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pd 1 blocking antibody  (MedChemExpress)


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    MedChemExpress pd 1 blocking antibody
    Pd 1 Blocking Antibody, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 54 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pd 1 blocking antibody/product/MedChemExpress
    Average 95 stars, based on 54 article reviews
    pd 1 blocking antibody - by Bioz Stars, 2026-06
    95/100 stars

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    Pd 1 Blocking Antibody, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    CLCA4 overexpression enhanced the therapeutic effect of <t>anti-PD-1.</t> (A) In vivo tumorigenicity assay in nude mice was performed to detect the therapeutic effect of CLCA4 overexpression combined with anti-PD-1 antibody. (B) Tumor growth curve was monitored from nude mice with different treatment groups. (C) Weights of tumors from nude mice with different treatments were detected. One-way ANOVA with Tukey's multiple comparisons test (mean ± standard deviation). (D) Analysis of the survival times of mice in each group ( n = 8 per group), and the experiment was terminated 60 days after tumor inoculation. Unpaired two-tailed t -test (mean ± standard deviation). (E) Immunofluorescence or immunohistochemistry staining was performed to detect the infiltration levels of CD8 + T cells, GZMB, Perforin + cells, Ki67 + , Bmi-1 + , and Oct4 + cells in tumors from different treatment groups. One-way ANOVA with Tukey's multiple comparisons test (mean ± standard deviation). (F) Hematoxylin-eosin staining of liver metastases in each group. (G) Quantitative analysis of the liver weight in each group. One-way ANOVA with Tukey's multiple comparisons test (mean ± standard deviation). (H) Quantitative analysis of the liver metastasis area/total liver area in each group. One-way ANOVA with Tukey's multiple comparisons test (mean ± standard deviation).
    Vivo Blocking Antibody Against Mouse Pd 1, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Bio X Cell antibodies blocking pd1
    (A) Experimental scheme consisting of bilateral VML surgery performed on the hindlimb quadriceps muscles, followed by unilateral subcutaneous inoculation of syngeneic cancer cells (CT26 or B16F10) on the right flank. Survival criteria comprised of tumor volume >1500 mm 3 or severe involuting ulceration. (B) CT26 and (C) B16F10 tumor growth kinetics of uninjured and VML-injured mice (n=8-10). (D) Experimental scheme introducing ICB therapy to the concurrent VML injury-tumor model. ICB therapy consisted of either combination αPD1/αCTLA4 (5 mg/kg each) or delayed αPD1 monotherapy (5 mg/kg) delivered via intraperitoneal injection every 3 days for 4 total doses. (E) CT26 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4 or (F) delayed αPD1 monotherapy. (G) B16F10 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4. (Statistics) Tumor growth curves: mean±SEM. Bar graphs: mean±SD (displaying earliest survival timepoint). Normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired two-tailed student t-test ( B ); otherwise, a non-parametric two-tailed Mann-Whitney test was used ( C, F, G ). Results representative of at least 2 independent experiments ( B, C ). Survival: Kaplan-Meier curve with Log-Rank Mantel-Cox test ( E-G ). Survival results combined from 2 independent experiments with separate results presented in supplemental figure 2 ( E-G ). NS: Not significant p>0.05, * p<0.05, ** p<0.01, *** p<0.001. CR: Complete Responder.
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    Sanofi bivalent pd 1 blocking antibody
    (A) Experimental scheme consisting of bilateral VML surgery performed on the hindlimb quadriceps muscles, followed by unilateral subcutaneous inoculation of syngeneic cancer cells (CT26 or B16F10) on the right flank. Survival criteria comprised of tumor volume >1500 mm 3 or severe involuting ulceration. (B) CT26 and (C) B16F10 tumor growth kinetics of uninjured and VML-injured mice (n=8-10). (D) Experimental scheme introducing ICB therapy to the concurrent VML injury-tumor model. ICB therapy consisted of either combination αPD1/αCTLA4 (5 mg/kg each) or delayed αPD1 monotherapy (5 mg/kg) delivered via intraperitoneal injection every 3 days for 4 total doses. (E) CT26 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4 or (F) delayed αPD1 monotherapy. (G) B16F10 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4. (Statistics) Tumor growth curves: mean±SEM. Bar graphs: mean±SD (displaying earliest survival timepoint). Normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired two-tailed student t-test ( B ); otherwise, a non-parametric two-tailed Mann-Whitney test was used ( C, F, G ). Results representative of at least 2 independent experiments ( B, C ). Survival: Kaplan-Meier curve with Log-Rank Mantel-Cox test ( E-G ). Survival results combined from 2 independent experiments with separate results presented in supplemental figure 2 ( E-G ). NS: Not significant p>0.05, * p<0.05, ** p<0.01, *** p<0.001. CR: Complete Responder.
    Bivalent Pd 1 Blocking Antibody, supplied by Sanofi, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    Bio X Cell pd 1 blocking antibody
