ct26  (ATCC)


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    Name:
    CT26 WT
    Description:

    Catalog Number:
    CRL-2638
    Price:
    None
    Applications:
    The cell line can be used with CT26.CL25 (ATCC CRL-2639) as a model for testing immunotherapy protocols and in studies on the host immune response.
    Host:
    Mus musculus, mouse
    Cell Type:
    fibroblast
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    Structured Review

    ATCC ct26
    Comparison of <t>CT26</t> and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).

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    Average 99 stars, based on 35 article reviews
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    ct26 - by Bioz Stars, 2021-01
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    Images

    1) Product Images from "Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector"

    Article Title: Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector

    Journal: Neuro-Oncology

    doi: 10.1093/neuonc/nor199

    Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).
    Figure Legend Snippet: Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).

    Techniques Used: In Vitro, Expressing, MTS Assay, Flow Cytometry, Cytometry

    CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.
    Figure Legend Snippet: CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.

    Techniques Used: Mouse Assay, Polymerase Chain Reaction, Plasmid Preparation

    2) Product Images from "Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector"

    Article Title: Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector

    Journal: Neuro-Oncology

    doi: 10.1093/neuonc/nor199

    Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).
    Figure Legend Snippet: Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).

    Techniques Used: In Vitro, Expressing, MTS Assay, Flow Cytometry, Cytometry

    CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.
    Figure Legend Snippet: CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.

    Techniques Used: Mouse Assay, Polymerase Chain Reaction, Plasmid Preparation

    3) Product Images from "Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector"

    Article Title: Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector

    Journal: Neuro-Oncology

    doi: 10.1093/neuonc/nor199

    Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).
    Figure Legend Snippet: Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).

    Techniques Used: In Vitro, Expressing, MTS Assay, Flow Cytometry, Cytometry

    CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.
    Figure Legend Snippet: CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.

    Techniques Used: Mouse Assay, Polymerase Chain Reaction, Plasmid Preparation

    4) Product Images from "Tumour and host cell PD-L1 is required to mediate suppression of anti-tumour immunity in mice"

    Article Title: Tumour and host cell PD-L1 is required to mediate suppression of anti-tumour immunity in mice

    Journal: Nature Communications

    doi: 10.1038/ncomms14572

    PD-L1 expression in malignant epithelial and immune cells of human tumours. IHC analysis of human non-small-cell lung cancer (NSCLC) ( a ) and triple-negative breast cancer (TNBC) ( b ) samples identified three distinct patterns of PD-L1 expression (brown) in the tumour epithelium, immune cells or both compartments. In mouse tumour models in vivo , PD-L1 RNA and surface protein expression were detectable in MC-38 or CT-26 tumour cells, as well as in myeloid (mye) and lymphoid (lym) cells ( c ). Treatment of wild-type MC-38 ( d ) or CT-26 ( e ) tumours with anti-PD-L1 blocking antibodies resulted in slowed tumour growth and tumour regressions. If not labelled in graph, data shown is from MC38 (open circles) and CT26 (filled circles). Treatment data is representative of multiple independent study repeats with the same antibody. CR, complete regression; TGI, tumour growth inhibition. Scale bar represents 20 μm. Error bars depict s.d. from the mean.
    Figure Legend Snippet: PD-L1 expression in malignant epithelial and immune cells of human tumours. IHC analysis of human non-small-cell lung cancer (NSCLC) ( a ) and triple-negative breast cancer (TNBC) ( b ) samples identified three distinct patterns of PD-L1 expression (brown) in the tumour epithelium, immune cells or both compartments. In mouse tumour models in vivo , PD-L1 RNA and surface protein expression were detectable in MC-38 or CT-26 tumour cells, as well as in myeloid (mye) and lymphoid (lym) cells ( c ). Treatment of wild-type MC-38 ( d ) or CT-26 ( e ) tumours with anti-PD-L1 blocking antibodies resulted in slowed tumour growth and tumour regressions. If not labelled in graph, data shown is from MC38 (open circles) and CT26 (filled circles). Treatment data is representative of multiple independent study repeats with the same antibody. CR, complete regression; TGI, tumour growth inhibition. Scale bar represents 20 μm. Error bars depict s.d. from the mean.

    Techniques Used: Expressing, Immunohistochemistry, In Vivo, Blocking Assay, Inhibition

    5) Product Images from "Imidazole Metalloporphyrins as Photosensitizers for Photodynamic Therapy: Role of Molecular Charge, Central Metal and Hydroxyl Radical Production"

    Article Title: Imidazole Metalloporphyrins as Photosensitizers for Photodynamic Therapy: Role of Molecular Charge, Central Metal and Hydroxyl Radical Production

    Journal: Cancer letters

    doi: 10.1016/j.canlet.2009.02.054

    Broad-band white light-fluence dependent inactivation of mitochondria of HeLa cervical cancer and murine CT26 colon adenocarcinoma cells in culture. (A) 1-Zn at 5 µM; (B) 2-Zn at 5 µM; (C) 2-Pd at 0.5 µM. Concentration dependent
    Figure Legend Snippet: Broad-band white light-fluence dependent inactivation of mitochondria of HeLa cervical cancer and murine CT26 colon adenocarcinoma cells in culture. (A) 1-Zn at 5 µM; (B) 2-Zn at 5 µM; (C) 2-Pd at 0.5 µM. Concentration dependent

    Techniques Used: Concentration Assay

    6) Product Images from "Improvements in the Oral Absorption and Anticancer Efficacy of an Oxaliplatin-Loaded Solid Formulation: Pharmacokinetic Properties in Rats and Nonhuman Primates and the Effects of Oral Metronomic Dosing on Colorectal Cancer"

    Article Title: Improvements in the Oral Absorption and Anticancer Efficacy of an Oxaliplatin-Loaded Solid Formulation: Pharmacokinetic Properties in Rats and Nonhuman Primates and the Effects of Oral Metronomic Dosing on Colorectal Cancer

    Journal: International Journal of Nanomedicine

    doi: 10.2147/IJN.S267424

    In vivo analyses of the inhibitory effects of the following on tumor growth in CT26 tumor-bearing mice: biweekly intravenous administration of 3.3 mg/kg OP [OP-IV (3.3)] and 10 mg/kg OP [OP-IV (10)]; once-daily oral administration of 10 mg/kg OP in aqueous solution (OP-S); once-daily oral administration of ODSF as 2.5 mg/kg OP [ODSF (2.5)]; once-daily oral administration of ODSF as 10 mg/kg OP [ODSF (10)]; and once-daily oral administration of ODSF as 20 mg/kg OP [ODSF (20)], for 21 days. ( A ) Tumor volumes in mice [ a P
    Figure Legend Snippet: In vivo analyses of the inhibitory effects of the following on tumor growth in CT26 tumor-bearing mice: biweekly intravenous administration of 3.3 mg/kg OP [OP-IV (3.3)] and 10 mg/kg OP [OP-IV (10)]; once-daily oral administration of 10 mg/kg OP in aqueous solution (OP-S); once-daily oral administration of ODSF as 2.5 mg/kg OP [ODSF (2.5)]; once-daily oral administration of ODSF as 10 mg/kg OP [ODSF (10)]; and once-daily oral administration of ODSF as 20 mg/kg OP [ODSF (20)], for 21 days. ( A ) Tumor volumes in mice [ a P

    Techniques Used: In Vivo, Mouse Assay

    7) Product Images from "Severe, but not mild heat-shock treatment induces immunogenic cell death in cancer cells"

    Article Title: Severe, but not mild heat-shock treatment induces immunogenic cell death in cancer cells

    Journal: Oncoimmunology

    doi: 10.1080/2162402X.2017.1311433

    sHS-treated tumor cells are immunogenic and elicit prophylactic immunity in mice. (A, B) The viability of untreated CT26 cells and cells treated with mHS (42°C, 1 h) or sHS (47°C, 1 h) followed by an incubation at 37°C for 5 h and 24 h. (C) The exposure of HSP70, HSP90 and calreticulin was determined by flow cytometry from AnnexinV+DAPI− cells. Graphs represent means ± SEM of n = 3 (* p
    Figure Legend Snippet: sHS-treated tumor cells are immunogenic and elicit prophylactic immunity in mice. (A, B) The viability of untreated CT26 cells and cells treated with mHS (42°C, 1 h) or sHS (47°C, 1 h) followed by an incubation at 37°C for 5 h and 24 h. (C) The exposure of HSP70, HSP90 and calreticulin was determined by flow cytometry from AnnexinV+DAPI− cells. Graphs represent means ± SEM of n = 3 (* p

    Techniques Used: Mouse Assay, Incubation, Flow Cytometry, Cytometry

    8) Product Images from "Intravenous administration of the selective toll-like receptor 7 agonist DSR-29133 leads to anti-tumor efficacy in murine solid tumor models which can be potentiated by combination with fractionated radiotherapy"

    Article Title: Intravenous administration of the selective toll-like receptor 7 agonist DSR-29133 leads to anti-tumor efficacy in murine solid tumor models which can be potentiated by combination with fractionated radiotherapy

    Journal: Oncotarget

    doi: 10.18632/oncotarget.7928

    DSR-29133 when combined with fractionated RT generates protective immunological memory ( A and B ) Kaplan-Meier curves of tumor naïve and long-term surviving (LTS) mice originally treated with DSR-29133 and RT, following contralateral rechallenge with either 5 × 10 5 CT26 cells (A) or 1 × 10 5 4T1 cells (B). ** P
    Figure Legend Snippet: DSR-29133 when combined with fractionated RT generates protective immunological memory ( A and B ) Kaplan-Meier curves of tumor naïve and long-term surviving (LTS) mice originally treated with DSR-29133 and RT, following contralateral rechallenge with either 5 × 10 5 CT26 cells (A) or 1 × 10 5 4T1 cells (B). ** P

    Techniques Used: Mouse Assay

    9) Product Images from "The Role and Therapeutic Potential of miRNAs in Colorectal Liver Metastasis"

    Article Title: The Role and Therapeutic Potential of miRNAs in Colorectal Liver Metastasis

    Journal: Scientific Reports

    doi: 10.1038/s41598-019-52225-2

    Restored expression of downregulated miRNAs inhibits anchorage independent growth of CRC cell lines. CRC cell lines (CT26, SW620, HCT116) were transfected with miR-378f, miR-605, miR-1976, or negative control (NC) mimics and plated into soft agar assays. Two weeks post plating, number of colonies were counted and presented as average number of colonies in 5 fields + standard deviation ( a ) with representative images of each below the graphs ( b ). Statistics generated using student t-test; N = 3, *p
    Figure Legend Snippet: Restored expression of downregulated miRNAs inhibits anchorage independent growth of CRC cell lines. CRC cell lines (CT26, SW620, HCT116) were transfected with miR-378f, miR-605, miR-1976, or negative control (NC) mimics and plated into soft agar assays. Two weeks post plating, number of colonies were counted and presented as average number of colonies in 5 fields + standard deviation ( a ) with representative images of each below the graphs ( b ). Statistics generated using student t-test; N = 3, *p

    Techniques Used: Expressing, Transfection, Negative Control, Standard Deviation, Generated

    Restored expression of downregulated miRNAs inhibits cell proliferation and induces apoptosis in CRC cell lines. CT26 ( a , d ), SW620 ( b , e ), HCT116 ( c , f ) cell lines were transfected with miR-378f, miR-605, miR-1976, or negative control (NC) mimics and subjected to CCK-8 assays to measure proliferation for up to 4 days ( a – c ) or apoptosis assays at 72 hrs post-transfection ( d – f ). Apoptosis graphs represent total percentage of apoptotic cells that were stained positive for AnnexinV or 7-AAD. Data presented as average absorbance or % of apoptotic cells +/− standard deviation; N = 3; student t-test used to calculate p-values (p-value represents the largest p-value at each time point compared to the normal mimic control), *p
    Figure Legend Snippet: Restored expression of downregulated miRNAs inhibits cell proliferation and induces apoptosis in CRC cell lines. CT26 ( a , d ), SW620 ( b , e ), HCT116 ( c , f ) cell lines were transfected with miR-378f, miR-605, miR-1976, or negative control (NC) mimics and subjected to CCK-8 assays to measure proliferation for up to 4 days ( a – c ) or apoptosis assays at 72 hrs post-transfection ( d – f ). Apoptosis graphs represent total percentage of apoptotic cells that were stained positive for AnnexinV or 7-AAD. Data presented as average absorbance or % of apoptotic cells +/− standard deviation; N = 3; student t-test used to calculate p-values (p-value represents the largest p-value at each time point compared to the normal mimic control), *p

    Techniques Used: Expressing, Transfection, Negative Control, CCK-8 Assay, Staining, Standard Deviation, Significance Assay

    Restored expression of downregulated miRNAs reduce the ability of CRC cell lines to migrate and invade. CRC cell lines (CT26, SW620, HCT116) transfected with miR-378f, miR-605, miR-1976, or negative control (NC) mimics were plated into migration ( a – c ), and invasion ( d – f ) assays. Migration and invasion data presented as average number of cells in 5 fields + standard deviation with representative images of each below the graphs. Larger purple stained cells in the representative images signify migrated or invaded cells. Statistics generated using student t-test; N = 3, *p
    Figure Legend Snippet: Restored expression of downregulated miRNAs reduce the ability of CRC cell lines to migrate and invade. CRC cell lines (CT26, SW620, HCT116) transfected with miR-378f, miR-605, miR-1976, or negative control (NC) mimics were plated into migration ( a – c ), and invasion ( d – f ) assays. Migration and invasion data presented as average number of cells in 5 fields + standard deviation with representative images of each below the graphs. Larger purple stained cells in the representative images signify migrated or invaded cells. Statistics generated using student t-test; N = 3, *p

    Techniques Used: Expressing, Transfection, Negative Control, Migration, Standard Deviation, Staining, Generated

    10) Product Images from "Nanoscale metal-organic frameworks for mitochondria-targeted radiotherapy-radiodynamic therapy"

    Article Title: Nanoscale metal-organic frameworks for mitochondria-targeted radiotherapy-radiodynamic therapy

    Journal: Nature Communications

    doi: 10.1038/s41467-018-06655-7

    In vivo anti-cancer efficacy of mitochondria-targeted RDT. a Tumor growth inhibition/regression curves in MC38 tumor-bearing mice treated with PBS, Hf-DBA, DBB-Ru, or Hf-DBB-Ru by intratumoral (i.t.) injection with (+) or without (−) X-ray irradiation or Hf-DBB-Ru by intravenous (i.v.) injection followed by X-ray irradiation. n = 6. b Excised tumor weights on day 22. n = 6. c Tumor growth inhibition/regression curves in CT26 tumor-bearing mice treated with PBS with (+) or without (−) X-ray irradiation or i.v. injected with Hf-DBB-Ru followed by X-ray irradiation. Black arrows refer to i.v. injection of different treatments and red arrows refer to X-ray irradiation. Excised tumor weights on day 21 shown in the inset. n = 6. ** P
    Figure Legend Snippet: In vivo anti-cancer efficacy of mitochondria-targeted RDT. a Tumor growth inhibition/regression curves in MC38 tumor-bearing mice treated with PBS, Hf-DBA, DBB-Ru, or Hf-DBB-Ru by intratumoral (i.t.) injection with (+) or without (−) X-ray irradiation or Hf-DBB-Ru by intravenous (i.v.) injection followed by X-ray irradiation. n = 6. b Excised tumor weights on day 22. n = 6. c Tumor growth inhibition/regression curves in CT26 tumor-bearing mice treated with PBS with (+) or without (−) X-ray irradiation or i.v. injected with Hf-DBB-Ru followed by X-ray irradiation. Black arrows refer to i.v. injection of different treatments and red arrows refer to X-ray irradiation. Excised tumor weights on day 21 shown in the inset. n = 6. ** P

