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Absolute Biotech Inc kpc cells
( a, b ) Peripheral blood immune profiling in the <t>KPC</t> flank model. <t>KPC</t> <t>cells</t> (1.0 x 10 6 ) cells were inoculated into the right flanks of 6-8-week-old C57BL/6J mice. Once tumors reach the target volume of 80-120 mm³ mice were randomized to treatment group (n=8/group) and treated with PBS or lyophilized iSTORM (iSTORM-L) at 5×10 7 CFU or 1×10 8 CFU/mouse, administered intraperitoneally, one bolus every 3 days, 4 doses total). Immune profiling in peripheral blood collected 15/16 days post the last treatment (23/24 days after the first dose) demonstrates that iSTROM fully retains immune-stimulatory activities and elicits a graded, dose-dependent activation of circulating T-cell compartments. Increasing iSTORM-L doses expanded activated CD4 + T cells (CD44 + CD69 + and ICOS + ) while concomitantly reducing exhaustion-associated PD-1 + and PD-1 + LAG3 + CD4 + subsets ( a ). CD8 + T cells displayed a parallel activation program, characterized by robust expansion of ICOS⁺ effector-like CD8 + T cells and uniformly low frequencies of PD-1 + or PD-1 + TIM3 + exhausted populations across all doses ( b ). c ) iSTORM-L induced dose-dependent tumor growth suppression in the KPC mice above. Tumor volumes (caliper measurements) were measured twice per week. Bar and whisker represent means and standard deviation, respectively.
Kpc Cells, supplied by Absolute Biotech Inc, 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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Images

1) Product Images from "CMTM6-Silencing Microbial Immunotherapy Reprograms PDAC Tumors and Restores T-cell Function"

Article Title: CMTM6-Silencing Microbial Immunotherapy Reprograms PDAC Tumors and Restores T-cell Function

Journal: bioRxiv

doi: 10.64898/2026.01.26.701790

( a, b ) Peripheral blood immune profiling in the KPC flank model. KPC cells (1.0 x 10 6 ) cells were inoculated into the right flanks of 6-8-week-old C57BL/6J mice. Once tumors reach the target volume of 80-120 mm³ mice were randomized to treatment group (n=8/group) and treated with PBS or lyophilized iSTORM (iSTORM-L) at 5×10 7 CFU or 1×10 8 CFU/mouse, administered intraperitoneally, one bolus every 3 days, 4 doses total). Immune profiling in peripheral blood collected 15/16 days post the last treatment (23/24 days after the first dose) demonstrates that iSTROM fully retains immune-stimulatory activities and elicits a graded, dose-dependent activation of circulating T-cell compartments. Increasing iSTORM-L doses expanded activated CD4 + T cells (CD44 + CD69 + and ICOS + ) while concomitantly reducing exhaustion-associated PD-1 + and PD-1 + LAG3 + CD4 + subsets ( a ). CD8 + T cells displayed a parallel activation program, characterized by robust expansion of ICOS⁺ effector-like CD8 + T cells and uniformly low frequencies of PD-1 + or PD-1 + TIM3 + exhausted populations across all doses ( b ). c ) iSTORM-L induced dose-dependent tumor growth suppression in the KPC mice above. Tumor volumes (caliper measurements) were measured twice per week. Bar and whisker represent means and standard deviation, respectively.
Figure Legend Snippet: ( a, b ) Peripheral blood immune profiling in the KPC flank model. KPC cells (1.0 x 10 6 ) cells were inoculated into the right flanks of 6-8-week-old C57BL/6J mice. Once tumors reach the target volume of 80-120 mm³ mice were randomized to treatment group (n=8/group) and treated with PBS or lyophilized iSTORM (iSTORM-L) at 5×10 7 CFU or 1×10 8 CFU/mouse, administered intraperitoneally, one bolus every 3 days, 4 doses total). Immune profiling in peripheral blood collected 15/16 days post the last treatment (23/24 days after the first dose) demonstrates that iSTROM fully retains immune-stimulatory activities and elicits a graded, dose-dependent activation of circulating T-cell compartments. Increasing iSTORM-L doses expanded activated CD4 + T cells (CD44 + CD69 + and ICOS + ) while concomitantly reducing exhaustion-associated PD-1 + and PD-1 + LAG3 + CD4 + subsets ( a ). CD8 + T cells displayed a parallel activation program, characterized by robust expansion of ICOS⁺ effector-like CD8 + T cells and uniformly low frequencies of PD-1 + or PD-1 + TIM3 + exhausted populations across all doses ( b ). c ) iSTORM-L induced dose-dependent tumor growth suppression in the KPC mice above. Tumor volumes (caliper measurements) were measured twice per week. Bar and whisker represent means and standard deviation, respectively.