    (A) Experimental scheme consisting of bilateral VML surgery performed on the hindlimb quadriceps muscles, followed by unilateral subcutaneous inoculation of syngeneic cancer cells (CT26 or B16F10) on the right flank. Survival criteria comprised of tumor volume >1500 mm 3 or severe involuting ulceration. (B) CT26 and (C) B16F10 tumor growth kinetics of uninjured and VML-injured mice (n=8-10). (D) Experimental scheme introducing ICB therapy to the concurrent VML injury-tumor model. ICB therapy consisted of either combination αPD1/αCTLA4 (5 mg/kg each) or delayed αPD1 monotherapy (5 mg/kg) delivered via intraperitoneal injection every 3 days for 4 total doses. (E) CT26 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4 or (F) delayed αPD1 monotherapy. (G) B16F10 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4. (Statistics) Tumor growth curves: mean±SEM. Bar graphs: mean±SD (displaying earliest survival timepoint). Normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired two-tailed student t-test ( B ); otherwise, a non-parametric two-tailed Mann-Whitney test was used ( C, F, G ). Results representative of at least 2 independent experiments ( B, C ). Survival: Kaplan-Meier curve with Log-Rank Mantel-Cox test ( E-G ). Survival results combined from 2 independent experiments with separate results presented in supplemental figure 2 ( E-G ). NS: Not significant p>0.05, * p<0.05, ** p<0.01, *** p<0.001. CR: Complete Responder.
    Pd 1 Blocking Antibody, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Selleck Chemicals anti-pd-1 blocking antibody
    (A) Experimental scheme consisting of bilateral VML surgery performed on the hindlimb quadriceps muscles, followed by unilateral subcutaneous inoculation of syngeneic cancer cells (CT26 or B16F10) on the right flank. Survival criteria comprised of tumor volume >1500 mm 3 or severe involuting ulceration. (B) CT26 and (C) B16F10 tumor growth kinetics of uninjured and VML-injured mice (n=8-10). (D) Experimental scheme introducing ICB therapy to the concurrent VML injury-tumor model. ICB therapy consisted of either combination αPD1/αCTLA4 (5 mg/kg each) or delayed αPD1 monotherapy (5 mg/kg) delivered via intraperitoneal injection every 3 days for 4 total doses. (E) CT26 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4 or (F) delayed αPD1 monotherapy. (G) B16F10 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4. (Statistics) Tumor growth curves: mean±SEM. Bar graphs: mean±SD (displaying earliest survival timepoint). Normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired two-tailed student t-test ( B ); otherwise, a non-parametric two-tailed Mann-Whitney test was used ( C, F, G ). Results representative of at least 2 independent experiments ( B, C ). Survival: Kaplan-Meier curve with Log-Rank Mantel-Cox test ( E-G ). Survival results combined from 2 independent experiments with separate results presented in supplemental figure 2 ( E-G ). NS: Not significant p>0.05, * p<0.05, ** p<0.01, *** p<0.001. CR: Complete Responder.
    Anti Pd 1 Blocking Antibody, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Selleck Chemicals anti-mouse pd-1 blocking antibody clone rmp1-14
    (A) Experimental scheme consisting of bilateral VML surgery performed on the hindlimb quadriceps muscles, followed by unilateral subcutaneous inoculation of syngeneic cancer cells (CT26 or B16F10) on the right flank. Survival criteria comprised of tumor volume >1500 mm 3 or severe involuting ulceration. (B) CT26 and (C) B16F10 tumor growth kinetics of uninjured and VML-injured mice (n=8-10). (D) Experimental scheme introducing ICB therapy to the concurrent VML injury-tumor model. ICB therapy consisted of either combination αPD1/αCTLA4 (5 mg/kg each) or delayed αPD1 monotherapy (5 mg/kg) delivered via intraperitoneal injection every 3 days for 4 total doses. (E) CT26 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4 or (F) delayed αPD1 monotherapy. (G) B16F10 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4. (Statistics) Tumor growth curves: mean±SEM. Bar graphs: mean±SD (displaying earliest survival timepoint). Normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired two-tailed student t-test ( B ); otherwise, a non-parametric two-tailed Mann-Whitney test was used ( C, F, G ). Results representative of at least 2 independent experiments ( B, C ). Survival: Kaplan-Meier curve with Log-Rank Mantel-Cox test ( E-G ). Survival results combined from 2 independent experiments with separate results presented in supplemental figure 2 ( E-G ). NS: Not significant p>0.05, * p<0.05, ** p<0.01, *** p<0.001. CR: Complete Responder.
    Anti Mouse Pd 1 Blocking Antibody Clone Rmp1 14, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    CLCA4 overexpression enhanced the therapeutic effect of anti-PD-1. (A) In vivo tumorigenicity assay in nude mice was performed to detect the therapeutic effect of CLCA4 overexpression combined with anti-PD-1 antibody. (B) Tumor growth curve was monitored from nude mice with different treatment groups. (C) Weights of tumors from nude mice with different treatments were detected. One-way ANOVA with Tukey's multiple comparisons test (mean ± standard deviation). (D) Analysis of the survival times of mice in each group ( n = 8 per group), and the experiment was terminated 60 days after tumor inoculation. Unpaired two-tailed t -test (mean ± standard deviation). (E) Immunofluorescence or immunohistochemistry staining was performed to detect the infiltration levels of CD8 + T cells, GZMB, Perforin + cells, Ki67 + , Bmi-1 + , and Oct4 + cells in tumors from different treatment groups. One-way ANOVA with Tukey's multiple comparisons test (mean ± standard deviation). (F) Hematoxylin-eosin staining of liver metastases in each group. (G) Quantitative analysis of the liver weight in each group. One-way ANOVA with Tukey's multiple comparisons test (mean ± standard deviation). (H) Quantitative analysis of the liver metastasis area/total liver area in each group. One-way ANOVA with Tukey's multiple comparisons test (mean ± standard deviation).