    Techniques Used: In Vivo, Inhibition, Mouse Assay, Injection, Irradiation

    11) Product Images from "Local angiotensin II contributes to tumor resistance to checkpoint immunotherapy"

    Article Title: Local angiotensin II contributes to tumor resistance to checkpoint immunotherapy

    Journal: Journal for Immunotherapy of Cancer

    doi: 10.1186/s40425-018-0401-3

    Local AngII in tumor microenvironment is involved in immune escape of tumor cells. a The influence of AngII-receptor blockers on 4T1 tumor growth in syngeneic BALB/c mice; candesartan (cand, 5mg/kg, i.p.; starting at day 5 after cell injection, daily ) for AT1R and PD123319 (5mg/kg, i.p.; starting from day 5 after cell injection, every other day) for AT2R, n =5. b The influence of AngII-receptor blockers on 4T1 cells proliferation in vitro as detected by MTT assay; candesartan (10μm/well) and PD123319 (10μm/well). c The influence of Ang II-receptor blockers on 4T1 tumor growth in T-cell immunodeficient BALB/c nude mice, n =5. d The expression of AGT, a precursor of AngII, was silenced in 4T1 cells and CT26 cells by shRNA. Hypoxia remarkably induced generation of Ang II in 4T1 and CT26 cells as detected by ELISA. AGT-silencing greatly decreased Ang II levels, especially under hypoxic condition. Data are presented as mean±SEM, n =3. e AGT silencing did not influence cell-proliferation of 4T1 cells in vitro as detected by MTT assay. f AGT silencing obviously inhibited tumor growth of 4T1cells in BALB/c mice comparing to negative control, and the depletion of CD8 + T cells in mice by in vivo administration of monoclonal antibody against CD8 greatly attenuated this effect ( n =6). Ns, no significance; *, P
    Figure Legend Snippet: Local AngII in tumor microenvironment is involved in immune escape of tumor cells. a The influence of AngII-receptor blockers on 4T1 tumor growth in syngeneic BALB/c mice; candesartan (cand, 5mg/kg, i.p.; starting at day 5 after cell injection, daily ) for AT1R and PD123319 (5mg/kg, i.p.; starting from day 5 after cell injection, every other day) for AT2R, n =5. b The influence of AngII-receptor blockers on 4T1 cells proliferation in vitro as detected by MTT assay; candesartan (10μm/well) and PD123319 (10μm/well). c The influence of Ang II-receptor blockers on 4T1 tumor growth in T-cell immunodeficient BALB/c nude mice, n =5. d The expression of AGT, a precursor of AngII, was silenced in 4T1 cells and CT26 cells by shRNA. Hypoxia remarkably induced generation of Ang II in 4T1 and CT26 cells as detected by ELISA. AGT-silencing greatly decreased Ang II levels, especially under hypoxic condition. Data are presented as mean±SEM, n =3. e AGT silencing did not influence cell-proliferation of 4T1 cells in vitro as detected by MTT assay. f AGT silencing obviously inhibited tumor growth of 4T1cells in BALB/c mice comparing to negative control, and the depletion of CD8 + T cells in mice by in vivo administration of monoclonal antibody against CD8 greatly attenuated this effect ( n =6). Ns, no significance; *, P

    Techniques Used: Mouse Assay, Injection, In Vitro, MTT Assay, Expressing, shRNA, Enzyme-linked Immunosorbent Assay, Negative Control, In Vivo

    12) Product Images from "Effects of isoflurane anesthesia on physiological parameters in murine subcutaneous tumor allografts measured via diffuse reflectance spectroscopy"

    Article Title: Effects of isoflurane anesthesia on physiological parameters in murine subcutaneous tumor allografts measured via diffuse reflectance spectroscopy

    Journal: Biomedical Optics Express

    doi: 10.1364/BOE.9.002871

    DRS was performed on Balb/c mouse (10 weeks old) to quantify physiological parameters (THC, StO 2 , HbO 2 , and μ s ’) in subcutaneous CT26 tumor allografts at a volume of 100 mm 3 (b, e), 500 mm 3 (c, f), and adjacent normal tissue (a, d) both with (d, e, f) and without isoflurane anesthesia (a, b, c). Anesthesia was constant at 1.5% isoflurane and 1 L/min O 2 .
    Figure Legend Snippet: DRS was performed on Balb/c mouse (10 weeks old) to quantify physiological parameters (THC, StO 2 , HbO 2 , and μ s ’) in subcutaneous CT26 tumor allografts at a volume of 100 mm 3 (b, e), 500 mm 3 (c, f), and adjacent normal tissue (a, d) both with (d, e, f) and without isoflurane anesthesia (a, b, c). Anesthesia was constant at 1.5% isoflurane and 1 L/min O 2 .

    Techniques Used:

    Comparison of the physiological parameters, THC, StO 2 , HbO 2 , and μ s ’ of subcutaneous CT26 tumor allografts and adjacent normal tissue both with (light gray) and without (dark gray) isoflurane anesthesia. Similar to previous findings, THC, StO 2 , and HbO 2 were reduced when comparing the no-anesthesia and 1.5% isoflurane conditions in adjacent normal tissue. Results demonstrate that isoflurane anesthesia causes experimentally-reduced HbO 2 values, and that StO 2 and HbO 2 decreased with increasing allograft tumor volumes, whereas THC increased and μ s ’ remained constant. Values are means ± SD. Significance is indicated by *(p
    Figure Legend Snippet: Comparison of the physiological parameters, THC, StO 2 , HbO 2 , and μ s ’ of subcutaneous CT26 tumor allografts and adjacent normal tissue both with (light gray) and without (dark gray) isoflurane anesthesia. Similar to previous findings, THC, StO 2 , and HbO 2 were reduced when comparing the no-anesthesia and 1.5% isoflurane conditions in adjacent normal tissue. Results demonstrate that isoflurane anesthesia causes experimentally-reduced HbO 2 values, and that StO 2 and HbO 2 decreased with increasing allograft tumor volumes, whereas THC increased and μ s ’ remained constant. Values are means ± SD. Significance is indicated by *(p

    Techniques Used:

    13) Product Images from "Cytokine Expression and Macrophage Localization in Xenograft and Allograft Tumor Models Stimulated with Lipopolysaccharide"

    Article Title: Cytokine Expression and Macrophage Localization in Xenograft and Allograft Tumor Models Stimulated with Lipopolysaccharide

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms19041261

    M1 macrophages and MDSCs in xenograft and allograft tumor models after LPS stimulation. HT29 and CT26 tumor-bearing mice were treated with LPS on the day 21 from tumor transplantation and splenocytes were isolated at 24 h. The expression levels of MHC class I ( A ), class II ( B ), CD80 ( C ), and Gr-1 ( D ) on CD11b + cells were analyzed by flow cytometry. Results are shown are representative of at least three independent experiments.
    Figure Legend Snippet: M1 macrophages and MDSCs in xenograft and allograft tumor models after LPS stimulation. HT29 and CT26 tumor-bearing mice were treated with LPS on the day 21 from tumor transplantation and splenocytes were isolated at 24 h. The expression levels of MHC class I ( A ), class II ( B ), CD80 ( C ), and Gr-1 ( D ) on CD11b + cells were analyzed by flow cytometry. Results are shown are representative of at least three independent experiments.

    Techniques Used: Mouse Assay, Transplantation Assay, Isolation, Expressing, Flow Cytometry, Cytometry

    Serum pro-inflammatory cytokine levels in xenograft and allograft tumor models after LPS stimulation. HT29 cells or CT26 cells were s.c. transplanted into BALB/c-nu/nu mice. On the day 21 after transplantation, 500 μg LPS was i.p. injected and peripheral blood was collected at indicated hour. The serum levels of TNF ( A ), IFN-γ ( B ), and IL-18 ( C ) were detected by ELISA. The data are presented as the mean ± SEM assessed by a Student’s two-tailed t -test. * p
    Figure Legend Snippet: Serum pro-inflammatory cytokine levels in xenograft and allograft tumor models after LPS stimulation. HT29 cells or CT26 cells were s.c. transplanted into BALB/c-nu/nu mice. On the day 21 after transplantation, 500 μg LPS was i.p. injected and peripheral blood was collected at indicated hour. The serum levels of TNF ( A ), IFN-γ ( B ), and IL-18 ( C ) were detected by ELISA. The data are presented as the mean ± SEM assessed by a Student’s two-tailed t -test. * p

    Techniques Used: Mouse Assay, Transplantation Assay, Injection, Enzyme-linked Immunosorbent Assay, Two Tailed Test

    Confocal images of CD80 and MRC1 expression cells in spleen and tumor with or without injection of LPS. HT29 and CT26 tumor-bearing mice were treated with LPS (+LPS) or PBS control (−LPS) on the day 21 from tumor transplantation and tumor and spleen were collected after 24 h from LPS treatment. ( A ) Spleen in HT29 tumor-bearing mice. ( B ) Tumor in HT29 tumor-bearing mice. ( C ) Spleen in CT26 tumor-bearing mice. ( D ) Tumor in CT26 tumor-bearing mice. CD80, MRC1, and cell nuclei (DAPI) are represented in green, red, and blue, respectively. Representative images from at least three independent experiments are shown. Each scale bar indicates 50 μm.
    Figure Legend Snippet: Confocal images of CD80 and MRC1 expression cells in spleen and tumor with or without injection of LPS. HT29 and CT26 tumor-bearing mice were treated with LPS (+LPS) or PBS control (−LPS) on the day 21 from tumor transplantation and tumor and spleen were collected after 24 h from LPS treatment. ( A ) Spleen in HT29 tumor-bearing mice. ( B ) Tumor in HT29 tumor-bearing mice. ( C ) Spleen in CT26 tumor-bearing mice. ( D ) Tumor in CT26 tumor-bearing mice. CD80, MRC1, and cell nuclei (DAPI) are represented in green, red, and blue, respectively. Representative images from at least three independent experiments are shown. Each scale bar indicates 50 μm.

    Techniques Used: Expressing, Injection, Mouse Assay, Transplantation Assay

    14) Product Images from "IGF1R blockade with ganitumab results in systemic effects on the GH–IGF axis in mice"

    Article Title: IGF1R blockade with ganitumab results in systemic effects on the GH–IGF axis in mice

    Journal: The Journal of endocrinology

    doi: 10.1530/JOE-13-0306

    Inhibition of mIGF1R activation by ganitumab in vivo . (A) (Left panel) Ganitumab inhibited IGF1-induced activation of mIGF1R in murine lungs. Each lane represents an individual mouse treated once with 1 mg/dose of ganitumab or hIgG1 for 6 h ( n =2 per group). In vitro cultures of CT26 cells were used as positive control for mIGF1R phosphorylation status. (Right panel) Densitometric analysis of IGF1R activation from the image on the left. Bars represent mean of the band intensity ± S.D. Values were normalized to total IGF1R levels from CT26-positive controls. Significant inhibition of pIGF1R was observed in ganitumab-treated mice receiving IGF1 challenge (* P
    Figure Legend Snippet: Inhibition of mIGF1R activation by ganitumab in vivo . (A) (Left panel) Ganitumab inhibited IGF1-induced activation of mIGF1R in murine lungs. Each lane represents an individual mouse treated once with 1 mg/dose of ganitumab or hIgG1 for 6 h ( n =2 per group). In vitro cultures of CT26 cells were used as positive control for mIGF1R phosphorylation status. (Right panel) Densitometric analysis of IGF1R activation from the image on the left. Bars represent mean of the band intensity ± S.D. Values were normalized to total IGF1R levels from CT26-positive controls. Significant inhibition of pIGF1R was observed in ganitumab-treated mice receiving IGF1 challenge (* P

    Techniques Used: Inhibition, Activation Assay, In Vivo, In Vitro, Positive Control, Mouse Assay

    Interaction of ganitumab with mIGF1R. (A) Ganitumab K D measurement. Binding affinity of ganitumab to mIGF1R(ECD)–mFc measured using the Biacore equilibrium method. (B) Ganitumab blockade of hIGF1 and hIGF2 binding. A binding assay with mIGF1R(ECD)–mFc was used to evaluate ganitumab blockade of ruthenium-labeled hIGF1 and hIGF2 ( n =2, mean±S.D.). (C) Ganitumab inhibition of mIGF1R phosphorylation. Serum-starved CT26 cells were pretreated with increasing concentrations of ganitumab before challenge with 2 nM IGF1 for 15 min. IGF1R phosphorylation was determined by immunoprecipitation and western blotting. pIGF1R, phosphorylated IGF1R; RU, relative units.
    Figure Legend Snippet: Interaction of ganitumab with mIGF1R. (A) Ganitumab K D measurement. Binding affinity of ganitumab to mIGF1R(ECD)–mFc measured using the Biacore equilibrium method. (B) Ganitumab blockade of hIGF1 and hIGF2 binding. A binding assay with mIGF1R(ECD)–mFc was used to evaluate ganitumab blockade of ruthenium-labeled hIGF1 and hIGF2 ( n =2, mean±S.D.). (C) Ganitumab inhibition of mIGF1R phosphorylation. Serum-starved CT26 cells were pretreated with increasing concentrations of ganitumab before challenge with 2 nM IGF1 for 15 min. IGF1R phosphorylation was determined by immunoprecipitation and western blotting. pIGF1R, phosphorylated IGF1R; RU, relative units.

    Techniques Used: Binding Assay, Labeling, Inhibition, Immunoprecipitation, Western Blot

    15) Product Images from "Efficiency of Conditionally Attenuated Salmonella enterica Serovar Typhimurium in Bacterium-Mediated Tumor Therapy"

    Article Title: Efficiency of Conditionally Attenuated Salmonella enterica Serovar Typhimurium in Bacterium-Mediated Tumor Therapy

    Journal: mBio

    doi: 10.1128/mBio.00254-15

    Tumor development upon infection with the arabinose-induced conditionally complemented Salmonella Δ rfaD variant. CT26 (A) and RenCa (B) tumor-bearing mice were infected i.v. with 5 × 10 6 bacteria. Tumor volumes were measured with a caliper. PBS served as a negative control, and SL7207 served as a positive control for comparison. (C) Body weight as an indicator of the general health status of infected mice. Induced (+) Δ araBAD ::P BAD rfaD bacteria exhibited greater virulence but also a stronger antitumor effect. (D) TNF-α levels in sera measured by ELISA at 1.5 hpi. Upon induction with arabinose (+), TNF-α was restored to WT levels. The mean and range are displayed. Results are representative of two independent experiments with five replicates per group.
    Figure Legend Snippet: Tumor development upon infection with the arabinose-induced conditionally complemented Salmonella Δ rfaD variant. CT26 (A) and RenCa (B) tumor-bearing mice were infected i.v. with 5 × 10 6 bacteria. Tumor volumes were measured with a caliper. PBS served as a negative control, and SL7207 served as a positive control for comparison. (C) Body weight as an indicator of the general health status of infected mice. Induced (+) Δ araBAD ::P BAD rfaD bacteria exhibited greater virulence but also a stronger antitumor effect. (D) TNF-α levels in sera measured by ELISA at 1.5 hpi. Upon induction with arabinose (+), TNF-α was restored to WT levels. The mean and range are displayed. Results are representative of two independent experiments with five replicates per group.

