) or UTD T cells by intravenous injection at 14 days post tumor challenge. C) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated as shown in B (n=6 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 74%). D) Survival curve of mice treated as shown in B. Mantel-Cox test. E) Schematic of the experimental design. Mice are injected intraperitoneally with AsPC-1 tumor cells and allowed to form peritoneal tumors. 7 days post tumor challenge, mice were adoptively transferred with meso-CAR-T cells (2e6) or UTD T cells by intravenous or intraperitoneal injections. F) Tumor growth kinetic (flux, photons/s, mean ± SEM) as measured by bioluminescence imaging (BLI) in mice treated as shown in E (n=6–7 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 91%). G) Tumor burden in each individual mouse from F as measured by BLI. H) Absolute numbers (mean ± SEM) of meso-CAR-T cells in the blood of AsPC-1 tumor-bearing mice from F, treated as indicated and as shown in E. Two-way ANOVA. I) Proportion of CD4 and CD8 T cells within CAR-T cells in the blood of mice in F, at day15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. J) Phenotype of CD4-positive and CD8-positive CAR-T cells in the peripheral blood of tumor-bearing mice from F, at day 15 following CAR-T cell adoptive transfer by intraperitoneal or intravenous injection. T stem cell memory cells (TSCM, CD45RA+CCR7+CD95+), central memory (CM, CD45RA-CCR7+), effector memory (CD45RA-CCR7-) and terminally differentiated effector memory (TEMRA, CD45RA+CCR7-) T cells. Unpaired Student’s t test. K) Expression of PD-1, TIM3 and CD39 markers (frequency, mean ± SEM) on the surface of CD4-positive and CD8-positive CAR-T cells in the blood of mice from F, at day 15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. **p<0.01, ***p<0.001, ****p<0.0001.
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    coefficient  (R&D Systems)
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    A) Schematic of dual-targeting Meso-FAP CAR TEAM T cells engineered to co-target PDAC tumor cells, through a <t>mesothelin-targeting</t> CAR, and tumor-associated CAFs, through a secreted FAP-targeting TEAM molecule. The secreted FAP TEAM molecule can redirect the cytotoxicity of both meso-CAR-T cells as well as CAR-negative bystander T cells that are present in the tumor microenvironment 8 . Created in BioRender.com . Escobar, Giulia. https://app.biorender.com/illustrations/66eeece9f2d42f9534e90be7?slideId=be6d217b-9bf9–4f4e-8420-dc13e4db9d9bB ). Schematic of the experimental design. Mice are implanted with subcutaneous AsPC-1 tumors cells and then adoptively transferred with meso-CAR-T cells (3e6) or UTD T cells by intravenous injection at 14 days post tumor challenge. C) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated as shown in B (n=6 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 74%). D) Survival curve of mice treated as shown in B. Mantel-Cox test. E) Schematic of the experimental design. Mice are injected intraperitoneally with AsPC-1 tumor cells and allowed to form peritoneal tumors. 7 days post tumor challenge, mice were adoptively transferred with meso-CAR-T cells (2e6) or UTD T cells by intravenous or intraperitoneal injections. F) Tumor growth kinetic (flux, photons/s, mean ± SEM) as measured by bioluminescence imaging (BLI) in mice treated as shown in E (n=6–7 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 91%). G) Tumor burden in each individual mouse from F as measured by BLI. H) Absolute numbers (mean ± SEM) of meso-CAR-T cells in the blood of AsPC-1 tumor-bearing mice from F, treated as indicated and as shown in E. Two-way ANOVA. I) Proportion of CD4 and CD8 T cells within CAR-T cells in the blood of mice in F, at day15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. J) Phenotype of CD4-positive and CD8-positive CAR-T cells in the peripheral blood of tumor-bearing mice from F, at day 15 following CAR-T cell adoptive transfer by intraperitoneal or intravenous injection. T stem cell memory cells (TSCM, CD45RA+CCR7+CD95+), central memory (CM, CD45RA-CCR7+), effector memory (CD45RA-CCR7-) and terminally differentiated effector memory (TEMRA, CD45RA+CCR7-) T cells. Unpaired Student’s t test. K) Expression of PD-1, TIM3 and CD39 markers (frequency, mean ± SEM) on the surface of CD4-positive and CD8-positive CAR-T cells in the blood of mice from F, at day 15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. **p<0.01, ***p<0.001, ****p<0.0001.
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    Image Search Results