    Journal: Genes & Diseases

    Article Title: Chloride channel accessory 4 suppresses stem cell-like properties of colorectal cancer and enhances anti-PD-1 immunotherapy

    doi: 10.1016/j.gendis.2025.101859

    Figure Lengend Snippet: CLCA4 overexpression enhanced the therapeutic effect of anti-PD-1. (A) In vivo tumorigenicity assay in nude mice was performed to detect the therapeutic effect of CLCA4 overexpression combined with anti-PD-1 antibody. (B) Tumor growth curve was monitored from nude mice with different treatment groups. (C) Weights of tumors from nude mice with different treatments were detected. One-way ANOVA with Tukey's multiple comparisons test (mean ± standard deviation). (D) Analysis of the survival times of mice in each group ( n = 8 per group), and the experiment was terminated 60 days after tumor inoculation. Unpaired two-tailed t -test (mean ± standard deviation). (E) Immunofluorescence or immunohistochemistry staining was performed to detect the infiltration levels of CD8 + T cells, GZMB, Perforin + cells, Ki67 + , Bmi-1 + , and Oct4 + cells in tumors from different treatment groups. One-way ANOVA with Tukey's multiple comparisons test (mean ± standard deviation). (F) Hematoxylin-eosin staining of liver metastases in each group. (G) Quantitative analysis of the liver weight in each group. One-way ANOVA with Tukey's multiple comparisons test (mean ± standard deviation). (H) Quantitative analysis of the liver metastasis area/total liver area in each group. One-way ANOVA with Tukey's multiple comparisons test (mean ± standard deviation).

    Article Snippet: After 7 days, mice were intraperitoneally treated with either an in vivo blocking antibody against mouse PD-1 (Clone: 29F.1A2, BioXcell, Cat# BP0273) or a rat IgG2a isotype control antibody (Clone: 2A3, BioXcell, Cat# BP0089).