    Techniques Used: Infection, Variant Assay, Mouse Assay, Negative Control, Positive Control, Enzyme-linked Immunosorbent Assay

    In vivo characterization of LPS variants in CT26-bearing BALB/c mice. Mice were infected i.v. with 5 × 10 6 CFU. (A and B) Blood, spleen, and tumor bacterial burdens were determined by plating serial dilutions of tissue homogenates. (A) CFU counts in different homogenates at 12 hpi. (B) CFU counts in different homogenates at 36 hpi. Much lower numbers of Δ rfaD and Δ rfaG LPS core mutant bacteria than WT bacteria were observed in the blood and spleen. (C) Body weight measurement as an indicator of general health status after infection of CT26-bearing mice with different LPS variants. Again, the Δ rfaD and Δ rfaG mutants are highly attenuated while the Δ rfaH , Δ rfaG , and Δ rfaL mutants are lethal within 3 days. The median and range are displayed. Results are representative of two independent experiments with five mice per group. *, P
    Figure Legend Snippet: In vivo characterization of LPS variants in CT26-bearing BALB/c mice. Mice were infected i.v. with 5 × 10 6 CFU. (A and B) Blood, spleen, and tumor bacterial burdens were determined by plating serial dilutions of tissue homogenates. (A) CFU counts in different homogenates at 12 hpi. (B) CFU counts in different homogenates at 36 hpi. Much lower numbers of Δ rfaD and Δ rfaG LPS core mutant bacteria than WT bacteria were observed in the blood and spleen. (C) Body weight measurement as an indicator of general health status after infection of CT26-bearing mice with different LPS variants. Again, the Δ rfaD and Δ rfaG mutants are highly attenuated while the Δ rfaH , Δ rfaG , and Δ rfaL mutants are lethal within 3 days. The median and range are displayed. Results are representative of two independent experiments with five mice per group. *, P

    Techniques Used: In Vivo, Mouse Assay, Infection, Mutagenesis

    Tumor development after infection with Salmonella LPS variants. CT26 (A), RenCa (B), and F1A11 (C) tumor-bearing mice were infected i.v. with 5 × 10 6 bacteria. Tumor volumes were measured with a caliper. PBS served as a negative control, and SL7207 served as a positive control for comparison. (D) TNF-α levels in sera measured by ELISA at 1.5 hpi with selected LPS variants. The Δ rfaG and Δ rfaD mutants induced a lower response than WT salmonellae . The median and range are displayed. Results are representative of two independent experiments with five replicates per group. The symbol † indicates that two out of five mice succumbed to the infection. *, P
    Figure Legend Snippet: Tumor development after infection with Salmonella LPS variants. CT26 (A), RenCa (B), and F1A11 (C) tumor-bearing mice were infected i.v. with 5 × 10 6 bacteria. Tumor volumes were measured with a caliper. PBS served as a negative control, and SL7207 served as a positive control for comparison. (D) TNF-α levels in sera measured by ELISA at 1.5 hpi with selected LPS variants. The Δ rfaG and Δ rfaD mutants induced a lower response than WT salmonellae . The median and range are displayed. Results are representative of two independent experiments with five replicates per group. The symbol † indicates that two out of five mice succumbed to the infection. *, P

    Techniques Used: Infection, Mouse Assay, Negative Control, Positive Control, Enzyme-linked Immunosorbent Assay

    16) Product Images from "Establishment of an Endoscopy-Guided Minimally Invasive Orthotopic Mouse Model of Colorectal Cancer"

    Article Title: Establishment of an Endoscopy-Guided Minimally Invasive Orthotopic Mouse Model of Colorectal Cancer

    Journal: Cancers

    doi: 10.3390/cancers12103007

    Microscopic tumor evaluation of the CT26/BALB/C model with H E ( A , B , D – H ) and immuno-histochemical staining for CK20 ( C ). Transverse section of the colon near the injection site with growth of the primary tumor. The malignant tumor with moderate atypia of the nuclei shows luminal ulceration ( A , yellow arrow) and infiltration of the muscularis propria layer ( A , B , red arrows) corresponding to a pT2 category in humans. ( C ) Cytoplasmic positivity of tumor cells for CK20. ( D ) Lympho-vascular invasion (red arrow) corresponding to an L1 category in humans near primary tumor site. ( E , F ) Scoring of stromal tumor-infiltrating lymphocytes (yellow circles) with a score of 1 (0–10% stromal TILs, E ) and a score of 6 ( > 50% stromal TILs, F ). ( G ) Mesenteric lymph node metastasis with tumor infiltrates (red arrows) and necrosis (yellow arrows). ( H ) Liver metastasis with tumor infiltrates (red arrows), normal liver tissue (yellow arrows).
    Figure Legend Snippet: Microscopic tumor evaluation of the CT26/BALB/C model with H E ( A , B , D – H ) and immuno-histochemical staining for CK20 ( C ). Transverse section of the colon near the injection site with growth of the primary tumor. The malignant tumor with moderate atypia of the nuclei shows luminal ulceration ( A , yellow arrow) and infiltration of the muscularis propria layer ( A , B , red arrows) corresponding to a pT2 category in humans. ( C ) Cytoplasmic positivity of tumor cells for CK20. ( D ) Lympho-vascular invasion (red arrow) corresponding to an L1 category in humans near primary tumor site. ( E , F ) Scoring of stromal tumor-infiltrating lymphocytes (yellow circles) with a score of 1 (0–10% stromal TILs, E ) and a score of 6 ( > 50% stromal TILs, F ). ( G ) Mesenteric lymph node metastasis with tumor infiltrates (red arrows) and necrosis (yellow arrows). ( H ) Liver metastasis with tumor infiltrates (red arrows), normal liver tissue (yellow arrows).

    Techniques Used: Staining, Injection

    Endoscopic score assigned during follow-up endoscopies on ( A ) BALB/C and ( B ) C57BL/6J mice with varying number of implanted CT26 or MC38 cells, respectively, over an observation period. Significant differences are marked, p values represent Bonferroni-corrected values (** p
    Figure Legend Snippet: Endoscopic score assigned during follow-up endoscopies on ( A ) BALB/C and ( B ) C57BL/6J mice with varying number of implanted CT26 or MC38 cells, respectively, over an observation period. Significant differences are marked, p values represent Bonferroni-corrected values (** p

    Techniques Used: Mouse Assay

    17) Product Images from "Improved Chemotherapeutic Activity by Morus alba Fruits through Immune Response of Toll-Like Receptor 4"

    Article Title: Improved Chemotherapeutic Activity by Morus alba Fruits through Immune Response of Toll-Like Receptor 4

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms161024139

    Cytoxicity of MFE in vitro . ( A ) The effect of MFE on the proliferation of CT26 tumor cells; ( B ) The effect of MFE on macrophage-mediated cytotoxicity against CT26 tumor cells. Macrophages were activated by MFE and co-cultured with CT26 tumor cells for additional 24 h at the ratio of 10:1 (macrophage to CT26). The values are presented as mean ± S.D. ** p
    Figure Legend Snippet: Cytoxicity of MFE in vitro . ( A ) The effect of MFE on the proliferation of CT26 tumor cells; ( B ) The effect of MFE on macrophage-mediated cytotoxicity against CT26 tumor cells. Macrophages were activated by MFE and co-cultured with CT26 tumor cells for additional 24 h at the ratio of 10:1 (macrophage to CT26). The values are presented as mean ± S.D. ** p

    Techniques Used: In Vitro, Cell Culture

    18) Product Images from "Cytotoxicity study of the interleukin-12-expressing recombinant Newcastle disease virus strain, rAF-IL12, towards CT26 colon cancer cells in vitro and in vivo"

    Article Title: Cytotoxicity study of the interleukin-12-expressing recombinant Newcastle disease virus strain, rAF-IL12, towards CT26 colon cancer cells in vitro and in vivo

    Journal: Cancer Cell International

    doi: 10.1186/s12935-020-01372-y

    Normalized gene expression level of KRAS, BRAF, MAPK1, NOTCH1, BAX, p53, CCL2, and VEGF-A in a CT26 cancer cells in vitro and b tumour excised from CT26 tumour-burden mice. Data are presented as mean ± S.E.M from three independent experiments. Statistically significant differences between the means were determined by One-Way ANOVA followed by Duncan post hoc test. Differences were considered significant when the p ≤ 0.05 as indicated by *
    Figure Legend Snippet: Normalized gene expression level of KRAS, BRAF, MAPK1, NOTCH1, BAX, p53, CCL2, and VEGF-A in a CT26 cancer cells in vitro and b tumour excised from CT26 tumour-burden mice. Data are presented as mean ± S.E.M from three independent experiments. Statistically significant differences between the means were determined by One-Way ANOVA followed by Duncan post hoc test. Differences were considered significant when the p ≤ 0.05 as indicated by *

    Techniques Used: Expressing, In Vitro, Mouse Assay

    Effects on the CT26 tumours for the negative control, AF2240-i, and rAF-IL12 groups. a Images of CT26 tumour harvested from negative control, AF2240-i, and rAF-IL12 groups following the 28-days of treatment. b The growth rate of the CT26 tumours from day-0 until day-28 of treatments. c Average weight of CT26 tumours harvested from mice after 28-days of treatment. Data are represented as mean ± S.E.M. of six mice per group. Mean values with statistical difference at p
    Figure Legend Snippet: Effects on the CT26 tumours for the negative control, AF2240-i, and rAF-IL12 groups. a Images of CT26 tumour harvested from negative control, AF2240-i, and rAF-IL12 groups following the 28-days of treatment. b The growth rate of the CT26 tumours from day-0 until day-28 of treatments. c Average weight of CT26 tumours harvested from mice after 28-days of treatment. Data are represented as mean ± S.E.M. of six mice per group. Mean values with statistical difference at p

    Techniques Used: Negative Control, Mouse Assay

    a Tumour sections assayed by DeadEnd colorimetric TUNEL system to indicate cell apoptosis in CT26 tumour-bearing Balb/c mice: a positive control (sample treated with DNAse I); b negative control; c tumour treated with AF2240-i; d tumour treated with rAF-IL12. Brown stained nuclei in the black circle indicate DNA fragmentation and nuclear condensation. Magnification: 100x; b The number of apoptotic cells per tumour section from the four aforementioned groups after 28 days of treatment. A total number of 200 cells per tumor section was used for the quantification analysis in the TUNEL assay. Data are presented as mean ± S.E.M. of six mice per group. Mean values with statistical difference at p ≤ 0.05 between groups are indicated with *
    Figure Legend Snippet: a Tumour sections assayed by DeadEnd colorimetric TUNEL system to indicate cell apoptosis in CT26 tumour-bearing Balb/c mice: a positive control (sample treated with DNAse I); b negative control; c tumour treated with AF2240-i; d tumour treated with rAF-IL12. Brown stained nuclei in the black circle indicate DNA fragmentation and nuclear condensation. Magnification: 100x; b The number of apoptotic cells per tumour section from the four aforementioned groups after 28 days of treatment. A total number of 200 cells per tumor section was used for the quantification analysis in the TUNEL assay. Data are presented as mean ± S.E.M. of six mice per group. Mean values with statistical difference at p ≤ 0.05 between groups are indicated with *

    Techniques Used: TUNEL Assay, Mouse Assay, Positive Control, Negative Control, Staining

    Viral copy number of AF2240-i and rAF-IL12 detected in CT26 cells at 24, 48, and 72 h post-infection as measured by RT-qPCR analysis based on NDV Fusion (F) gene for viral replication kinetics. The copy number was calculated based on the formula generated from the qPCR standard curve of the NDV: X = (y−58.149)/−3.371; where X is the viral copy number; y is the value mean Cq; 58.149 is the y-intercept value; and −3.371 is the slope of the standard curve. Data are presented as mean ± S.E.M from triplicate determinations. Statistically significant differences between the means were determined by One-Way ANOVA followed by Duncan post hoc test. Differences were considered significant when the * p ≤ 0.05
    Figure Legend Snippet: Viral copy number of AF2240-i and rAF-IL12 detected in CT26 cells at 24, 48, and 72 h post-infection as measured by RT-qPCR analysis based on NDV Fusion (F) gene for viral replication kinetics. The copy number was calculated based on the formula generated from the qPCR standard curve of the NDV: X = (y−58.149)/−3.371; where X is the viral copy number; y is the value mean Cq; 58.149 is the y-intercept value; and −3.371 is the slope of the standard curve. Data are presented as mean ± S.E.M from triplicate determinations. Statistically significant differences between the means were determined by One-Way ANOVA followed by Duncan post hoc test. Differences were considered significant when the * p ≤ 0.05

    Techniques Used: Infection, Quantitative RT-PCR, Generated, Real-time Polymerase Chain Reaction

    MTT assay showing the cytotoxicity activity of AF2240-i and rAF-IL12 against CT26 and 3T3 cells 72 h post-infection. Percentage of viability of two cell lines (CT26 and 3T3) when treated with seven doses of virus treatment (AF2240-i or rAF-IL12) after 72 h. The IC 50 value (half-maximal inhibitory concentration, HA unit) for AF2240-i-CT26 = 291 ± 0.67; rAF-IL12-CT26 = 276 ± 0.88; AF2240-3T3 = n.d.; rAF-IL12-3T3 = n.d. Data are presented as mean ± S.E.M from triplicate determinations
    Figure Legend Snippet: MTT assay showing the cytotoxicity activity of AF2240-i and rAF-IL12 against CT26 and 3T3 cells 72 h post-infection. Percentage of viability of two cell lines (CT26 and 3T3) when treated with seven doses of virus treatment (AF2240-i or rAF-IL12) after 72 h. The IC 50 value (half-maximal inhibitory concentration, HA unit) for AF2240-i-CT26 = 291 ± 0.67; rAF-IL12-CT26 = 276 ± 0.88; AF2240-3T3 = n.d.; rAF-IL12-3T3 = n.d. Data are presented as mean ± S.E.M from triplicate determinations