    A) Schematic of dual-targeting Meso-FAP CAR TEAM T cells engineered to co-target PDAC tumor cells, through a mesothelin-targeting CAR, and tumor-associated CAFs, through a secreted FAP-targeting TEAM molecule. The secreted FAP TEAM molecule can redirect the cytotoxicity of both meso-CAR-T cells as well as CAR-negative bystander T cells that are present in the tumor microenvironment 8 . Created in BioRender.com . Escobar, Giulia. https://app.biorender.com/illustrations/66eeece9f2d42f9534e90be7?slideId=be6d217b-9bf9–4f4e-8420-dc13e4db9d9bB ). Schematic of the experimental design. Mice are implanted with subcutaneous AsPC-1 tumors cells and then adoptively transferred with meso-CAR-T cells (3e6) or UTD T cells by intravenous injection at 14 days post tumor challenge. C) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated as shown in B (n=6 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 74%). D) Survival curve of mice treated as shown in B. Mantel-Cox test. E) Schematic of the experimental design. Mice are injected intraperitoneally with AsPC-1 tumor cells and allowed to form peritoneal tumors. 7 days post tumor challenge, mice were adoptively transferred with meso-CAR-T cells (2e6) or UTD T cells by intravenous or intraperitoneal injections. F) Tumor growth kinetic (flux, photons/s, mean ± SEM) as measured by bioluminescence imaging (BLI) in mice treated as shown in E (n=6–7 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 91%). G) Tumor burden in each individual mouse from F as measured by BLI. H) Absolute numbers (mean ± SEM) of meso-CAR-T cells in the blood of AsPC-1 tumor-bearing mice from F, treated as indicated and as shown in E. Two-way ANOVA. I) Proportion of CD4 and CD8 T cells within CAR-T cells in the blood of mice in F, at day15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. J) Phenotype of CD4-positive and CD8-positive CAR-T cells in the peripheral blood of tumor-bearing mice from F, at day 15 following CAR-T cell adoptive transfer by intraperitoneal or intravenous injection. T stem cell memory cells (TSCM, CD45RA+CCR7+CD95+), central memory (CM, CD45RA-CCR7+), effector memory (CD45RA-CCR7-) and terminally differentiated effector memory (TEMRA, CD45RA+CCR7-) T cells. Unpaired Student’s t test. K) Expression of PD-1, TIM3 and CD39 markers (frequency, mean ± SEM) on the surface of CD4-positive and CD8-positive CAR-T cells in the blood of mice from F, at day 15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. **p<0.01, ***p<0.001, ****p<0.0001.

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    Article Title: Ibrutinib and PD-1 blockade potentiate mesothelin-targeting CAR-T cell therapy in preclinical models of pancreatic cancer

    doi: 10.1158/1078-0432.CCR-25-2907

    Figure Lengend Snippet: A) Schematic of dual-targeting Meso-FAP CAR TEAM T cells engineered to co-target PDAC tumor cells, through a mesothelin-targeting CAR, and tumor-associated CAFs, through a secreted FAP-targeting TEAM molecule. The secreted FAP TEAM molecule can redirect the cytotoxicity of both meso-CAR-T cells as well as CAR-negative bystander T cells that are present in the tumor microenvironment 8 . Created in BioRender.com . Escobar, Giulia. https://app.biorender.com/illustrations/66eeece9f2d42f9534e90be7?slideId=be6d217b-9bf9–4f4e-8420-dc13e4db9d9bB ). Schematic of the experimental design. Mice are implanted with subcutaneous AsPC-1 tumors cells and then adoptively transferred with meso-CAR-T cells (3e6) or UTD T cells by intravenous injection at 14 days post tumor challenge. C) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated as shown in B (n=6 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 74%). D) Survival curve of mice treated as shown in B. Mantel-Cox test. E) Schematic of the experimental design. Mice are injected intraperitoneally with AsPC-1 tumor cells and allowed to form peritoneal tumors. 7 days post tumor challenge, mice were adoptively transferred with meso-CAR-T cells (2e6) or UTD T cells by intravenous or intraperitoneal injections. F) Tumor growth kinetic (flux, photons/s, mean ± SEM) as measured by bioluminescence imaging (BLI) in mice treated as shown in E (n=6–7 mice per group). Two-way ANOVA. HD53 was used to generate meso-CAR-T cells (transduction: 72%, viability at infusion: 91%). G) Tumor burden in each individual mouse from F as measured by BLI. H) Absolute numbers (mean ± SEM) of meso-CAR-T cells in the blood of AsPC-1 tumor-bearing mice from F, treated as indicated and as shown in E. Two-way ANOVA. I) Proportion of CD4 and CD8 T cells within CAR-T cells in the blood of mice in F, at day15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. J) Phenotype of CD4-positive and CD8-positive CAR-T cells in the peripheral blood of tumor-bearing mice from F, at day 15 following CAR-T cell adoptive transfer by intraperitoneal or intravenous injection. T stem cell memory cells (TSCM, CD45RA+CCR7+CD95+), central memory (CM, CD45RA-CCR7+), effector memory (CD45RA-CCR7-) and terminally differentiated effector memory (TEMRA, CD45RA+CCR7-) T cells. Unpaired Student’s t test. K) Expression of PD-1, TIM3 and CD39 markers (frequency, mean ± SEM) on the surface of CD4-positive and CD8-positive CAR-T cells in the blood of mice from F, at day 15 post adoptive CAR-T cell transfer by intravenous or intraperitoneal injection. Unpaired Student’s t test. **p<0.01, ***p<0.001, ****p<0.0001.