    Techniques: Over Expression, In Vivo, Tumorigenicity Assay, Standard Deviation, Two Tailed Test, Immunofluorescence, Immunohistochemistry, Staining

    (A) Experimental scheme consisting of bilateral VML surgery performed on the hindlimb quadriceps muscles, followed by unilateral subcutaneous inoculation of syngeneic cancer cells (CT26 or B16F10) on the right flank. Survival criteria comprised of tumor volume >1500 mm 3 or severe involuting ulceration. (B) CT26 and (C) B16F10 tumor growth kinetics of uninjured and VML-injured mice (n=8-10). (D) Experimental scheme introducing ICB therapy to the concurrent VML injury-tumor model. ICB therapy consisted of either combination αPD1/αCTLA4 (5 mg/kg each) or delayed αPD1 monotherapy (5 mg/kg) delivered via intraperitoneal injection every 3 days for 4 total doses. (E) CT26 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4 or (F) delayed αPD1 monotherapy. (G) B16F10 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4. (Statistics) Tumor growth curves: mean±SEM. Bar graphs: mean±SD (displaying earliest survival timepoint). Normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired two-tailed student t-test ( B ); otherwise, a non-parametric two-tailed Mann-Whitney test was used ( C, F, G ). Results representative of at least 2 independent experiments ( B, C ). Survival: Kaplan-Meier curve with Log-Rank Mantel-Cox test ( E-G ). Survival results combined from 2 independent experiments with separate results presented in supplemental figure 2 ( E-G ). NS: Not significant p>0.05, * p<0.05, ** p<0.01, *** p<0.001. CR: Complete Responder.

    Journal: bioRxiv

    Article Title: Tissue Injury and Biomaterial Treatment Modulate Tumor Growth and Response to Immunotherapy

    doi: 10.64898/2026.02.02.703323

    Figure Lengend Snippet: (A) Experimental scheme consisting of bilateral VML surgery performed on the hindlimb quadriceps muscles, followed by unilateral subcutaneous inoculation of syngeneic cancer cells (CT26 or B16F10) on the right flank. Survival criteria comprised of tumor volume >1500 mm 3 or severe involuting ulceration. (B) CT26 and (C) B16F10 tumor growth kinetics of uninjured and VML-injured mice (n=8-10). (D) Experimental scheme introducing ICB therapy to the concurrent VML injury-tumor model. ICB therapy consisted of either combination αPD1/αCTLA4 (5 mg/kg each) or delayed αPD1 monotherapy (5 mg/kg) delivered via intraperitoneal injection every 3 days for 4 total doses. (E) CT26 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4 or (F) delayed αPD1 monotherapy. (G) B16F10 tumor growth and survival curves of uninjured and VML injured mice treated with αPD1/αCTLA4. (Statistics) Tumor growth curves: mean±SEM. Bar graphs: mean±SD (displaying earliest survival timepoint). Normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired two-tailed student t-test ( B ); otherwise, a non-parametric two-tailed Mann-Whitney test was used ( C, F, G ). Results representative of at least 2 independent experiments ( B, C ). Survival: Kaplan-Meier curve with Log-Rank Mantel-Cox test ( E-G ). Survival results combined from 2 independent experiments with separate results presented in supplemental figure 2 ( E-G ). NS: Not significant p>0.05, * p<0.05, ** p<0.01, *** p<0.001. CR: Complete Responder.

    Article Snippet: ICB therapy consisted of monoclonal antibodies blocking PD1 (clone RPM1-14, BioXCell BP0146) and CTLA4 (clone 9H10, BioXCell BP0131) delivered via intraperitoneal (IP) injection at 5mg/kg body weight each prepared in sterile dilution buffer ( InVivo Pure pH 7.0, BioXCell IP0070).