    Techniques Used: MTT Assay, Activity Assay, Infection, Concentration Assay

    Cell cycle analysis of CT2 cells at different cell cycle phase. a Histogram of cell cycle analysis showing distribution of CT26 cells at different cell cycle phase (G 0 , G 1 , S, and G 2 ) after 72 h period of treatment with AF2240-i and rAF-IL12. The G 0 peak appeared first in the histogram followed by G 1 , S, and G 2 peaks indicating the percentage of cells population in those aforementioned cell cycle phases. Percentage of cells population in each peak was calculated from a total number of 10, 000 cells in each flow cytometry run. b Percentage of cells population at different cell cycle phase analysed by flow cytometer following treatment with AF2240-i (291 HA titre) and rAF-IL12 (276 HA titre) in CT26 cells. Data are presented as mean ± S.E.M from triplicate determinations. Mean values with statistical difference at p
    Figure Legend Snippet: Cell cycle analysis of CT2 cells at different cell cycle phase. a Histogram of cell cycle analysis showing distribution of CT26 cells at different cell cycle phase (G 0 , G 1 , S, and G 2 ) after 72 h period of treatment with AF2240-i and rAF-IL12. The G 0 peak appeared first in the histogram followed by G 1 , S, and G 2 peaks indicating the percentage of cells population in those aforementioned cell cycle phases. Percentage of cells population in each peak was calculated from a total number of 10, 000 cells in each flow cytometry run. b Percentage of cells population at different cell cycle phase analysed by flow cytometer following treatment with AF2240-i (291 HA titre) and rAF-IL12 (276 HA titre) in CT26 cells. Data are presented as mean ± S.E.M from triplicate determinations. Mean values with statistical difference at p

    Techniques Used: Cell Cycle Assay, Flow Cytometry

    Annexin V/FITC assay in CT26 cells following AF2240-i (291 HA titre) and rAF-IL12 (276 HA titre) 72 h post-infection. a Typical quadrant analysis of Annexin V/FITC flow cytometry of CT26 cells apoptosis. The lower left quadrant of each group indicated the viable cells population; the lower right quadrant indicated the early apoptotic cells population; the upper right quadrant indicated the late apoptotic cells population; and the upper left quadrant indicated the necrotic cells population. Two fluorescent dyes were used in this assay which are FITC (x-axis) and PE (y-axis). b Percentage of viable, early apoptotic, and late apoptotic cells population analysed by quantitative analysis. Data are presented as mean ± S.E.M from triplicate determinations. Mean values with statistical difference at p
    Figure Legend Snippet: Annexin V/FITC assay in CT26 cells following AF2240-i (291 HA titre) and rAF-IL12 (276 HA titre) 72 h post-infection. a Typical quadrant analysis of Annexin V/FITC flow cytometry of CT26 cells apoptosis. The lower left quadrant of each group indicated the viable cells population; the lower right quadrant indicated the early apoptotic cells population; the upper right quadrant indicated the late apoptotic cells population; and the upper left quadrant indicated the necrotic cells population. Two fluorescent dyes were used in this assay which are FITC (x-axis) and PE (y-axis). b Percentage of viable, early apoptotic, and late apoptotic cells population analysed by quantitative analysis. Data are presented as mean ± S.E.M from triplicate determinations. Mean values with statistical difference at p

    Techniques Used: Infection, Flow Cytometry

    19) Product Images from "Infliximab does not increase colonic cancer risk associated to murine chronic colitis"

    Article Title: Infliximab does not increase colonic cancer risk associated to murine chronic colitis

    Journal: World Journal of Gastroenterology

    doi: 10.3748/wjg.v22.i44.9727

    Effect of Infliximab on proliferation and vitality of colonic cancer cell line CT26: MTT assay. A: MTT performed without cell pre-treatment; B: MTT performed following 24 h cell pre-incubation with TNFα.
    Figure Legend Snippet: Effect of Infliximab on proliferation and vitality of colonic cancer cell line CT26: MTT assay. A: MTT performed without cell pre-treatment; B: MTT performed following 24 h cell pre-incubation with TNFα.

    Techniques Used: MTT Assay, Incubation

    20) Product Images from "Tumor-Targeted Immunotherapy by Using Primary Adipose-Derived Stem Cells and an Antigen-Specific Protein Vaccine"

    Article Title: Tumor-Targeted Immunotherapy by Using Primary Adipose-Derived Stem Cells and an Antigen-Specific Protein Vaccine

    Journal: Cancers

    doi: 10.3390/cancers10110446

    In vivo antibody depletion reduces the antitumor effect of the ADSC-E7’-eGFP–PE(ΔIII)-E7-KDEL3 combined treatment. ( A ) Time course of the experiment; ( B ) tumor volume measurements of syngeneic tumor models with different treatments were conducted at indicated days after the subcutaneous injection of CT26 cells; * p
    Figure Legend Snippet: In vivo antibody depletion reduces the antitumor effect of the ADSC-E7’-eGFP–PE(ΔIII)-E7-KDEL3 combined treatment. ( A ) Time course of the experiment; ( B ) tumor volume measurements of syngeneic tumor models with different treatments were conducted at indicated days after the subcutaneous injection of CT26 cells; * p

    Techniques Used: In Vivo, Injection

    Histological assessment of tumor angiogenesis. Representative fluorescence images of tumor sections from mice inoculated with ( A ) CT26 cells or ( B ) LLC1 cells, which were stained with anti-CD31 (red) after 28 days to detect tumor-associated blood vessels. The quantitative results were determined by the average blood vessel area per microscopic field in tumor sections from mice inoculated with ( C ) CT26 cells or ( D ) LLC1 cells. Values are means + SEM; * p
    Figure Legend Snippet: Histological assessment of tumor angiogenesis. Representative fluorescence images of tumor sections from mice inoculated with ( A ) CT26 cells or ( B ) LLC1 cells, which were stained with anti-CD31 (red) after 28 days to detect tumor-associated blood vessels. The quantitative results were determined by the average blood vessel area per microscopic field in tumor sections from mice inoculated with ( C ) CT26 cells or ( D ) LLC1 cells. Values are means + SEM; * p

    Techniques Used: Fluorescence, Mouse Assay, Staining

    The tumor inhibition of the combined treatment by subcutaneously inoculated ADSC-E7’-eGFP and the protein vaccine. ( A ) Time course of the experiment. Representative bioluminescence images of mice subcutaneously injected with ( B ) 2 × 10 5 CT26 cells with indicated treatment or ( C ) 2 × 10 5 LLC1 cells with indicated treatment. Tumor volume measurements of syngeneic tumor models were conducted at indicated days after subcutaneous injection of ( D ) CT26 cells or ( E ) LLC1 cells; ** p
    Figure Legend Snippet: The tumor inhibition of the combined treatment by subcutaneously inoculated ADSC-E7’-eGFP and the protein vaccine. ( A ) Time course of the experiment. Representative bioluminescence images of mice subcutaneously injected with ( B ) 2 × 10 5 CT26 cells with indicated treatment or ( C ) 2 × 10 5 LLC1 cells with indicated treatment. Tumor volume measurements of syngeneic tumor models were conducted at indicated days after subcutaneous injection of ( D ) CT26 cells or ( E ) LLC1 cells; ** p

    Techniques Used: Inhibition, Mouse Assay, Injection

    The tumor inhibition of the combined treatment by the systemic administration of ADSC-E7’-eGFP and the protein vaccine. The GFP immunohistochemical staining of ( A ) the CT26 tumor with or without the systemic administration of ADSC-E7’-eGFP cells; or ( B ) the LLC1 tumor with or without the systemic administration of ADSC-E7’-eGFP cells. ( C ) Time course of the experiment. Two representative bioluminescence images of mice subcutaneously injected with ( D ) 2 × 10 5 CT26 cells with indicated treatment; or ( E ) 2 × 10 5 LLC1 cells with indicated treatment. Tumor volume measurements of syngeneic tumor models were conducted at indicated days after subcutaneous injection of ( F ) CT26 cells; or ( G ) LLC1 cells; * p
    Figure Legend Snippet: The tumor inhibition of the combined treatment by the systemic administration of ADSC-E7’-eGFP and the protein vaccine. The GFP immunohistochemical staining of ( A ) the CT26 tumor with or without the systemic administration of ADSC-E7’-eGFP cells; or ( B ) the LLC1 tumor with or without the systemic administration of ADSC-E7’-eGFP cells. ( C ) Time course of the experiment. Two representative bioluminescence images of mice subcutaneously injected with ( D ) 2 × 10 5 CT26 cells with indicated treatment; or ( E ) 2 × 10 5 LLC1 cells with indicated treatment. Tumor volume measurements of syngeneic tumor models were conducted at indicated days after subcutaneous injection of ( F ) CT26 cells; or ( G ) LLC1 cells; * p

    Techniques Used: Inhibition, Immunohistochemistry, Staining, Mouse Assay, Injection

    Evaluation of apoptosis in tumor tissues by TUNEL staining. Representative fluorescence images of ( A ) the CT26 tumor with different treatments; or ( B ) the LLC1 tumor with different treatments. Apoptotic-positive cells were shown in green (arrows) and the cellular nucleus was stained by DAPI and shown in blue. ( C , D ) The number of apoptotic-positive cells in the microscopic fields were calculated. The quantitative results are presented as means + standard error of means (SEM); *** indicates p
    Figure Legend Snippet: Evaluation of apoptosis in tumor tissues by TUNEL staining. Representative fluorescence images of ( A ) the CT26 tumor with different treatments; or ( B ) the LLC1 tumor with different treatments. Apoptotic-positive cells were shown in green (arrows) and the cellular nucleus was stained by DAPI and shown in blue. ( C , D ) The number of apoptotic-positive cells in the microscopic fields were calculated. The quantitative results are presented as means + standard error of means (SEM); *** indicates p

    Techniques Used: TUNEL Assay, Staining, Fluorescence

    21) Product Images from "Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector"

    Article Title: Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector

    Journal: Neuro-Oncology

    doi: 10.1093/neuonc/nor199

    Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).
    Figure Legend Snippet: Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).

    Techniques Used: In Vitro, Expressing, MTS Assay, Flow Cytometry, Cytometry

    CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.
    Figure Legend Snippet: CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.

    Techniques Used: Mouse Assay, Polymerase Chain Reaction, Plasmid Preparation

    22) Product Images from "Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector"

    Article Title: Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector

    Journal: Neuro-Oncology

    doi: 10.1093/neuonc/nor199

    Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).
    Figure Legend Snippet: Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).

    Techniques Used: In Vitro, Expressing, MTS Assay, Flow Cytometry, Cytometry

    CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.
    Figure Legend Snippet: CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.

    Techniques Used: Mouse Assay, Polymerase Chain Reaction, Plasmid Preparation

    23) Product Images from "Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector"

    Article Title: Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector

    Journal: Neuro-Oncology

    doi: 10.1093/neuonc/nor199

    Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).
    Figure Legend Snippet: Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).

    Techniques Used: In Vitro, Expressing, MTS Assay, Flow Cytometry, Cytometry

    CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.
    Figure Legend Snippet: CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.

    Techniques Used: Mouse Assay, Polymerase Chain Reaction, Plasmid Preparation

    24) Product Images from "Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector"

    Article Title: Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector

    Journal: Neuro-Oncology

    doi: 10.1093/neuonc/nor199

    Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).
    Figure Legend Snippet: Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).

    Techniques Used: In Vitro, Expressing, MTS Assay, Flow Cytometry, Cytometry

    CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.
    Figure Legend Snippet: CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.

    Techniques Used: Mouse Assay, Polymerase Chain Reaction, Plasmid Preparation

    25) Product Images from "Cherenkov luminescence imaging is a fast and relevant preclinical tool to assess tumour hypoxia in vivo"

    Article Title: Cherenkov luminescence imaging is a fast and relevant preclinical tool to assess tumour hypoxia in vivo

    Journal: EJNMMI Research

    doi: 10.1186/s13550-018-0464-7

    Imaging of hypoxia within CT26 tumour bearing mice ( n = 13), PET-MRI a – d Representative PET-MRI images showing the global co-localisation of FMISO uptake and BOLD MRI signal. Images were acquired 120 min post-injection of 10 MBq of [ 18 F]-Fluoromisonidazole (FMISO). PET. a Representative maximum-intensity-projection FMISO PET Image; b Transversal slice showing FMISO uptake within the tumour; c T2*-weighted MRI and d BOLD image derived from T2* mapping. White dashed lines: tumour limits, white arrows: oxygenated tumour area (increased BOLD signal), black circle: hypoxic tumour areas (decreased BOLD signal). CLI ( e ): Representative FMISO CLI image of the same mouse as for a to d acquired just after the PET-MRI scan. f Tumour-to-background ratio for PET, MRI and CLI following the injection of FMISO determined by the ratio of the signal from the tumour and a contralateral irrelevant region of interest (muscle); n = 13, *** p
    Figure Legend Snippet: Imaging of hypoxia within CT26 tumour bearing mice ( n = 13), PET-MRI a – d Representative PET-MRI images showing the global co-localisation of FMISO uptake and BOLD MRI signal. Images were acquired 120 min post-injection of 10 MBq of [ 18 F]-Fluoromisonidazole (FMISO). PET. a Representative maximum-intensity-projection FMISO PET Image; b Transversal slice showing FMISO uptake within the tumour; c T2*-weighted MRI and d BOLD image derived from T2* mapping. White dashed lines: tumour limits, white arrows: oxygenated tumour area (increased BOLD signal), black circle: hypoxic tumour areas (decreased BOLD signal). CLI ( e ): Representative FMISO CLI image of the same mouse as for a to d acquired just after the PET-MRI scan. f Tumour-to-background ratio for PET, MRI and CLI following the injection of FMISO determined by the ratio of the signal from the tumour and a contralateral irrelevant region of interest (muscle); n = 13, *** p

    Techniques Used: Imaging, Mouse Assay, Positron Emission Tomography, Magnetic Resonance Imaging, Injection, Derivative Assay

    26) Product Images from "Adipose triglyceride lipase activity regulates cancer cell proliferation via AMP-kinase and mTOR signaling"

    Article Title: Adipose triglyceride lipase activity regulates cancer cell proliferation via AMP-kinase and mTOR signaling

    Journal: Biochimica et Biophysica Acta. Molecular and Cell Biology of Lipids

    doi: 10.1016/j.bbalip.2020.158737

    TG catabolism and proliferation of Control/ATGL-OE cancer cells. (A, B) Proliferation of Control/ATGL-OE (A) B16 and (B) CT26 cells was analyzed with a hemocytometer at the indicated timepoints. (C) TG hydrolase activity of Control/ATGL-OE cancer cells and white adipose tissue (WAT) in the presence and absence of 50 ng/ml CGI-58 and 40 μM Atglistatin© (AI) was determined using cell/tissue lysates and a radiolabeled TG substrate. (D) TG content of Control/ATGL-OE cancer cells was determined after Folch extraction using a commercially available kit. (E) FA content of Control/ATGL-OE cancer cells was determined after Folch extraction using a commercially available kit. Data are presented as mean values of n = 3–6 ± standard deviation. Significance was determined by student's t-test (*p ≤ 0.05, **p ≤ 0.01 versus control group, # p ≤ 0.05, ## p ≤ 0.01 versus ATGL-OE group; $ p ≤ 0.05, $$ p ≤ 0.01 versus ATGL-OE + CGI-58 group).
    Figure Legend Snippet: TG catabolism and proliferation of Control/ATGL-OE cancer cells. (A, B) Proliferation of Control/ATGL-OE (A) B16 and (B) CT26 cells was analyzed with a hemocytometer at the indicated timepoints. (C) TG hydrolase activity of Control/ATGL-OE cancer cells and white adipose tissue (WAT) in the presence and absence of 50 ng/ml CGI-58 and 40 μM Atglistatin© (AI) was determined using cell/tissue lysates and a radiolabeled TG substrate. (D) TG content of Control/ATGL-OE cancer cells was determined after Folch extraction using a commercially available kit. (E) FA content of Control/ATGL-OE cancer cells was determined after Folch extraction using a commercially available kit. Data are presented as mean values of n = 3–6 ± standard deviation. Significance was determined by student's t-test (*p ≤ 0.05, **p ≤ 0.01 versus control group, # p ≤ 0.05, ## p ≤ 0.01 versus ATGL-OE group; $ p ≤ 0.05, $$ p ≤ 0.01 versus ATGL-OE + CGI-58 group).