    Article Snippet: To analyze soluble mesothelin in the culture supernatant, the Human Mesothelin DuoSet ELISA (R&D Systems, DY3265) kit was used according to manufacturer protocol.

    Techniques: Injection, Transduction, Imaging, Adoptive Transfer Assay, Expressing

    A) Representative histograms of ADAM-10 and ADAM-17 expression in the indicated pancreatic cancer cell lines as measured by flow cytometry. B) Representative flow histograms of mesothelin expression in the indicated pancreatic cancer cell lines. C-E) Representative flow histograms (C) and quantification (C-E; mean ± SEM; frequency and mean fluorescence intensity, MFI) of mesothelin expression in AsPC-1, CAPAN-2 and BxPC-3 tumor cells either left untreated (DMSO) or treated with the indicated concentrations of aderbasib for 72 hours. Mesothelin knock-out (Meso-KO) AsPC-1 tumor cells are included as a negative control. Shown is one of two independent experiments per tumor cell line. One-way ANOVA with Dunnett’s multiple comparison test, vs DMSO-treated condition. F) Quantification (mean ± SEM) of soluble mesothelin by ELISA in the culture supernatant of the indicated pancreatic tumor cell lines treated for 72 hours with increasing concentrations of aderbasib. Meso-KO AsPC-1 cells are included as a negative control. One-way ANOVA with Dunnett’s multiple comparison test, vs DMSO-treated condition. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    Article Title: Ibrutinib and PD-1 blockade potentiate mesothelin-targeting CAR-T cell therapy in preclinical models of pancreatic cancer

    doi: 10.1158/1078-0432.CCR-25-2907

    Figure Lengend Snippet: A) Representative histograms of ADAM-10 and ADAM-17 expression in the indicated pancreatic cancer cell lines as measured by flow cytometry. B) Representative flow histograms of mesothelin expression in the indicated pancreatic cancer cell lines. C-E) Representative flow histograms (C) and quantification (C-E; mean ± SEM; frequency and mean fluorescence intensity, MFI) of mesothelin expression in AsPC-1, CAPAN-2 and BxPC-3 tumor cells either left untreated (DMSO) or treated with the indicated concentrations of aderbasib for 72 hours. Mesothelin knock-out (Meso-KO) AsPC-1 tumor cells are included as a negative control. Shown is one of two independent experiments per tumor cell line. One-way ANOVA with Dunnett’s multiple comparison test, vs DMSO-treated condition. F) Quantification (mean ± SEM) of soluble mesothelin by ELISA in the culture supernatant of the indicated pancreatic tumor cell lines treated for 72 hours with increasing concentrations of aderbasib. Meso-KO AsPC-1 cells are included as a negative control. One-way ANOVA with Dunnett’s multiple comparison test, vs DMSO-treated condition. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

    Article Snippet: To analyze soluble mesothelin in the culture supernatant, the Human Mesothelin DuoSet ELISA (R&D Systems, DY3265) kit was used according to manufacturer protocol.