Techniques Used: Activation Assay, Whisker Assay, Standard Deviation



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CO exposure increases MHC-I and PD-L1 expression in pancreatic cancer cells. Human and mouse pancreatic cancer cell lines were exposed to CO in the air at a concentration of 250 ppm for 48 hours before being harvested for analysis of gene and protein expression. (A) Log 10 -fold change in RNA levels for antigen processing and presentation proteins, MHC-I molecules, and PD-L1 in human pancreatic cancer cells (Panc1) exposed to CO relative to air. Data are means ± standard deviation. CO-treated samples; n=3; air-treated samples, n=3. (B) Gene set enrichment analysis of pathways that promote immunotherapy response and were upregulated in human pancreatic cancer cells (Panc1) exposed to CO relative to those exposed to air. Data are means ± standard deviation; CO-treated samples; n=3; air-treated samples, n=3. (C) Western blots from cell lysates obtained from human pancreatic cancer cells (Panc1) or mouse pancreatic cancer cells <t>(KPC)</t> exposed to CO or air. β-actin served as a loading control. (D) Flow cytometric analysis of Panc1 or <t>KPC</t> <t>cells</t> exposed to CO or air in the presence or absence of increasing concentrations of IFN-γ. Cells were analyzed for expression of MHC-I (HLA in humans; H2Kb in mice) or PD-L1. Results represent the mean ± standard deviation of 3 independent experiments. *, P<0.05; **, P<0.01; ***, P < 0.001; Panc1 with CO + IFN-γ, n=8; Panc1 with air + IFN-γ, n=8; KPC with CO + IFN-γ, n=8; KPC with air + IFN-γ, n=8; P values were determined by unpaired t-test.
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CO exposure increases MHC-I and PD-L1 expression in pancreatic cancer cells. Human and mouse pancreatic cancer cell lines were exposed to CO in the air at a concentration of 250 ppm for 48 hours before being harvested for analysis of gene and protein expression. (A) Log 10 -fold change in RNA levels for antigen processing and presentation proteins, MHC-I molecules, and PD-L1 in human pancreatic cancer cells (Panc1) exposed to CO relative to air. Data are means ± standard deviation. CO-treated samples; n=3; air-treated samples, n=3. (B) Gene set enrichment analysis of pathways that promote immunotherapy response and were upregulated in human pancreatic cancer cells (Panc1) exposed to CO relative to those exposed to air. Data are means ± standard deviation; CO-treated samples; n=3; air-treated samples, n=3. (C) Western blots from cell lysates obtained from human pancreatic cancer cells (Panc1) or mouse pancreatic cancer cells <t>(KPC)</t> exposed to CO or air. β-actin served as a loading control. (D) Flow cytometric analysis of Panc1 or <t>KPC</t> <t>cells</t> exposed to CO or air in the presence or absence of increasing concentrations of IFN-γ. Cells were analyzed for expression of MHC-I (HLA in humans; H2Kb in mice) or PD-L1. Results represent the mean ± standard deviation of 3 independent experiments. *, P<0.05; **, P<0.01; ***, P < 0.001; Panc1 with CO + IFN-γ, n=8; Panc1 with air + IFN-γ, n=8; KPC with CO + IFN-γ, n=8; KPC with air + IFN-γ, n=8; P values were determined by unpaired t-test.
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CO exposure increases MHC-I and PD-L1 expression in pancreatic cancer cells. Human and mouse pancreatic cancer cell lines were exposed to CO in the air at a concentration of 250 ppm for 48 hours before being harvested for analysis of gene and protein expression. (A) Log 10 -fold change in RNA levels for antigen processing and presentation proteins, MHC-I molecules, and PD-L1 in human pancreatic cancer cells (Panc1) exposed to CO relative to air. Data are means ± standard deviation. CO-treated samples; n=3; air-treated samples, n=3. (B) Gene set enrichment analysis of pathways that promote immunotherapy response and were upregulated in human pancreatic cancer cells (Panc1) exposed to CO relative to those exposed to air. Data are means ± standard deviation; CO-treated samples; n=3; air-treated samples, n=3. (C) Western blots from cell lysates obtained from human pancreatic cancer cells (Panc1) or mouse pancreatic cancer cells <t>(KPC)</t> exposed to CO or air. β-actin served as a loading control. (D) Flow cytometric analysis of Panc1 or <t>KPC</t> <t>cells</t> exposed to CO or air in the presence or absence of increasing concentrations of IFN-γ. Cells were analyzed for expression of MHC-I (HLA in humans; H2Kb in mice) or PD-L1. Results represent the mean ± standard deviation of 3 independent experiments. *, P<0.05; **, P<0.01; ***, P < 0.001; Panc1 with CO + IFN-γ, n=8; Panc1 with air + IFN-γ, n=8; KPC with CO + IFN-γ, n=8; KPC with air + IFN-γ, n=8; P values were determined by unpaired t-test.
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CO exposure increases MHC-I and PD-L1 expression in pancreatic cancer cells. Human and mouse pancreatic cancer cell lines were exposed to CO in the air at a concentration of 250 ppm for 48 hours before being harvested for analysis of gene and protein expression. (A) Log 10 -fold change in RNA levels for antigen processing and presentation proteins, MHC-I molecules, and PD-L1 in human pancreatic cancer cells (Panc1) exposed to CO relative to air. Data are means ± standard deviation. CO-treated samples; n=3; air-treated samples, n=3. (B) Gene set enrichment analysis of pathways that promote immunotherapy response and were upregulated in human pancreatic cancer cells (Panc1) exposed to CO relative to those exposed to air. Data are means ± standard deviation; CO-treated samples; n=3; air-treated samples, n=3. (C) Western blots from cell lysates obtained from human pancreatic cancer cells (Panc1) or mouse pancreatic cancer cells <t>(KPC)</t> exposed to CO or air. β-actin served as a loading control. (D) Flow cytometric analysis of Panc1 or <t>KPC</t> <t>cells</t> exposed to CO or air in the presence or absence of increasing concentrations of IFN-γ. Cells were analyzed for expression of MHC-I (HLA in humans; H2Kb in mice) or PD-L1. Results represent the mean ± standard deviation of 3 independent experiments. *, P<0.05; **, P<0.01; ***, P < 0.001; Panc1 with CO + IFN-γ, n=8; Panc1 with air + IFN-γ, n=8; KPC with CO + IFN-γ, n=8; KPC with air + IFN-γ, n=8; P values were determined by unpaired t-test.
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( a, b ) Peripheral blood immune profiling in the <t>KPC</t> flank model. <t>KPC</t> <t>cells</t> (1.0 x 10 6 ) cells were inoculated into the right flanks of 6-8-week-old C57BL/6J mice. Once tumors reach the target volume of 80-120 mm³ mice were randomized to treatment group (n=8/group) and treated with PBS or lyophilized iSTORM (iSTORM-L) at 5×10 7 CFU or 1×10 8 CFU/mouse, administered intraperitoneally, one bolus every 3 days, 4 doses total). Immune profiling in peripheral blood collected 15/16 days post the last treatment (23/24 days after the first dose) demonstrates that iSTROM fully retains immune-stimulatory activities and elicits a graded, dose-dependent activation of circulating T-cell compartments. Increasing iSTORM-L doses expanded activated CD4 + T cells (CD44 + CD69 + and ICOS + ) while concomitantly reducing exhaustion-associated PD-1 + and PD-1 + LAG3 + CD4 + subsets ( a ). CD8 + T cells displayed a parallel activation program, characterized by robust expansion of ICOS⁺ effector-like CD8 + T cells and uniformly low frequencies of PD-1 + or PD-1 + TIM3 + exhausted populations across all doses ( b ). c ) iSTORM-L induced dose-dependent tumor growth suppression in the KPC mice above. Tumor volumes (caliper measurements) were measured twice per week. Bar and whisker represent means and standard deviation, respectively.
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Image Search Results