    Techniques Used: Activity Assay, Standard Deviation

    TG catabolism and proliferation of shControl/shATGL cancer cells. (A) TG hydrolase activity of shControl/shATGL cancer cells and white adipose tissue (WAT) was determined using cell/tissue lysates and a radiolabeled TG substrate. (B) TG content of shControl/shATGL cancer cells was determined after Folch extraction using a commercially available kit. (C) FA content of shControl/shATGL cancer cells was determined after Folch extraction using a commercially available kit. (D, E) Proliferation of shControl/shATGL (D) B16 and (E) CT26 cells was analyzed using a hemocytometer at the indicated timepoints. (F) Weights of shControl/shATGL allografts 14 days after cancer cell injection. Data are presented as mean values of n = 3–6 ± standard deviation. Significance was determined by student's t-test (*p ≤ 0.05, **p ≤ 0.01).
    Figure Legend Snippet: TG catabolism and proliferation of shControl/shATGL cancer cells. (A) TG hydrolase activity of shControl/shATGL cancer cells and white adipose tissue (WAT) was determined using cell/tissue lysates and a radiolabeled TG substrate. (B) TG content of shControl/shATGL cancer cells was determined after Folch extraction using a commercially available kit. (C) FA content of shControl/shATGL cancer cells was determined after Folch extraction using a commercially available kit. (D, E) Proliferation of shControl/shATGL (D) B16 and (E) CT26 cells was analyzed using a hemocytometer at the indicated timepoints. (F) Weights of shControl/shATGL allografts 14 days after cancer cell injection. Data are presented as mean values of n = 3–6 ± standard deviation. Significance was determined by student's t-test (*p ≤ 0.05, **p ≤ 0.01).

    Techniques Used: Activity Assay, Injection, Standard Deviation

    The effect of Atglistatin on TG catabolism and proliferation of cancer cells. (A, B) Proliferation of (A) B16 and (B) CT26 cells in the presence and absence of 40 μM Atglistatin© (AI), 25 μM HSL inhibitor (HI), 20 μM MGL inhibitor (MI), or DMSO as control was determined with a hemocytometer at the indicated timepoints. (C) Tumor weights of mice injected with B16, C26, CT26, or LLC cancer cells and fed an HFD containing 200 μmol/kg Atglistatin© or a control HFD. (D) TG hydrolase activities of cancer cells treated with 40 μM Atglistatin©, 25 μM HI, or DMSO as vehicle control were determined using cell lysates and a radiolabeled TG substrate. (E) TG content of cancer cells treated with 40 μM Atglistatin© or DMSO as vehicle control was determined after Folch extraction using a commercially available kit. (F) FA content of cancer cells treated with 40 μM Atglistatin© or DMSO as vehicle control was determined after Folch extraction using a commercially available kit. Data are presented as mean values of n = 3–6 ± standard deviation. Significance was determined by student's t-test (*p ≤ 0.05, **p ≤ 0.01).
    Figure Legend Snippet: The effect of Atglistatin on TG catabolism and proliferation of cancer cells. (A, B) Proliferation of (A) B16 and (B) CT26 cells in the presence and absence of 40 μM Atglistatin© (AI), 25 μM HSL inhibitor (HI), 20 μM MGL inhibitor (MI), or DMSO as control was determined with a hemocytometer at the indicated timepoints. (C) Tumor weights of mice injected with B16, C26, CT26, or LLC cancer cells and fed an HFD containing 200 μmol/kg Atglistatin© or a control HFD. (D) TG hydrolase activities of cancer cells treated with 40 μM Atglistatin©, 25 μM HI, or DMSO as vehicle control were determined using cell lysates and a radiolabeled TG substrate. (E) TG content of cancer cells treated with 40 μM Atglistatin© or DMSO as vehicle control was determined after Folch extraction using a commercially available kit. (F) FA content of cancer cells treated with 40 μM Atglistatin© or DMSO as vehicle control was determined after Folch extraction using a commercially available kit. Data are presented as mean values of n = 3–6 ± standard deviation. Significance was determined by student's t-test (*p ≤ 0.05, **p ≤ 0.01).

    Techniques Used: Mouse Assay, Injection, Standard Deviation

    The effect of Atglistatin© on proliferation of cancer cells. (A-C) Proliferation of (A) C26, (B) HepG2, and (C) LLC cells in the presence and absence of 40 μM Atglistatin© (AI), 25 μM HSL inhibitor (HI), 20 μM MGL inhibitor (MI), or DMSO as control. (D-F) Proliferation of (D) WT/AKO B lymphoma cells, (E) shControl/shATGL B16, and (F) shControl/shATGL CT26 cells in the presence and absence of 40 μM Atglistatin©. Proliferation was determined by seeding equal amounts of cells and counting the cells using a hemocytometer at the indicated timepoints. Data are presented as mean values of n = 6 ± standard deviation. Significance was determined by student's t-test (*p ≤ 0.05, **p ≤ 0.01).
    Figure Legend Snippet: The effect of Atglistatin© on proliferation of cancer cells. (A-C) Proliferation of (A) C26, (B) HepG2, and (C) LLC cells in the presence and absence of 40 μM Atglistatin© (AI), 25 μM HSL inhibitor (HI), 20 μM MGL inhibitor (MI), or DMSO as control. (D-F) Proliferation of (D) WT/AKO B lymphoma cells, (E) shControl/shATGL B16, and (F) shControl/shATGL CT26 cells in the presence and absence of 40 μM Atglistatin©. Proliferation was determined by seeding equal amounts of cells and counting the cells using a hemocytometer at the indicated timepoints. Data are presented as mean values of n = 6 ± standard deviation. Significance was determined by student's t-test (*p ≤ 0.05, **p ≤ 0.01).

    Techniques Used: Standard Deviation

    27) Product Images from "Inhibition of hypoxia-inducible factors limits tumor progression in a mouse model of colorectal cancer"

    Article Title: Inhibition of hypoxia-inducible factors limits tumor progression in a mouse model of colorectal cancer

    Journal: Carcinogenesis

    doi: 10.1093/carcin/bgu004

    Effects of ACF on colorectal cell lines are HIF dependent. ( A ) Cytoplasmic/nuclear fractionation of CT26 and CMT93 lysates under normoxia (21% O 2 ) and hypoxia (0.5% O 2 ) with or without ACF treatment and immunoblotting for HIF-1α, NF-κB
    Figure Legend Snippet: Effects of ACF on colorectal cell lines are HIF dependent. ( A ) Cytoplasmic/nuclear fractionation of CT26 and CMT93 lysates under normoxia (21% O 2 ) and hypoxia (0.5% O 2 ) with or without ACF treatment and immunoblotting for HIF-1α, NF-κB

    Techniques Used: Fractionation

    28) Product Images from "A novel function of API5 (apoptosis inhibitor 5), TLR4-dependent activation of antigen presenting cells"

    Article Title: A novel function of API5 (apoptosis inhibitor 5), TLR4-dependent activation of antigen presenting cells

    Journal: Oncoimmunology

    doi: 10.1080/2162402X.2018.1472187

    Long-term antigen-specific CD8 ± T cell memory and tumor protective effect produced by API5 treated DC vaccination. Mice (5 mice per group) were vaccinated with PBS or API5 treated mature DC loaded OVA (A), E7 (C) or AH1-A5 twice at one week intervals. (E). Seven weeks after second vaccination, mice were challenged with or without EG.7, TC-1 or CT26 tumor cells, respectively. One week after tumor challenge, splenocytes of mice were collected and assessed for the abundance of antigen specific CD8+ T cells by flow cytometry. The tumor free survival of EG.7 (B), TC-1 (D) or CT26 (F) tumor challenged mice cells were followed for up to 30 days after tumor challenge. Data are presented as mean ± SD (* = p
    Figure Legend Snippet: Long-term antigen-specific CD8 ± T cell memory and tumor protective effect produced by API5 treated DC vaccination. Mice (5 mice per group) were vaccinated with PBS or API5 treated mature DC loaded OVA (A), E7 (C) or AH1-A5 twice at one week intervals. (E). Seven weeks after second vaccination, mice were challenged with or without EG.7, TC-1 or CT26 tumor cells, respectively. One week after tumor challenge, splenocytes of mice were collected and assessed for the abundance of antigen specific CD8+ T cells by flow cytometry. The tumor free survival of EG.7 (B), TC-1 (D) or CT26 (F) tumor challenged mice cells were followed for up to 30 days after tumor challenge. Data are presented as mean ± SD (* = p

    Techniques Used: Produced, Mouse Assay, Flow Cytometry, Cytometry

    API5-mediated DC vaccination produces antigen-specific CD8 ± T cells and prevents tumor formation. Wild type C57BL/6 mice (5 mice per group) were immunized with 1) PBS, 2) immature DC, 3) immature DC loaded with antigen peptide, 4) API5 treated mature DC, 5) API5 treated mature DC loaded with antigen peptide, and 6) LPS treated mature DC loaded with antigen peptide, twice at one week intervals. One week following respective vaccination, the abundance of OVA (A), E7 (C) or AH1-A5 (E) specific CD8+ and IFN-γ+ T cells in splenocytes of mice were measured using flow cytometry. Kaplan-Meier survival analysis of mice(5 mice per group) challenged with TC-1 (B), EG.7 (D) or CT26 (F) tumor cells, at one week after the second DC vaccination. Data are presented as mean ± SD (* = p
    Figure Legend Snippet: API5-mediated DC vaccination produces antigen-specific CD8 ± T cells and prevents tumor formation. Wild type C57BL/6 mice (5 mice per group) were immunized with 1) PBS, 2) immature DC, 3) immature DC loaded with antigen peptide, 4) API5 treated mature DC, 5) API5 treated mature DC loaded with antigen peptide, and 6) LPS treated mature DC loaded with antigen peptide, twice at one week intervals. One week following respective vaccination, the abundance of OVA (A), E7 (C) or AH1-A5 (E) specific CD8+ and IFN-γ+ T cells in splenocytes of mice were measured using flow cytometry. Kaplan-Meier survival analysis of mice(5 mice per group) challenged with TC-1 (B), EG.7 (D) or CT26 (F) tumor cells, at one week after the second DC vaccination. Data are presented as mean ± SD (* = p

    Techniques Used: Mouse Assay, Flow Cytometry, Cytometry

    API5-treated DC vaccination reduces tumor growth and prolongs survival. Mice (5 mice per group) were challenged with EG.7 (A), TC-1 (C) or CT26 (E) tumor cells. Three and ten days after tumor challenge, mice were treated with 1) PBS, 2) immature DC, 3) immature DC loaded with antigen peptide, 4) API5 treated mature DC, 5) API5 treated mature DC loaded with antigen peptide, and 6) LPS treated mature DC loaded with antigen peptide, in the footpad twice at one week intervals. Tumor volume was measured using digital caliper. (B, D, F) Mice survival were assessed using Kaplan-Meier analysis. Data are presented as mean ± SD (* = p ≤ 0.05, ** = p ≤ 0.01).
    Figure Legend Snippet: API5-treated DC vaccination reduces tumor growth and prolongs survival. Mice (5 mice per group) were challenged with EG.7 (A), TC-1 (C) or CT26 (E) tumor cells. Three and ten days after tumor challenge, mice were treated with 1) PBS, 2) immature DC, 3) immature DC loaded with antigen peptide, 4) API5 treated mature DC, 5) API5 treated mature DC loaded with antigen peptide, and 6) LPS treated mature DC loaded with antigen peptide, in the footpad twice at one week intervals. Tumor volume was measured using digital caliper. (B, D, F) Mice survival were assessed using Kaplan-Meier analysis. Data are presented as mean ± SD (* = p ≤ 0.05, ** = p ≤ 0.01).

    Techniques Used: Mouse Assay

    29) Product Images from "SiRNA-Mediated Reduction of ?-Actinin-1 Inhibits Pressure-Induced Murine Tumor Cell Wound Implantation and Enhances Tumor-Free Survival 1"

    Article Title: SiRNA-Mediated Reduction of ?-Actinin-1 Inhibits Pressure-Induced Murine Tumor Cell Wound Implantation and Enhances Tumor-Free Survival 1

    Journal:

    doi:

    Effect of α-actinin-1 reduction on pressure-mediated CT26 tumor cell wound implantation. The 15 mm Hg-increased pressure (closed bars) stimulates the adhesion of siNT-transfected, 51 Cr-labeled CT26 cells to murine surgical wounds compared with
    Figure Legend Snippet: Effect of α-actinin-1 reduction on pressure-mediated CT26 tumor cell wound implantation. The 15 mm Hg-increased pressure (closed bars) stimulates the adhesion of siNT-transfected, 51 Cr-labeled CT26 cells to murine surgical wounds compared with

    Techniques Used: Transfection, Labeling

    Effect of siRNA-mediated reduction of α-actinin-1 on pressure-stimulated murine colon cancer cell adhesion to collagen I. (A) Typical reduction of α-actinin-1 protein in CT26 cells transfected with siRNA targeted to α-actinin-1
    Figure Legend Snippet: Effect of siRNA-mediated reduction of α-actinin-1 on pressure-stimulated murine colon cancer cell adhesion to collagen I. (A) Typical reduction of α-actinin-1 protein in CT26 cells transfected with siRNA targeted to α-actinin-1

    Techniques Used: Transfection

    Effect of preoperative siRNA-mediated α-actinin-1 silencing on murine tumor development and survival after exposure to increased pressure. Exposure of CT26 cells to elevated pressure increases the rate of surgical wound implantation, whereas preoperative
    Figure Legend Snippet: Effect of preoperative siRNA-mediated α-actinin-1 silencing on murine tumor development and survival after exposure to increased pressure. Exposure of CT26 cells to elevated pressure increases the rate of surgical wound implantation, whereas preoperative

    Techniques Used:

    Effect of increased pressure and α-actinin-1 reduction on CT26 cell proliferation. CT26 cells were transfected with either siACTN1 or siNT and, after 48 hours, were exposed to either 15 mm Hg-increased pressure or ambient pressure conditions.
    Figure Legend Snippet: Effect of increased pressure and α-actinin-1 reduction on CT26 cell proliferation. CT26 cells were transfected with either siACTN1 or siNT and, after 48 hours, were exposed to either 15 mm Hg-increased pressure or ambient pressure conditions.