    Techniques: Expressing, In Vitro, Flow Cytometry, Fluorescence, Knock-Out, Negative Control, Comparison, Enzyme-linked Immunosorbent Assay

    A) Fold change over timepoint 0 of the green area (mean ± SEM) of GFP-positive pancreatic tumor cells cultured alone or together with untransduced T cells (UTD) or meso-CAR-T cells in the absence (DMSO) or presence of 5uM aderbasib. Healthy donor (HD) 105 was used to manufacture meso-CAR-T cells. Two-way ANOVA is calculated between the meso-CAR + DMSO and the meso-CAR + aderbasib groups and between the UTD + DMSO and UTD + aderbasib groups. B) Schematic of the experimental design. AsPC-1-tumor bearing mice received aderbasib treatment by oral gavage (60mg/kg) starting 3 days prior and up to 14 days post adoptive transfer of 3e6 meso-CAR-T cells. C) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated with UTD T cells or 3e6 meso-CAR-T cells either as monotherapy or in combination with aderbasib (treatment window is indicated by the lilac square. n=6 mice per group). HD53 was used to manufacture meso-CAR-T cells (transduction: 66%, viability at infusion: >80%). Two-way ANOVA. D) Absolute numbers (mean ± SEM) of meso-CAR-T cells in the blood of AsPC-1 tumor-bearing mice treated as indicated and as shown in B. E) Schematic of the experimental design. AsPC-1 tumor-bearing mice received aderbasib treatment by oral gavage (60mg/kg) starting 4 days post CAR-T cell transfer (1.5e6 cells) and up to day 25. F) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated with UTD T cells or 1.5e6 meso-CAR-T cells either as monotherapy or in combination with aderbasib (treatment window is indicated by the lilac square; n=4–6 mice per group). Two-way ANOVA. HD207 was used to generate meso-CAR-T cells (transduction: 68%, viability at infusion: >80%). G) Representative flow histograms and quantification (frequency and MFI, mean ± SEM) of mesothelin expression in AsPC-1 (GFP+) tumors harvested at day 28 from mice treated with UTD T cells alone or in combination with aderbasib from F. Statistical significance was determined using unpaired Student’s t test. *p<0.05, **p<0.01, ****p<0.0001.

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    Article Title: Ibrutinib and PD-1 blockade potentiate mesothelin-targeting CAR-T cell therapy in preclinical models of pancreatic cancer

    doi: 10.1158/1078-0432.CCR-25-2907

    Figure Lengend Snippet: A) Fold change over timepoint 0 of the green area (mean ± SEM) of GFP-positive pancreatic tumor cells cultured alone or together with untransduced T cells (UTD) or meso-CAR-T cells in the absence (DMSO) or presence of 5uM aderbasib. Healthy donor (HD) 105 was used to manufacture meso-CAR-T cells. Two-way ANOVA is calculated between the meso-CAR + DMSO and the meso-CAR + aderbasib groups and between the UTD + DMSO and UTD + aderbasib groups. B) Schematic of the experimental design. AsPC-1-tumor bearing mice received aderbasib treatment by oral gavage (60mg/kg) starting 3 days prior and up to 14 days post adoptive transfer of 3e6 meso-CAR-T cells. C) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated with UTD T cells or 3e6 meso-CAR-T cells either as monotherapy or in combination with aderbasib (treatment window is indicated by the lilac square. n=6 mice per group). HD53 was used to manufacture meso-CAR-T cells (transduction: 66%, viability at infusion: >80%). Two-way ANOVA. D) Absolute numbers (mean ± SEM) of meso-CAR-T cells in the blood of AsPC-1 tumor-bearing mice treated as indicated and as shown in B. E) Schematic of the experimental design. AsPC-1 tumor-bearing mice received aderbasib treatment by oral gavage (60mg/kg) starting 4 days post CAR-T cell transfer (1.5e6 cells) and up to day 25. F) Tumor growth kinetic (tumor volume, mean ± SEM) in AsPC-1 tumor-bearing mice treated with UTD T cells or 1.5e6 meso-CAR-T cells either as monotherapy or in combination with aderbasib (treatment window is indicated by the lilac square; n=4–6 mice per group). Two-way ANOVA. HD207 was used to generate meso-CAR-T cells (transduction: 68%, viability at infusion: >80%). G) Representative flow histograms and quantification (frequency and MFI, mean ± SEM) of mesothelin expression in AsPC-1 (GFP+) tumors harvested at day 28 from mice treated with UTD T cells alone or in combination with aderbasib from F. Statistical significance was determined using unpaired Student’s t test. *p<0.05, **p<0.01, ****p<0.0001.

    Article Snippet: To analyze soluble mesothelin in the culture supernatant, the Human Mesothelin DuoSet ELISA (R&D Systems, DY3265) kit was used according to manufacturer protocol.

    Techniques: In Vitro, In Vivo, Cell Culture, Adoptive Transfer Assay, Transduction, Expressing