CO exposure increases MHC-I and PD-L1 expression in pancreatic cancer cells. Human and mouse pancreatic cancer cell lines were exposed to CO in the air at a concentration of 250 ppm for 48 hours before being harvested for analysis of gene and protein expression. (A) Log 10 -fold change in RNA levels for antigen processing and presentation proteins, MHC-I molecules, and PD-L1 in human pancreatic cancer cells (Panc1) exposed to CO relative to air. Data are means ± standard deviation. CO-treated samples; n=3; air-treated samples, n=3. (B) Gene set enrichment analysis of pathways that promote immunotherapy response and were upregulated in human pancreatic cancer cells (Panc1) exposed to CO relative to those exposed to air. Data are means ± standard deviation; CO-treated samples; n=3; air-treated samples, n=3. (C) Western blots from cell lysates obtained from human pancreatic cancer cells (Panc1) or mouse pancreatic cancer cells (KPC) exposed to CO or air. β-actin served as a loading control. (D) Flow cytometric analysis of Panc1 or KPC cells exposed to CO or air in the presence or absence of increasing concentrations of IFN-γ. Cells were analyzed for expression of MHC-I (HLA in humans; H2Kb in mice) or PD-L1. Results represent the mean ± standard deviation of 3 independent experiments. *, P<0.05; **, P<0.01; ***, P < 0.001; Panc1 with CO + IFN-γ, n=8; Panc1 with air + IFN-γ, n=8; KPC with CO + IFN-γ, n=8; KPC with air + IFN-γ, n=8; P values were determined by unpaired t-test.