    Techniques Used: Transfection

    30) Product Images from "Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector"

    Article Title: Brain tumor eradication and prolonged survival from intratumoral conversion of 5-fluorocytosine to 5-fluorouracil using a nonlytic retroviral replicating vector

    Journal: Neuro-Oncology

    doi: 10.1093/neuonc/nor199

    Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).
    Figure Legend Snippet: Comparison of CT26 and Tu-2449 in vitro susceptibility to Toca 511 (511) or MLV expressing GFP (MLV-GFP) vectors. Sensitivity to 5-FC was determined by measuring cell viability (MTS assay) over time in the absence or presence of titrating amounts of 5-FC (A). IC 50 values were calculated for CT26 and Tu-2449 cell lines at 4.2 μM (0.5 μg/mL) and 1.5 μM (0.19 μg/mL), respectively. Flow cytometry analysis was done to measure GFP positive cells transduced by MLV-GFP at an MOI of 1.0 or 0.1 (B).

    Techniques Used: In Vitro, Expressing, MTS Assay, Flow Cytometry, Cytometry

    CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.
    Figure Legend Snippet: CT26 in BALB/c brain metastasis tumor model survival analysis. Groups of 10 female BALB/c mice (9 weeks of age) were implanted IC with 1E4 CT26 tumor cells then dosed IC with vehicle (Control) or IC with Toca 511 at 3 dose levels expressed as transducing units per gram of brain (TU/g) ranging from a dose level of E4 to a dose level of E6 TU/g. Following 9 days, to allow spread of Toca 511, mice were treated IP BID for 7 consecutive days with either PBS or 5-FC (500 mg/kg) as indicated. The cycle of 7 days on drug followed by 10 days off drug was repeated until the conclusion of the study. Survival analysis up to day 95 was performed. DNA and RNA PCR analysis to detect integrated vector in various tissues and viral particles in sera were performed on the mice terminated at day 95.

    Techniques Used: Mouse Assay, Polymerase Chain Reaction, Plasmid Preparation

    31) Product Images from "Targeting hepatitis B virus antigens to dendritic cells by heat shock protein to improve DNA vaccine potency"

    Article Title: Targeting hepatitis B virus antigens to dendritic cells by heat shock protein to improve DNA vaccine potency

    Journal: World Journal of Gastroenterology : WJG

    doi: 10.3748/wjg.v13.i44.5911

    A: Tumor incidence after CT26-HBeAg challenge of Balb/c mice; B: Tumor growth after CT26-HBeAg challenge of Balb/c mice.
    Figure Legend Snippet: A: Tumor incidence after CT26-HBeAg challenge of Balb/c mice; B: Tumor growth after CT26-HBeAg challenge of Balb/c mice.

    Techniques Used: Mouse Assay

    32) Product Images from "Subcellular Singlet Oxygen and Cell Death: Location Matters"

    Article Title: Subcellular Singlet Oxygen and Cell Death: Location Matters

    Journal: Frontiers in Chemistry

    doi: 10.3389/fchem.2020.592941

    HEK cell and CT26 cells with mitochondrially localized FAP show dramatically different sensitivity to singlet oxygen generation. (A) Populations of cells with initially similar FAP expression (MG-ester-FAP signal) were collected within the indicated gate region to narrow the fluorescence distribution, with the population falling in the gate shown as a fluorescence histogram in green on the right, with the associated population medians. (B) The phototoxic dose–response curves of collected cells reveal that CT26 cells are remarkably resistant to mitochondrially generated singlet oxygen compared to the HEK cells with similar expression levels.
    Figure Legend Snippet: HEK cell and CT26 cells with mitochondrially localized FAP show dramatically different sensitivity to singlet oxygen generation. (A) Populations of cells with initially similar FAP expression (MG-ester-FAP signal) were collected within the indicated gate region to narrow the fluorescence distribution, with the population falling in the gate shown as a fluorescence histogram in green on the right, with the associated population medians. (B) The phototoxic dose–response curves of collected cells reveal that CT26 cells are remarkably resistant to mitochondrially generated singlet oxygen compared to the HEK cells with similar expression levels.

    Techniques Used: Expressing, Fluorescence, Generated

    33) Product Images from "Bacteriolytic therapy can generate a potent immune response against experimental tumors"

    Article Title: Bacteriolytic therapy can generate a potent immune response against experimental tumors

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi: 10.1073/pnas.0406242101

    Photographs of mice used for challenge experiments. A mouse surgically cured of a CT26 tumor was not resistant to a challenge of CT26 cells in the opposite flank ( a ), whereas a mouse cured with C. novyi-NT was resistant ( b ). ( c ) CT26 tumors and RENCA
    Figure Legend Snippet: Photographs of mice used for challenge experiments. A mouse surgically cured of a CT26 tumor was not resistant to a challenge of CT26 cells in the opposite flank ( a ), whereas a mouse cured with C. novyi-NT was resistant ( b ). ( c ) CT26 tumors and RENCA

    Techniques Used: Mouse Assay

    34) Product Images from "Antigen-specific oncolytic MV-based tumor vaccines through presentation of selected tumor-associated antigens on infected cells or virus-like particles"

    Article Title: Antigen-specific oncolytic MV-based tumor vaccines through presentation of selected tumor-associated antigens on infected cells or virus-like particles

    Journal: Scientific Reports

    doi: 10.1038/s41598-017-16928-8

    Antigen-specific cellular and humoral immunity induced by CLDN6-presenting MV. ( a ) Schematic depiction of immunization experiments. ( b ) IFN-γ ELISpot analysis using splenocytes of vaccinated mice with indicated viruses expressing CLDN6 or MLV-gag. Viruses expressing VLPs, but no antigen (MV vac2 -gag) served as negative controls. Splenocytes isolated 21 days after boost immunization and analyzed for IFN-γ-production after incubation with ConA, viral antigen (MV bulk), specific or unspecific peptides (CLDN6 or ISQ, respectively), or without stimulation (mock). ( c ) Virus neutralizing titers (VNT) of with indicated viruses vaccinated animals’ sera were analyzed for neutralization of MV. LLOD = VNT 20. ( d ) Flow cytometry histograms of CLDN6-expressing CT26 cells stained with sera of representative mice vaccinated with indicated viruses before (solid black line), after prime (solid grey line), or after booster (filled grey area) vaccination. Staining with anti-CLDN6 mAb served as positive control ( e ) Analysis of CLDN6-specific antibody concentration in serum samples of vaccinated mice determined by FACS as shown in panel D according to MFI of stained cell populations. Dots represent single animals (n = 5–6); horizontal line represents mean per group. Statistical differences between groups were assessed by Mann-Whitney test ( b ) or two-way ANOVA ( d ); *P
    Figure Legend Snippet: Antigen-specific cellular and humoral immunity induced by CLDN6-presenting MV. ( a ) Schematic depiction of immunization experiments. ( b ) IFN-γ ELISpot analysis using splenocytes of vaccinated mice with indicated viruses expressing CLDN6 or MLV-gag. Viruses expressing VLPs, but no antigen (MV vac2 -gag) served as negative controls. Splenocytes isolated 21 days after boost immunization and analyzed for IFN-γ-production after incubation with ConA, viral antigen (MV bulk), specific or unspecific peptides (CLDN6 or ISQ, respectively), or without stimulation (mock). ( c ) Virus neutralizing titers (VNT) of with indicated viruses vaccinated animals’ sera were analyzed for neutralization of MV. LLOD = VNT 20. ( d ) Flow cytometry histograms of CLDN6-expressing CT26 cells stained with sera of representative mice vaccinated with indicated viruses before (solid black line), after prime (solid grey line), or after booster (filled grey area) vaccination. Staining with anti-CLDN6 mAb served as positive control ( e ) Analysis of CLDN6-specific antibody concentration in serum samples of vaccinated mice determined by FACS as shown in panel D according to MFI of stained cell populations. Dots represent single animals (n = 5–6); horizontal line represents mean per group. Statistical differences between groups were assessed by Mann-Whitney test ( b ) or two-way ANOVA ( d ); *P

    Techniques Used: Enzyme-linked Immunospot, Mouse Assay, Expressing, Isolation, Incubation, Neutralization, Flow Cytometry, Cytometry, Staining, Positive Control, Concentration Assay, FACS, MANN-WHITNEY

    35) Product Images from "Cherenkov luminescence imaging is a fast and relevant preclinical tool to assess tumour hypoxia in vivo"

    Article Title: Cherenkov luminescence imaging is a fast and relevant preclinical tool to assess tumour hypoxia in vivo

    Journal: EJNMMI Research

    doi: 10.1186/s13550-018-0464-7

    Imaging of hypoxia within CT26 tumour bearing mice ( n = 13), PET-MRI a – d Representative PET-MRI images showing the global co-localisation of FMISO uptake and BOLD MRI signal. Images were acquired 120 min post-injection of 10 MBq of [ 18 F]-Fluoromisonidazole (FMISO). PET. a Representative maximum-intensity-projection FMISO PET Image; b Transversal slice showing FMISO uptake within the tumour; c T2*-weighted MRI and d BOLD image derived from T2* mapping. White dashed lines: tumour limits, white arrows: oxygenated tumour area (increased BOLD signal), black circle: hypoxic tumour areas (decreased BOLD signal). CLI ( e ): Representative FMISO CLI image of the same mouse as for a to d acquired just after the PET-MRI scan. f Tumour-to-background ratio for PET, MRI and CLI following the injection of FMISO determined by the ratio of the signal from the tumour and a contralateral irrelevant region of interest (muscle); n = 13, *** p
    Figure Legend Snippet: Imaging of hypoxia within CT26 tumour bearing mice ( n = 13), PET-MRI a – d Representative PET-MRI images showing the global co-localisation of FMISO uptake and BOLD MRI signal. Images were acquired 120 min post-injection of 10 MBq of [ 18 F]-Fluoromisonidazole (FMISO). PET. a Representative maximum-intensity-projection FMISO PET Image; b Transversal slice showing FMISO uptake within the tumour; c T2*-weighted MRI and d BOLD image derived from T2* mapping. White dashed lines: tumour limits, white arrows: oxygenated tumour area (increased BOLD signal), black circle: hypoxic tumour areas (decreased BOLD signal). CLI ( e ): Representative FMISO CLI image of the same mouse as for a to d acquired just after the PET-MRI scan. f Tumour-to-background ratio for PET, MRI and CLI following the injection of FMISO determined by the ratio of the signal from the tumour and a contralateral irrelevant region of interest (muscle); n = 13, *** p

    Techniques Used: Imaging, Mouse Assay, Positron Emission Tomography, Magnetic Resonance Imaging, Injection, Derivative Assay

    36) Product Images from "Characterization of an engineered human purine nucleoside phosphorylase fused to an anti-her2/neu single chain Fv for use in ADEPT"

    Article Title: Characterization of an engineered human purine nucleoside phosphorylase fused to an anti-her2/neu single chain Fv for use in ADEPT

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    doi: 10.1186/1756-9966-28-147

    Enzymatic activity of hDM-αH-C6.5 MH3B1 . (A) , Lineweaver-Burk plot of enzyme activity of hDM-αH-C6.5 MH3B1 with F-dAdo as substrate. Conversion of F-dAdo to F-Ade was followed spectrophotometrically in real time by the increase in absorbance at 280 nm. Concentration of F-dAdo is in μM and v is based on mili-units of absorbance/min. (B) , Proliferation of CT26 and CT26HER2/ neu cells and (C) , MCF-7HER2 cells in the presence or absence of F-dAdo or hDM-αH-C6.5 MH3B1 was determined in 72 hours by MTS. (D) , 0.2 μM of hPNP-αH-C6.5 MH3B1 was incubated with CT26HER2/ neu or MCF-7 cells in the presence of 1.5 or 6 μM of F-dAdo respectively for 72 hours and cellular proliferation determined by MTS assay. Error bars for each graph represent standard deviation within each set of values.
    Figure Legend Snippet: Enzymatic activity of hDM-αH-C6.5 MH3B1 . (A) , Lineweaver-Burk plot of enzyme activity of hDM-αH-C6.5 MH3B1 with F-dAdo as substrate. Conversion of F-dAdo to F-Ade was followed spectrophotometrically in real time by the increase in absorbance at 280 nm. Concentration of F-dAdo is in μM and v is based on mili-units of absorbance/min. (B) , Proliferation of CT26 and CT26HER2/ neu cells and (C) , MCF-7HER2 cells in the presence or absence of F-dAdo or hDM-αH-C6.5 MH3B1 was determined in 72 hours by MTS. (D) , 0.2 μM of hPNP-αH-C6.5 MH3B1 was incubated with CT26HER2/ neu or MCF-7 cells in the presence of 1.5 or 6 μM of F-dAdo respectively for 72 hours and cellular proliferation determined by MTS assay. Error bars for each graph represent standard deviation within each set of values.

    Techniques Used: Activity Assay, Concentration Assay, Incubation, MTS Assay, Standard Deviation

    hDM-αH-C6.5 MH3B1 specifically associates with HER2/ neu expressing cells and causes cytotoxicty in the presence of F-dAdo irrespective of expression of tumor antigen or cell growth rate . (A) , hDM-αH-C6.5 MH3B1 associates with HER2/ neu expressing cells resulting in concentration dependent cytotoxicity upon addition of 1.5 or 6 μM F-dAdo to CT26HER2/ neu or MCF-7HER2 cells respectively. Different concentrations of hDM-αH-C6.5 MH3B1 were incubated with cells, unbound enzyme washed away, F-dAdo added and 72 hours later cellular proliferation was determined by MTS assay. (B) , CT26HER2/ neu and CT26 cells were seeded at different ratios and grown overnight. hDM-αH-C6.5 MH3B1 was incubated with cells for 45 minutes, and washed away. Cells were then grown in the presence of 1.5 μM F-dAdo for 72 hours and cell proliferation determined by MTS assay. (C) , MCF-7HER2 cells were grown overnight (O/N) in the presence of 10% serum, washed and growth continued for 72 hours in the presence of varying amounts of serum. The column labeled overnight (O/N) represents the number of cells prior to switching to different amounts of serum. The number of cells was determined by visually counting the cells. (D) , Viability of MCF-7HER2 cells in the presence of different amounts of fetal bovine serum and 1.5 μM F-Ade was determined after 72 hours of incubation by MTS assay. Error bars for each graph represent standard deviation within each set of values.
    Figure Legend Snippet: hDM-αH-C6.5 MH3B1 specifically associates with HER2/ neu expressing cells and causes cytotoxicty in the presence of F-dAdo irrespective of expression of tumor antigen or cell growth rate . (A) , hDM-αH-C6.5 MH3B1 associates with HER2/ neu expressing cells resulting in concentration dependent cytotoxicity upon addition of 1.5 or 6 μM F-dAdo to CT26HER2/ neu or MCF-7HER2 cells respectively. Different concentrations of hDM-αH-C6.5 MH3B1 were incubated with cells, unbound enzyme washed away, F-dAdo added and 72 hours later cellular proliferation was determined by MTS assay. (B) , CT26HER2/ neu and CT26 cells were seeded at different ratios and grown overnight. hDM-αH-C6.5 MH3B1 was incubated with cells for 45 minutes, and washed away. Cells were then grown in the presence of 1.5 μM F-dAdo for 72 hours and cell proliferation determined by MTS assay. (C) , MCF-7HER2 cells were grown overnight (O/N) in the presence of 10% serum, washed and growth continued for 72 hours in the presence of varying amounts of serum. The column labeled overnight (O/N) represents the number of cells prior to switching to different amounts of serum. The number of cells was determined by visually counting the cells. (D) , Viability of MCF-7HER2 cells in the presence of different amounts of fetal bovine serum and 1.5 μM F-Ade was determined after 72 hours of incubation by MTS assay. Error bars for each graph represent standard deviation within each set of values.