    Techniques: Muscles, Injection, Two Tailed Test, MANN-WHITNEY

    VML Injury Impacts Anti-Tumor CD8 + T Cell Response. (A) Flow cytometric profiling of CT26 tumor-infiltrating CD8 + T cells, (B) PD1 expression on CD8 + T cells, and (C) CT26 tumor-specific CD8 + T cells marked by AH1-loaded MHC class I tetramer in uninjured and VML injured mice. (D) Single-cell RNA-sequencing (scRNAseq) of CT26 tumor-infiltrating T cells from uninjured and VML injured mice. UMAP depicting main T cell clusters (e.g., CD8, CD4, Treg, unconventional). (E) T cell UMAP separated by tumor-reactive AH1-Tetramer + CD8 + T cells (top) and other T cells (bottom) colored by cells from uninjured (gray) and VML injured (green) mice. (F) Differential gene expression and (G, H) GSEA using Hallmark or (I) curated list of T cell-related pathways with top leading edge genes comparing tumor-reactive AH1-Tetramer + CD8 + T cells of uninjured and VML injured mice. (J) Intracellular cytokine staining following ex vivo stimulation of IFNγ-producing effector cell types in CT26 tumors of uninjured and VML injured mice. (Statistics) Bar graphs: mean±SD. Normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired two-tailed student t-test ( A-C, J ). Results representative of at least 2 independent experiments ( A-C ). NS: Not significant p>0.05, * p<0.05, ** p<0.01. UMAP: Uniform manifold approximation and projection. GSEA: Gene set enrichment analysis.

    Journal: bioRxiv

    Article Title: Tissue Injury and Biomaterial Treatment Modulate Tumor Growth and Response to Immunotherapy

    doi: 10.64898/2026.02.02.703323

    Figure Lengend Snippet: VML Injury Impacts Anti-Tumor CD8 + T Cell Response. (A) Flow cytometric profiling of CT26 tumor-infiltrating CD8 + T cells, (B) PD1 expression on CD8 + T cells, and (C) CT26 tumor-specific CD8 + T cells marked by AH1-loaded MHC class I tetramer in uninjured and VML injured mice. (D) Single-cell RNA-sequencing (scRNAseq) of CT26 tumor-infiltrating T cells from uninjured and VML injured mice. UMAP depicting main T cell clusters (e.g., CD8, CD4, Treg, unconventional). (E) T cell UMAP separated by tumor-reactive AH1-Tetramer + CD8 + T cells (top) and other T cells (bottom) colored by cells from uninjured (gray) and VML injured (green) mice. (F) Differential gene expression and (G, H) GSEA using Hallmark or (I) curated list of T cell-related pathways with top leading edge genes comparing tumor-reactive AH1-Tetramer + CD8 + T cells of uninjured and VML injured mice. (J) Intracellular cytokine staining following ex vivo stimulation of IFNγ-producing effector cell types in CT26 tumors of uninjured and VML injured mice. (Statistics) Bar graphs: mean±SD. Normally distributed data (Shapiro-Wilk test, α=0.05) was analyzed using an unpaired two-tailed student t-test ( A-C, J ). Results representative of at least 2 independent experiments ( A-C ). NS: Not significant p>0.05, * p<0.05, ** p<0.01. UMAP: Uniform manifold approximation and projection. GSEA: Gene set enrichment analysis.

    Article Snippet: ICB therapy consisted of monoclonal antibodies blocking PD1 (clone RPM1-14, BioXCell BP0146) and CTLA4 (clone 9H10, BioXCell BP0131) delivered via intraperitoneal (IP) injection at 5mg/kg body weight each prepared in sterile dilution buffer ( InVivo Pure pH 7.0, BioXCell IP0070).

    Techniques: Expressing, Single Cell, RNA Sequencing, Gene Expression, Staining, Ex Vivo, Two Tailed Test