Journal: Biomaterials

Article Title: Potentiating the effect of immunotherapy in pancreatic cancer using gas-entrapping materials

doi: 10.1016/j.biomaterials.2025.123097

Figure Lengend Snippet: CO exposure increases MHC-I and PD-L1 expression in pancreatic cancer cells. Human and mouse pancreatic cancer cell lines were exposed to CO in the air at a concentration of 250 ppm for 48 hours before being harvested for analysis of gene and protein expression. (A) Log 10 -fold change in RNA levels for antigen processing and presentation proteins, MHC-I molecules, and PD-L1 in human pancreatic cancer cells (Panc1) exposed to CO relative to air. Data are means ± standard deviation. CO-treated samples; n=3; air-treated samples, n=3. (B) Gene set enrichment analysis of pathways that promote immunotherapy response and were upregulated in human pancreatic cancer cells (Panc1) exposed to CO relative to those exposed to air. Data are means ± standard deviation; CO-treated samples; n=3; air-treated samples, n=3. (C) Western blots from cell lysates obtained from human pancreatic cancer cells (Panc1) or mouse pancreatic cancer cells (KPC) exposed to CO or air. β-actin served as a loading control. (D) Flow cytometric analysis of Panc1 or KPC cells exposed to CO or air in the presence or absence of increasing concentrations of IFN-γ. Cells were analyzed for expression of MHC-I (HLA in humans; H2Kb in mice) or PD-L1. Results represent the mean ± standard deviation of 3 independent experiments. *, P<0.05; **, P<0.01; ***, P < 0.001; Panc1 with CO + IFN-γ, n=8; Panc1 with air + IFN-γ, n=8; KPC with CO + IFN-γ, n=8; KPC with air + IFN-γ, n=8; P values were determined by unpaired t-test.

Article Snippet: To generate syngeneic tumors, 3 × 10 6 KPC cells were injected into the right flank of C57BL/6J mice (Jackson Laboratory, Bar Harbor, ME, USA).

Techniques: Expressing, Concentration Assay, Standard Deviation, Western Blot, Control

Enhanced anti-tumor effects for combined treatment with CO-GeMs and ICIs. (A) Volumes and weights of subcutaneous allograft pancreatic tumors. Once tumors reached a volume of approximately 100 mm 3 mice received intratumoral injection of CO-GeMs and anti-PD-1 antibody, alone and in combination, or with IgG control. Results represent the mean ± standard deviation of 7 mice/group. Statistical analysis on day 19 post initiation of treatment. *, P<0.05; **, P<0.01; ***, P < 0.001; P values determined by one-way ANOVA. (B) Representative immunohistochemical staining for CD8 and CD45 in tumors treated with anti-PD-1 antibody with or without CO-GeM exposure in mice treated as in (A). (C) Quantification of CD8+ and CD45+ cells in subcutaneous allograft tumors from mice treated as in (A). The results represent the mean ± standard deviation of 10 images/group. NS, not significant; *, p < 0.05, ***, P <0.001. P values were determined by one-way ANOVA. (D) Luciferase emission as determined by bioluminescence imaging and Kaplan-Meier survival curves of allograft hepatic metastases induced in C57BL/6J mice using luc-expressing KPC cells. Results represent mean ± standard deviation of 5–7 mice/group. IgG control, n=5; CO, n=6; anti-PD-1, n=7; anti-PD-1 + CO, n=7. P values were determined by one-way ANOVA. NS, not significant; *, p < 0.05; **, p < 0.01.

Journal: Biomaterials

Article Title: Potentiating the effect of immunotherapy in pancreatic cancer using gas-entrapping materials