    Techniques Used: Expressing, Concentration Assay, Incubation, MTS Assay, Labeling, Standard Deviation

    37) Product Images from "Nanoscale metal-organic frameworks for mitochondria-targeted radiotherapy-radiodynamic therapy"

    Article Title: Nanoscale metal-organic frameworks for mitochondria-targeted radiotherapy-radiodynamic therapy

    Journal: Nature Communications

    doi: 10.1038/s41467-018-06655-7

    In vivo anti-cancer efficacy of mitochondria-targeted RDT. a Tumor growth inhibition/regression curves in MC38 tumor-bearing mice treated with PBS, Hf-DBA, DBB-Ru, or Hf-DBB-Ru by intratumoral (i.t.) injection with (+) or without (−) X-ray irradiation or Hf-DBB-Ru by intravenous (i.v.) injection followed by X-ray irradiation. n = 6. b Excised tumor weights on day 22. n = 6. c Tumor growth inhibition/regression curves in CT26 tumor-bearing mice treated with PBS with (+) or without (−) X-ray irradiation or i.v. injected with Hf-DBB-Ru followed by X-ray irradiation. Black arrows refer to i.v. injection of different treatments and red arrows refer to X-ray irradiation. Excised tumor weights on day 21 shown in the inset. n = 6. ** P
    Figure Legend Snippet: In vivo anti-cancer efficacy of mitochondria-targeted RDT. a Tumor growth inhibition/regression curves in MC38 tumor-bearing mice treated with PBS, Hf-DBA, DBB-Ru, or Hf-DBB-Ru by intratumoral (i.t.) injection with (+) or without (−) X-ray irradiation or Hf-DBB-Ru by intravenous (i.v.) injection followed by X-ray irradiation. n = 6. b Excised tumor weights on day 22. n = 6. c Tumor growth inhibition/regression curves in CT26 tumor-bearing mice treated with PBS with (+) or without (−) X-ray irradiation or i.v. injected with Hf-DBB-Ru followed by X-ray irradiation. Black arrows refer to i.v. injection of different treatments and red arrows refer to X-ray irradiation. Excised tumor weights on day 21 shown in the inset. n = 6. ** P

    Techniques Used: In Vivo, Inhibition, Mouse Assay, Injection, Irradiation

    38) Product Images from "Local angiotensin II contributes to tumor resistance to checkpoint immunotherapy"

    Article Title: Local angiotensin II contributes to tumor resistance to checkpoint immunotherapy

    Journal: Journal for Immunotherapy of Cancer

    doi: 10.1186/s40425-018-0401-3

    Local AngII in tumor microenvironment is involved in immune escape of tumor cells. a The influence of AngII-receptor blockers on 4T1 tumor growth in syngeneic BALB/c mice; candesartan (cand, 5mg/kg, i.p.; starting at day 5 after cell injection, daily ) for AT1R and PD123319 (5mg/kg, i.p.; starting from day 5 after cell injection, every other day) for AT2R, n =5. b The influence of AngII-receptor blockers on 4T1 cells proliferation in vitro as detected by MTT assay; candesartan (10μm/well) and PD123319 (10μm/well). c The influence of Ang II-receptor blockers on 4T1 tumor growth in T-cell immunodeficient BALB/c nude mice, n =5. d The expression of AGT, a precursor of AngII, was silenced in 4T1 cells and CT26 cells by shRNA. Hypoxia remarkably induced generation of Ang II in 4T1 and CT26 cells as detected by ELISA. AGT-silencing greatly decreased Ang II levels, especially under hypoxic condition. Data are presented as mean±SEM, n =3. e AGT silencing did not influence cell-proliferation of 4T1 cells in vitro as detected by MTT assay. f AGT silencing obviously inhibited tumor growth of 4T1cells in BALB/c mice comparing to negative control, and the depletion of CD8 + T cells in mice by in vivo administration of monoclonal antibody against CD8 greatly attenuated this effect ( n =6). Ns, no significance; *, P
    Figure Legend Snippet: Local AngII in tumor microenvironment is involved in immune escape of tumor cells. a The influence of AngII-receptor blockers on 4T1 tumor growth in syngeneic BALB/c mice; candesartan (cand, 5mg/kg, i.p.; starting at day 5 after cell injection, daily ) for AT1R and PD123319 (5mg/kg, i.p.; starting from day 5 after cell injection, every other day) for AT2R, n =5. b The influence of AngII-receptor blockers on 4T1 cells proliferation in vitro as detected by MTT assay; candesartan (10μm/well) and PD123319 (10μm/well). c The influence of Ang II-receptor blockers on 4T1 tumor growth in T-cell immunodeficient BALB/c nude mice, n =5. d The expression of AGT, a precursor of AngII, was silenced in 4T1 cells and CT26 cells by shRNA. Hypoxia remarkably induced generation of Ang II in 4T1 and CT26 cells as detected by ELISA. AGT-silencing greatly decreased Ang II levels, especially under hypoxic condition. Data are presented as mean±SEM, n =3. e AGT silencing did not influence cell-proliferation of 4T1 cells in vitro as detected by MTT assay. f AGT silencing obviously inhibited tumor growth of 4T1cells in BALB/c mice comparing to negative control, and the depletion of CD8 + T cells in mice by in vivo administration of monoclonal antibody against CD8 greatly attenuated this effect ( n =6). Ns, no significance; *, P

    Techniques Used: Mouse Assay, Injection, In Vitro, MTT Assay, Expressing, shRNA, Enzyme-linked Immunosorbent Assay, Negative Control, In Vivo

    39) Product Images from "Apoptosis of tumor infiltrating effector TIM-3+CD8+ T cells in colon cancer"

    Article Title: Apoptosis of tumor infiltrating effector TIM-3+CD8+ T cells in colon cancer

    Journal: Scientific Reports

    doi: 10.1038/srep15659

    Tumor infiltrating CD8+ T cells are functionally active and inhibit tumor growth in mouse CT26 colon tumor model. CT-26 tumor cells were inoculated in BALB/c mice and tumor-infiltrating CD8+ T cells were sorted on day 28- post tumor inoculation. ( a ) Tumor-infiltrating CD8+ T cells secrete IFN-γ following culture with irradiated CT-26 tumor cells. Splenic CD8+ T cells from the tumor-bearing mice secrete minimum IFN-γ. ( b ) Both tumor-infiltrating and splenic CD8+ T cells of tumor-bearing mice execute cytolysis activity on CT26 tumor cells in vitro . The effect is higher by tumor-infiltrating compared to splenic CD8+ T cells. Splenic CD8+ T cells from naïve non tumor-bearing mice execute minimum cytolysis, served as control. ( c ) Upon adoptive transfer in another tumor-bearing mice, the tumor-infiltrating CD8+ T cells inhibit tumor growth. Transfer of naïve CD8+ T cells from spleens of non tumor-bearing naïve mice served as control. Data are mean ± SD of at least 3 similar experiments.
    Figure Legend Snippet: Tumor infiltrating CD8+ T cells are functionally active and inhibit tumor growth in mouse CT26 colon tumor model. CT-26 tumor cells were inoculated in BALB/c mice and tumor-infiltrating CD8+ T cells were sorted on day 28- post tumor inoculation. ( a ) Tumor-infiltrating CD8+ T cells secrete IFN-γ following culture with irradiated CT-26 tumor cells. Splenic CD8+ T cells from the tumor-bearing mice secrete minimum IFN-γ. ( b ) Both tumor-infiltrating and splenic CD8+ T cells of tumor-bearing mice execute cytolysis activity on CT26 tumor cells in vitro . The effect is higher by tumor-infiltrating compared to splenic CD8+ T cells. Splenic CD8+ T cells from naïve non tumor-bearing mice execute minimum cytolysis, served as control. ( c ) Upon adoptive transfer in another tumor-bearing mice, the tumor-infiltrating CD8+ T cells inhibit tumor growth. Transfer of naïve CD8+ T cells from spleens of non tumor-bearing naïve mice served as control. Data are mean ± SD of at least 3 similar experiments.

    Techniques Used: Mouse Assay, Irradiation, Activity Assay, In Vitro, Adoptive Transfer Assay

    TIM-3 and PD-1 expression with T-bet and Eomes co-induction of tumor infiltrating CD8+ T cells in mouse CT26 colon tumor model. CT-26 tumor cells were inoculated subcutaneously in BALB/c mice and were allowed to form solid tumor. Mice were sacrificed on day 28- post tumor inoculation. Splenocytes from naïve non tumor-bearing mice served as controls. ( a ) Majority of tumor-infiltrating CD8+ T cells express TIM-3. CD3+ cells were analyzed for CD8 and TIM-3 expression. ( b ) Majority of tumor-infiltrating TIM-3+ CD8+ T cells co-expresses PD-1. ( c ) Majority of tumor-infiltrating CD8+ T cells are with co-induced of T-bet and Eomes. Data are mean ± SD of at least 3 similar experiments (n = 6; *** = p
    Figure Legend Snippet: TIM-3 and PD-1 expression with T-bet and Eomes co-induction of tumor infiltrating CD8+ T cells in mouse CT26 colon tumor model. CT-26 tumor cells were inoculated subcutaneously in BALB/c mice and were allowed to form solid tumor. Mice were sacrificed on day 28- post tumor inoculation. Splenocytes from naïve non tumor-bearing mice served as controls. ( a ) Majority of tumor-infiltrating CD8+ T cells express TIM-3. CD3+ cells were analyzed for CD8 and TIM-3 expression. ( b ) Majority of tumor-infiltrating TIM-3+ CD8+ T cells co-expresses PD-1. ( c ) Majority of tumor-infiltrating CD8+ T cells are with co-induced of T-bet and Eomes. Data are mean ± SD of at least 3 similar experiments (n = 6; *** = p

    Techniques Used: Expressing, Mouse Assay

    Tumor-derived galectin-9 acts on TIM-3 and induces apoptosis of TIM-3+ tumor-infiltrating CD8+ T cells in CT26 mouse colon tumor model. CT-26 tumor cells were inoculated in BALB/c mice and were allowed to form solid tumor. ( a ) The frequency of tumor-infiltrating CD8+ T cells decreases with tumor progression, as revealed by the comparison of CD8+ or CD4+ T cell percentages in all cells of the single-cell suspension of tumors on the stated days post tumor inoculation. ( b ) Higher apoptosis of tumor-infiltrating compared to splenic CD8+ T cells of tumor-bearing mice on day 28- post tumor inoculation. Splenic CD8+ T cells from naïve mice served as control. ( c ) Higher TIM-3 expression in apoptotic compared to non-apoptotic population of tumor-infiltrating CD8+ T cells on day 28- post tumor inoculation. ( d ) Decreased apoptosis of tumor-infiltrating CD8+ T cells, including the TIM-3+ CD8+ T cells, following in vitro culture with Anti- TIM-3 antibody. ( e ) CT26 tumor cells secrete galectin-9, as measured in tumor tissues on the stated days post tumor inoculation. ( f ) Recombinant galectin-9 increases and anti- TIM-3 antibody decreases apoptosis of tumor-infiltrating CD8+ T cells following in vitro culture. ( g ) Anti- TIM-3 antibody treatment i nhibits tumor growth in mice. The treatment increases tumor-infiltrating CD8+ T cell frequency, which is associated with decreased apoptosis of TIM-3+ CD8+ T cells on day 21- post tumor inoculation. Data are mean ± SD of at least 3 similar experiments (n = 6; *** = p
    Figure Legend Snippet: Tumor-derived galectin-9 acts on TIM-3 and induces apoptosis of TIM-3+ tumor-infiltrating CD8+ T cells in CT26 mouse colon tumor model. CT-26 tumor cells were inoculated in BALB/c mice and were allowed to form solid tumor. ( a ) The frequency of tumor-infiltrating CD8+ T cells decreases with tumor progression, as revealed by the comparison of CD8+ or CD4+ T cell percentages in all cells of the single-cell suspension of tumors on the stated days post tumor inoculation. ( b ) Higher apoptosis of tumor-infiltrating compared to splenic CD8+ T cells of tumor-bearing mice on day 28- post tumor inoculation. Splenic CD8+ T cells from naïve mice served as control. ( c ) Higher TIM-3 expression in apoptotic compared to non-apoptotic population of tumor-infiltrating CD8+ T cells on day 28- post tumor inoculation. ( d ) Decreased apoptosis of tumor-infiltrating CD8+ T cells, including the TIM-3+ CD8+ T cells, following in vitro culture with Anti- TIM-3 antibody. ( e ) CT26 tumor cells secrete galectin-9, as measured in tumor tissues on the stated days post tumor inoculation. ( f ) Recombinant galectin-9 increases and anti- TIM-3 antibody decreases apoptosis of tumor-infiltrating CD8+ T cells following in vitro culture. ( g ) Anti- TIM-3 antibody treatment i nhibits tumor growth in mice. The treatment increases tumor-infiltrating CD8+ T cell frequency, which is associated with decreased apoptosis of TIM-3+ CD8+ T cells on day 21- post tumor inoculation. Data are mean ± SD of at least 3 similar experiments (n = 6; *** = p

    Techniques Used: Derivative Assay, Mouse Assay, Expressing, In Vitro, Recombinant

    More effector cytokine secretion by TIM-3+ compared to TIM-3- population of tumor infiltrating CD8+ T cells in mouse CT26 colon tumor model. CT26 tumor cells were inoculated in BALB/c mice and were allowed to form solid tumor. The TIM-3+ population of tumor-infiltrating CD8+ T cells produces higher level of IFN-γ, TNF-α and IL-2 compared to that by the TIM-3- population on day 28- post tumor inoculation. Dot-plots demonstrate cytokine frequencies of TIM-3+ and TIM-3- populations of a single mouse representing each experimental group. Data are mean ± SD of at least 3 similar experiments (n = 6; *** = p
    Figure Legend Snippet: More effector cytokine secretion by TIM-3+ compared to TIM-3- population of tumor infiltrating CD8+ T cells in mouse CT26 colon tumor model. CT26 tumor cells were inoculated in BALB/c mice and were allowed to form solid tumor. The TIM-3+ population of tumor-infiltrating CD8+ T cells produces higher level of IFN-γ, TNF-α and IL-2 compared to that by the TIM-3- population on day 28- post tumor inoculation. Dot-plots demonstrate cytokine frequencies of TIM-3+ and TIM-3- populations of a single mouse representing each experimental group. Data are mean ± SD of at least 3 similar experiments (n = 6; *** = p

    Techniques Used: Mouse Assay

    40) Product Images from "Compressive Stress Inhibits Proliferation in Tumor Spheroids through a Volume Limitation"

    Article Title: Compressive Stress Inhibits Proliferation in Tumor Spheroids through a Volume Limitation

    Journal: Biophysical Journal

    doi: 10.1016/j.bpj.2014.08.031

    Multicellular spheroids and mechanical stress. ( A ) Growth of a CT26 MCS from Day 0 to Day 10 (scale bar, 200 μ m). ( B ) Principle of the experiment. Dextran is added to the culture medium, and does not penetrate the MCS. This results in a moderate
    Figure Legend Snippet: Multicellular spheroids and mechanical stress. ( A ) Growth of a CT26 MCS from Day 0 to Day 10 (scale bar, 200 μ m). ( B ) Principle of the experiment. Dextran is added to the culture medium, and does not penetrate the MCS. This results in a moderate

    Techniques Used:

    Macroscopic correlation between CT26 MCS volume reduction obtained in 5 min and the growth rate obtained by the growth curve fitting over 15 days. A linear regression gives a correlation of 0.98. To see this figure in color, go online.
    Figure Legend Snippet: Macroscopic correlation between CT26 MCS volume reduction obtained in 5 min and the growth rate obtained by the growth curve fitting over 15 days. A linear regression gives a correlation of 0.98. To see this figure in color, go online.