    Treatment of Injury with Pro-Regenerative Biologics Impacts Cancer Progression. (A) CT26 tumor growth kinetics of uninjured, untreated VML-injured, and extracellular matrix (ECM) scaffold-treated VML-injured mice (n=6-8). (B) Experiment compilation of CT26 tumor volume fold changes (normalized to the uninjured group within each experiment) of untreated and ECM-treated VML-injured groups at day 14 post-inoculation (n=10 independent experiments). (C) B16F10 tumor growth kinetics of uninjured, untreated VML-injured, and ECM-treated VML-injured mice (n=8). (D) CT26 tumor growth kinetics of uninjured, untreated VML-injured, and Schistosoma mansoni regenerative soluble egg antigen (rSEA)-treated VML-injured mice (n=8). (E) Survival curves of untreated and ECM-treated VML-injured mice bearing CT26 tumors treated with delayed αPD1 monotherapy or (F) bearing B16F10 tumors treated with αPD1/αCTLA4. (G) Schematic of patient selection criteria for retrospective cohort study using TriNetX database. (H) Overall survival curve for breast cancer patients treated with ICB therapy and complete mastectomy (CPT 19303), with versus without biological implant placement (CPT 15777), on or up to 3 months after ICB therapy. (I) Summary table of distribution of common cancer treatments (e.g., chemotherapy, radiation) between both patient cohorts. (Statistics) Tumor growth curves: mean±SEM. Bar graphs: mean±SD (earliest survival timepoint or experiment endpoint). Experiment Compilation: Each datapoint represents an independent experiment, with fold change represented as geometric mean±geometric SD on a Log2 scale ( B ). Data was analyzed using an ordinary one-way ANOVA with Tukey’s multiple comparisons test ( A-D ). Survival: Kaplan-Meier curve with Log-Rank Mantel-Cox test ( E, F, I ). Survival results combined from 2 independent experiments with separate results presented in supplemental figures ( E, F ). Survival experiments were conducted in tandem with uninjured controls, thereby untreated VML data are the same as in  and  ( E, F ). Categorical data in clinical cancer treatment table was analyzed using Fisher’s exact test ( I ). NS: Not significant p>0.05, * p<0.05, ** p<0.01. CR: Complete Responder.

    Journal: bioRxiv

    Article Title: Tissue Injury and Biomaterial Treatment Modulate Tumor Growth and Response to Immunotherapy

    doi: 10.64898/2026.02.02.703323

    Figure Lengend Snippet: Treatment of Injury with Pro-Regenerative Biologics Impacts Cancer Progression. (A) CT26 tumor growth kinetics of uninjured, untreated VML-injured, and extracellular matrix (ECM) scaffold-treated VML-injured mice (n=6-8). (B) Experiment compilation of CT26 tumor volume fold changes (normalized to the uninjured group within each experiment) of untreated and ECM-treated VML-injured groups at day 14 post-inoculation (n=10 independent experiments). (C) B16F10 tumor growth kinetics of uninjured, untreated VML-injured, and ECM-treated VML-injured mice (n=8). (D) CT26 tumor growth kinetics of uninjured, untreated VML-injured, and Schistosoma mansoni regenerative soluble egg antigen (rSEA)-treated VML-injured mice (n=8). (E) Survival curves of untreated and ECM-treated VML-injured mice bearing CT26 tumors treated with delayed αPD1 monotherapy or (F) bearing B16F10 tumors treated with αPD1/αCTLA4. (G) Schematic of patient selection criteria for retrospective cohort study using TriNetX database. (H) Overall survival curve for breast cancer patients treated with ICB therapy and complete mastectomy (CPT 19303), with versus without biological implant placement (CPT 15777), on or up to 3 months after ICB therapy. (I) Summary table of distribution of common cancer treatments (e.g., chemotherapy, radiation) between both patient cohorts. (Statistics) Tumor growth curves: mean±SEM. Bar graphs: mean±SD (earliest survival timepoint or experiment endpoint). Experiment Compilation: Each datapoint represents an independent experiment, with fold change represented as geometric mean±geometric SD on a Log2 scale ( B ). Data was analyzed using an ordinary one-way ANOVA with Tukey’s multiple comparisons test ( A-D ). Survival: Kaplan-Meier curve with Log-Rank Mantel-Cox test ( E, F, I ). Survival results combined from 2 independent experiments with separate results presented in supplemental figures ( E, F ). Survival experiments were conducted in tandem with uninjured controls, thereby untreated VML data are the same as in and ( E, F ). Categorical data in clinical cancer treatment table was analyzed using Fisher’s exact test ( I ). NS: Not significant p>0.05, * p<0.05, ** p<0.01. CR: Complete Responder.

    Article Snippet: ICB therapy consisted of monoclonal antibodies blocking PD1 (clone RPM1-14, BioXCell BP0146) and CTLA4 (clone 9H10, BioXCell BP0131) delivered via intraperitoneal (IP) injection at 5mg/kg body weight each prepared in sterile dilution buffer ( InVivo Pure pH 7.0, BioXCell IP0070).

    Techniques: Selection