doi: 10.1016/j.biomaterials.2025.123097

Figure Lengend Snippet: Enhanced anti-tumor effects for combined treatment with CO-GeMs and ICIs. (A) Volumes and weights of subcutaneous allograft pancreatic tumors. Once tumors reached a volume of approximately 100 mm 3 mice received intratumoral injection of CO-GeMs and anti-PD-1 antibody, alone and in combination, or with IgG control. Results represent the mean ± standard deviation of 7 mice/group. Statistical analysis on day 19 post initiation of treatment. *, P<0.05; **, P<0.01; ***, P < 0.001; P values determined by one-way ANOVA. (B) Representative immunohistochemical staining for CD8 and CD45 in tumors treated with anti-PD-1 antibody with or without CO-GeM exposure in mice treated as in (A). (C) Quantification of CD8+ and CD45+ cells in subcutaneous allograft tumors from mice treated as in (A). The results represent the mean ± standard deviation of 10 images/group. NS, not significant; *, p < 0.05, ***, P <0.001. P values were determined by one-way ANOVA. (D) Luciferase emission as determined by bioluminescence imaging and Kaplan-Meier survival curves of allograft hepatic metastases induced in C57BL/6J mice using luc-expressing KPC cells. Results represent mean ± standard deviation of 5–7 mice/group. IgG control, n=5; CO, n=6; anti-PD-1, n=7; anti-PD-1 + CO, n=7. P values were determined by one-way ANOVA. NS, not significant; *, p < 0.05; **, p < 0.01.

Article Snippet: To generate syngeneic tumors, 3 × 10 6 KPC cells were injected into the right flank of C57BL/6J mice (Jackson Laboratory, Bar Harbor, ME, USA).

Techniques: Injection, Control, Standard Deviation, Immunohistochemical staining, Staining, Luciferase, Imaging, Expressing

( a, b ) Peripheral blood immune profiling in the KPC flank model. KPC cells (1.0 x 10 6 ) cells were inoculated into the right flanks of 6-8-week-old C57BL/6J mice. Once tumors reach the target volume of 80-120 mm³ mice were randomized to treatment group (n=8/group) and treated with PBS or lyophilized iSTORM (iSTORM-L) at 5×10 7 CFU or 1×10 8 CFU/mouse, administered intraperitoneally, one bolus every 3 days, 4 doses total). Immune profiling in peripheral blood collected 15/16 days post the last treatment (23/24 days after the first dose) demonstrates that iSTROM fully retains immune-stimulatory activities and elicits a graded, dose-dependent activation of circulating T-cell compartments. Increasing iSTORM-L doses expanded activated CD4 + T cells (CD44 + CD69 + and ICOS + ) while concomitantly reducing exhaustion-associated PD-1 + and PD-1 + LAG3 + CD4 + subsets ( a ). CD8 + T cells displayed a parallel activation program, characterized by robust expansion of ICOS⁺ effector-like CD8 + T cells and uniformly low frequencies of PD-1 + or PD-1 + TIM3 + exhausted populations across all doses ( b ). c ) iSTORM-L induced dose-dependent tumor growth suppression in the KPC mice above. Tumor volumes (caliper measurements) were measured twice per week. Bar and whisker represent means and standard deviation, respectively.

Journal: bioRxiv

Article Title: CMTM6-Silencing Microbial Immunotherapy Reprograms PDAC Tumors and Restores T-cell Function

doi: 10.64898/2026.01.26.701790

Figure Lengend Snippet: ( a, b ) Peripheral blood immune profiling in the KPC flank model. KPC cells (1.0 x 10 6 ) cells were inoculated into the right flanks of 6-8-week-old C57BL/6J mice. Once tumors reach the target volume of 80-120 mm³ mice were randomized to treatment group (n=8/group) and treated with PBS or lyophilized iSTORM (iSTORM-L) at 5×10 7 CFU or 1×10 8 CFU/mouse, administered intraperitoneally, one bolus every 3 days, 4 doses total). Immune profiling in peripheral blood collected 15/16 days post the last treatment (23/24 days after the first dose) demonstrates that iSTROM fully retains immune-stimulatory activities and elicits a graded, dose-dependent activation of circulating T-cell compartments. Increasing iSTORM-L doses expanded activated CD4 + T cells (CD44 + CD69 + and ICOS + ) while concomitantly reducing exhaustion-associated PD-1 + and PD-1 + LAG3 + CD4 + subsets ( a ). CD8 + T cells displayed a parallel activation program, characterized by robust expansion of ICOS⁺ effector-like CD8 + T cells and uniformly low frequencies of PD-1 + or PD-1 + TIM3 + exhausted populations across all doses ( b ). c ) iSTORM-L induced dose-dependent tumor growth suppression in the KPC mice above. Tumor volumes (caliper measurements) were measured twice per week. Bar and whisker represent means and standard deviation, respectively.

Article Snippet: KPC cells (Kerafast, catalog# EUP012-FP, MA, United States) were maintained in DMEM-High Glucose (Gibco TM , catalog# 11965092, NY, United States) supplemented with 10% FBS (Sigma-Aldrich, catalog# F4135, MO, United States).

Techniques: Activation Assay, Whisker Assay, Standard Deviation