    Techniques Used:

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    Transduction:

    Article Title: Central role of liver in anticancer and radioprotective activities of Toll-like receptor 5 agonist
    Article Snippet: .. Murine mammary carcinoma 4T1, B-cell lymphoma A20, and colon undifferentiated carcinoma CT26 cells (American Type Culture Collection) were transduced with constitutive luciferase expression constructs and were cultured in RPMI plus 10% (vol/vol) FBS with standard supplements and antibiotics. .. Primary human hepatocytes were purchased from BD Biosciences.

    Luciferase:

    Article Title: Central role of liver in anticancer and radioprotective activities of Toll-like receptor 5 agonist
    Article Snippet: .. Murine mammary carcinoma 4T1, B-cell lymphoma A20, and colon undifferentiated carcinoma CT26 cells (American Type Culture Collection) were transduced with constitutive luciferase expression constructs and were cultured in RPMI plus 10% (vol/vol) FBS with standard supplements and antibiotics. .. Primary human hepatocytes were purchased from BD Biosciences.

    Construct:

    Article Title: Central role of liver in anticancer and radioprotective activities of Toll-like receptor 5 agonist
    Article Snippet: .. Murine mammary carcinoma 4T1, B-cell lymphoma A20, and colon undifferentiated carcinoma CT26 cells (American Type Culture Collection) were transduced with constitutive luciferase expression constructs and were cultured in RPMI plus 10% (vol/vol) FBS with standard supplements and antibiotics. .. Primary human hepatocytes were purchased from BD Biosciences.

    Mouse Assay:

    Article Title: Instant immunity through chemically programmable vaccination and covalent self-assembly
    Article Snippet: .. Mouse colon carcinoma cell line CT26 (syngeneic with BALB/C mice) were purchased from American Type Culture Collection (ATCC) and were maintained in DMEM supplemented with 4 mM L-glutamine, 1.5 g/L sodium bicarbonate, 4.5 g/L glucose, 1 mM sodium pyruvate, 10% FCS, and antibiotics. .. B16F10 mouse melanoma cell line (syngeneic with C57BL6) was purchased from ATCC and maintained in RPMI medium 1640 containing 10% FCS and antibiotics.

    other:

    Article Title: Lymphotoxin ? receptor mediates caspase-dependent tumor cell apoptosis in vitro and tumor suppression in vivo despite induction of NF-?B activation
    Article Snippet: Mouse colon carcinoma cell line CT26 was also obtained from ATCC.

    Cell Culture:

    Article Title: Central role of liver in anticancer and radioprotective activities of Toll-like receptor 5 agonist
    Article Snippet: .. Murine mammary carcinoma 4T1, B-cell lymphoma A20, and colon undifferentiated carcinoma CT26 cells (American Type Culture Collection) were transduced with constitutive luciferase expression constructs and were cultured in RPMI plus 10% (vol/vol) FBS with standard supplements and antibiotics. .. Primary human hepatocytes were purchased from BD Biosciences.

    Article Title: 64Cu-DOTA-Anti-CTLA-4 mAb Enabled PET Visualization of CTLA-4 on the T-Cell Infiltrating Tumor Tissues
    Article Snippet: .. Cell culture CT26 was purchased from American Type Culture Collection and cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum, 4 mM L-glutamine, 10 U/mL penicillin, and 10 mg/mL streptomycin at 37°C in a humidified atmosphere containing 5% CO2 . .. Preparation of subcutaneous tumor model mice Female BALB/c and BALB/c (nu/nu) nude mice (4–6 weeks old) were purchased from CLEA Japan Inc. Tumor-bearing BALB/c and BALB/c nude mice were prepared by subcutaneously implanting CT26 cells (1–4×106 cells).

    Article Title: microRNA-451a regulates colorectal cancer proliferation in response to radiation
    Article Snippet: .. CT26 cells (ATCC) were cultured in RPMI-1640 medium supplemented with 10% FBS and antibiotics. .. SW480 and SW620 cells (ATCC) were cultured in Leibovitz’s L-15 Medium with 10% FBS, L-glutamine, antibiotics under 0% CO2 conditions.

    Expressing:

    Article Title: Central role of liver in anticancer and radioprotective activities of Toll-like receptor 5 agonist
    Article Snippet: .. Murine mammary carcinoma 4T1, B-cell lymphoma A20, and colon undifferentiated carcinoma CT26 cells (American Type Culture Collection) were transduced with constitutive luciferase expression constructs and were cultured in RPMI plus 10% (vol/vol) FBS with standard supplements and antibiotics. .. Primary human hepatocytes were purchased from BD Biosciences.

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  • 99
    ATCC ct26 cells
    miR-451a is robustly induced by radiation in human and mouse colorectal carcinoma. a Design of the screen for miRs induced by radiation. Heatmap depicts miRs with more than 2 fold change from the affymetrix microRNA array v4.0 across both tumor types. b Levels of the two most upregulated and downregulated miRs 6 h post 2 Gy radiation were validated by qRT-PCR using specific Taqman probes for each microRNA. Mean fold change after normalization to a housekeeping RNA, RNU48, is depicted. c Most abundant ( > 10 counts) miRs in <t>CT26</t> mouse colorectal carcinomas at 6 h post 10 Gy treatment. Bars represent mean + SD of 3 mice in 0 Gy group and 2 mice in 10 Gy group. RNA was extracted from tumors and miR profiles were analyzed using the Nanostring miR panel
    Ct26 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 30 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ct26 cells/product/ATCC
    Average 99 stars, based on 30 article reviews
    Price from $9.99 to $1999.99
    ct26 cells - by Bioz Stars, 2021-01
    99/100 stars
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    88
    ATCC ct26 colon carcinoma cell line
    Mechanism of antitumour activity of mutation specific poly-epitope vaccines in <t>CT26</t> tumour-bearing mice a , BALB/c mice ( n = 5) were vaccinated either with pentatope (35 μg) or the corresponding mixture of five RNA monotopes (7 μg each). T-cell responses in peptide-stimulated splenocytes of mice were measured ex vivo via ELISpot (medium control subtracted mean ± s.e.m.). b, c , BALB/c mice ( n = 10) were inoculated i.v. with CT26 tumour cells and left untreated or injected with irrelevant, CT26-M19 or pentatope1 or 2 RNA in absence ( b ) or presence of a CD8 T cell depleting antibody or a CD40L blocking antibody ( c ). Mean ± s.e.m. of tumour nodules per lung are shown. d , Immunofluorescence analyses of tumour-infiltrating lymphocytes in pentatope2-vaccinated mice. Upper panel, lung tumour tissue stained for CD4 and CD8 or CD4 and FoxP3. Scale bar, 50 μm. Lower panel left, proportion of infiltrating cells in sections of irrelevant (CD4: n = 13; CD8 = 9; FoxP3: n = 13) or pentatope (CD4: n = 17; CD8: n = 6; FoxP3: n = 10) RNA-treated animals. Lower panel right, tumour area in sections of control ( n = 22) and pentatope2-treated ( n = 20) animals (mean ± s.e.m.).
    Ct26 Colon Carcinoma Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 88/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ct26 colon carcinoma cell line/product/ATCC
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    85
    ATCC culture ct26 colorectal cancer cell line
    Tumor suppression and survival advantage in Ad-Endo-PMSC-treated mice. A. Images of representative <t>CT26</t> tumor-bearing mice after intraperitoneal treatment. Ad-Endo-PMSCs effectively inhibited the peritoneal dissemination and growth of <t>colorectal</t> cancer. B. Significant increases in survival rates and prolonged survival times were observed in Ad-Endo-PMSC-treated mice compared to control groups. p
    Culture Ct26 Colorectal Cancer Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/culture ct26 colorectal cancer cell line/product/ATCC
    Average 85 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    culture ct26 colorectal cancer cell line - by Bioz Stars, 2021-01
    85/100 stars
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    Image Search Results


    miR-451a is robustly induced by radiation in human and mouse colorectal carcinoma. a Design of the screen for miRs induced by radiation. Heatmap depicts miRs with more than 2 fold change from the affymetrix microRNA array v4.0 across both tumor types. b Levels of the two most upregulated and downregulated miRs 6 h post 2 Gy radiation were validated by qRT-PCR using specific Taqman probes for each microRNA. Mean fold change after normalization to a housekeeping RNA, RNU48, is depicted. c Most abundant ( > 10 counts) miRs in CT26 mouse colorectal carcinomas at 6 h post 10 Gy treatment. Bars represent mean + SD of 3 mice in 0 Gy group and 2 mice in 10 Gy group. RNA was extracted from tumors and miR profiles were analyzed using the Nanostring miR panel

    Journal: BMC Cancer

    Article Title: microRNA-451a regulates colorectal cancer proliferation in response to radiation

    doi: 10.1186/s12885-018-4370-1

    Figure Lengend Snippet: miR-451a is robustly induced by radiation in human and mouse colorectal carcinoma. a Design of the screen for miRs induced by radiation. Heatmap depicts miRs with more than 2 fold change from the affymetrix microRNA array v4.0 across both tumor types. b Levels of the two most upregulated and downregulated miRs 6 h post 2 Gy radiation were validated by qRT-PCR using specific Taqman probes for each microRNA. Mean fold change after normalization to a housekeeping RNA, RNU48, is depicted. c Most abundant ( > 10 counts) miRs in CT26 mouse colorectal carcinomas at 6 h post 10 Gy treatment. Bars represent mean + SD of 3 mice in 0 Gy group and 2 mice in 10 Gy group. RNA was extracted from tumors and miR profiles were analyzed using the Nanostring miR panel

    Article Snippet: CT26 cells (ATCC) were cultured in RPMI-1640 medium supplemented with 10% FBS and antibiotics.

    Techniques: Quantitative RT-PCR, Mouse Assay

    Mechanism of antitumour activity of mutation specific poly-epitope vaccines in CT26 tumour-bearing mice a , BALB/c mice ( n = 5) were vaccinated either with pentatope (35 μg) or the corresponding mixture of five RNA monotopes (7 μg each). T-cell responses in peptide-stimulated splenocytes of mice were measured ex vivo via ELISpot (medium control subtracted mean ± s.e.m.). b, c , BALB/c mice ( n = 10) were inoculated i.v. with CT26 tumour cells and left untreated or injected with irrelevant, CT26-M19 or pentatope1 or 2 RNA in absence ( b ) or presence of a CD8 T cell depleting antibody or a CD40L blocking antibody ( c ). Mean ± s.e.m. of tumour nodules per lung are shown. d , Immunofluorescence analyses of tumour-infiltrating lymphocytes in pentatope2-vaccinated mice. Upper panel, lung tumour tissue stained for CD4 and CD8 or CD4 and FoxP3. Scale bar, 50 μm. Lower panel left, proportion of infiltrating cells in sections of irrelevant (CD4: n = 13; CD8 = 9; FoxP3: n = 13) or pentatope (CD4: n = 17; CD8: n = 6; FoxP3: n = 10) RNA-treated animals. Lower panel right, tumour area in sections of control ( n = 22) and pentatope2-treated ( n = 20) animals (mean ± s.e.m.).

    Journal: Nature

    Article Title: Mutant MHC class II epitopes drive therapeutic immune responses to cancer

    doi: 10.1038/nature14426

    Figure Lengend Snippet: Mechanism of antitumour activity of mutation specific poly-epitope vaccines in CT26 tumour-bearing mice a , BALB/c mice ( n = 5) were vaccinated either with pentatope (35 μg) or the corresponding mixture of five RNA monotopes (7 μg each). T-cell responses in peptide-stimulated splenocytes of mice were measured ex vivo via ELISpot (medium control subtracted mean ± s.e.m.). b, c , BALB/c mice ( n = 10) were inoculated i.v. with CT26 tumour cells and left untreated or injected with irrelevant, CT26-M19 or pentatope1 or 2 RNA in absence ( b ) or presence of a CD8 T cell depleting antibody or a CD40L blocking antibody ( c ). Mean ± s.e.m. of tumour nodules per lung are shown. d , Immunofluorescence analyses of tumour-infiltrating lymphocytes in pentatope2-vaccinated mice. Upper panel, lung tumour tissue stained for CD4 and CD8 or CD4 and FoxP3. Scale bar, 50 μm. Lower panel left, proportion of infiltrating cells in sections of irrelevant (CD4: n = 13; CD8 = 9; FoxP3: n = 13) or pentatope (CD4: n = 17; CD8: n = 6; FoxP3: n = 10) RNA-treated animals. Lower panel right, tumour area in sections of control ( n = 22) and pentatope2-treated ( n = 20) animals (mean ± s.e.m.).

    Article Snippet: B16F10 melanoma cell line, CT26 colon carcinoma cell line and 4T1-luc2-tdtomato (4T1-Luc) cells were purchased in 2010, 2011 and 2011, respectively (ATCC CRL-6475 lot no. 58078645, ATCC CRL-2638 lot no. 58494154, Caliper 125669 lot no. 101648).

    Techniques: Activity Assay, Mutagenesis, Mouse Assay, Ex Vivo, Enzyme-linked Immunospot, Injection, Blocking Assay, Immunofluorescence, Staining

    Tumor suppression and survival advantage in Ad-Endo-PMSC-treated mice. A. Images of representative CT26 tumor-bearing mice after intraperitoneal treatment. Ad-Endo-PMSCs effectively inhibited the peritoneal dissemination and growth of colorectal cancer. B. Significant increases in survival rates and prolonged survival times were observed in Ad-Endo-PMSC-treated mice compared to control groups. p

    Journal: International Journal of Medical Sciences

    Article Title: Suppression of Peritoneal Tumorigenesis by Placenta-Derived Mesenchymal Stem Cells Expressing Endostatin on Colorectal Cancer

    doi: 10.7150/ijms.8758

    Figure Lengend Snippet: Tumor suppression and survival advantage in Ad-Endo-PMSC-treated mice. A. Images of representative CT26 tumor-bearing mice after intraperitoneal treatment. Ad-Endo-PMSCs effectively inhibited the peritoneal dissemination and growth of colorectal cancer. B. Significant increases in survival rates and prolonged survival times were observed in Ad-Endo-PMSC-treated mice compared to control groups. p

    Article Snippet: Cell lines and culture CT26 colorectal cancer cell line and transformed human embryonic kidney cell line 293T cells were purchased from ATCC (American Type Culture Collection, Rockville, MD).

    Techniques: Mouse Assay