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schematic of castration resistant prostate cancer mouse model (crpc)  (Celgene)

 
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    Celgene schematic of castration resistant prostate cancer mouse model (crpc)
    A) Proliferation assays using DNA-PK knockdown (siDNA-PK) and pharmacological inhibition of DNA-PK (NU7441,1 μM) in <t>CRPC</t> cell lines using Trypan Blue(left) and Pico Green (right) assay respectively. Cell counts were obtained at 1, 4, and 6 days post transfection for knockdown experiments, and at day 0 (prior to treatment), 4, and 6 for inhibitor experiments. Relative cell number was calculated for each day normalizing to their appropriate controls. Data are represented as mean ± SD of biological triplicate. Student t-test statistical analyses were used where *p<0.05, ***p<0.001 compared to control. B) Representative FACS plots of BrdU incorporation after 24-hour treatment with 1 μM NU7441 and vehicle control (DMSO). Quantification of active S phase FACS data are presented as mean ± SD of biological triplicate. C) RNA-Seq schematic of C4-2 cell line treated with vehicle control (DMSO) and DNA-PK inhibitor (NU7441, 1 μM) in triplicate for 24 hours before RNA was harvested. MA plot was generated by comparing NU7441 treated cells to vehicle control showing gene expression modulation with the number of transcripts up-regulated (top) and down-regulated (bottom). GSEA using Hallmark geneset from MSigDB analysis was used to identify enriched and de-enriched pathways for DNA-PKi treated cells compared to vehicle control using FDR<0.25. Each pathway is depicted by a ribbon in the circos plot where blue ribbons identify pathways enriched exclusively by DNA-PKi and green ribbons identify pathways de-enriched by NU7441 treatment.
    Schematic Of Castration Resistant Prostate Cancer Mouse Model (Crpc), supplied by Celgene, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/schematic+of+castration+resistant+prostate+cancer+mouse+model+(crpc)/schematic+of+castration+resistant+prostate+cancer+mouse+model++crpc+/pmc06744985-401-3-12
    Average 90 stars, based on 1 article reviews
    schematic of castration resistant prostate cancer mouse model (crpc) - by Bioz Stars, 2026-09
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    1) Product Images from "Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies"

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies

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

    doi: 10.1158/1078-0432.CCR-18-2207

    A) Proliferation assays using DNA-PK knockdown (siDNA-PK) and pharmacological inhibition of DNA-PK (NU7441,1 μM) in CRPC cell lines using Trypan Blue(left) and Pico Green (right) assay respectively. Cell counts were obtained at 1, 4, and 6 days post transfection for knockdown experiments, and at day 0 (prior to treatment), 4, and 6 for inhibitor experiments. Relative cell number was calculated for each day normalizing to their appropriate controls. Data are represented as mean ± SD of biological triplicate. Student t-test statistical analyses were used where *p<0.05, ***p<0.001 compared to control. B) Representative FACS plots of BrdU incorporation after 24-hour treatment with 1 μM NU7441 and vehicle control (DMSO). Quantification of active S phase FACS data are presented as mean ± SD of biological triplicate. C) RNA-Seq schematic of C4-2 cell line treated with vehicle control (DMSO) and DNA-PK inhibitor (NU7441, 1 μM) in triplicate for 24 hours before RNA was harvested. MA plot was generated by comparing NU7441 treated cells to vehicle control showing gene expression modulation with the number of transcripts up-regulated (top) and down-regulated (bottom). GSEA using Hallmark geneset from MSigDB analysis was used to identify enriched and de-enriched pathways for DNA-PKi treated cells compared to vehicle control using FDR<0.25. Each pathway is depicted by a ribbon in the circos plot where blue ribbons identify pathways enriched exclusively by DNA-PKi and green ribbons identify pathways de-enriched by NU7441 treatment.
    Figure Legend Snippet: A) Proliferation assays using DNA-PK knockdown (siDNA-PK) and pharmacological inhibition of DNA-PK (NU7441,1 μM) in CRPC cell lines using Trypan Blue(left) and Pico Green (right) assay respectively. Cell counts were obtained at 1, 4, and 6 days post transfection for knockdown experiments, and at day 0 (prior to treatment), 4, and 6 for inhibitor experiments. Relative cell number was calculated for each day normalizing to their appropriate controls. Data are represented as mean ± SD of biological triplicate. Student t-test statistical analyses were used where *p<0.05, ***p<0.001 compared to control. B) Representative FACS plots of BrdU incorporation after 24-hour treatment with 1 μM NU7441 and vehicle control (DMSO). Quantification of active S phase FACS data are presented as mean ± SD of biological triplicate. C) RNA-Seq schematic of C4-2 cell line treated with vehicle control (DMSO) and DNA-PK inhibitor (NU7441, 1 μM) in triplicate for 24 hours before RNA was harvested. MA plot was generated by comparing NU7441 treated cells to vehicle control showing gene expression modulation with the number of transcripts up-regulated (top) and down-regulated (bottom). GSEA using Hallmark geneset from MSigDB analysis was used to identify enriched and de-enriched pathways for DNA-PKi treated cells compared to vehicle control using FDR<0.25. Each pathway is depicted by a ribbon in the circos plot where blue ribbons identify pathways enriched exclusively by DNA-PKi and green ribbons identify pathways de-enriched by NU7441 treatment.

    Techniques Used: Knockdown, Inhibition, Transfection, Control, BrdU Incorporation Assay, RNA Sequencing, Generated, Gene Expression

    A) Dose response proliferation assays using NU7441 (DNA-PK inhibitor) and CC-115 (dual DNA-PK/TOR kinase inhibitor) in HSPC and CRPC cell lines using Pico Green assay at 6 days post treatment compared to vehicle control. B) RNA-Seq schematic of C4-2 cell line treated with 1 μM of CC-115 in triplicate for 24 hours before RNA was harvested. MA plots was generated for CC-115 treatment compared to control showing gene expression modulation with the number of transcripts up-regulated (top) and down-regulated (bottom). C) GSEA using Hallmark geneset from MSigDB analysis was used to identify enriched and de-enriched pathways for NU7441 and CC-115 treated cells compared to control using FDR<0.25. Each pathway is depicted by a ribbon in the circos plot where blue ribbons identify pathways de-enriched exclusively by NU7441, dark blue = exclusive enrichment by NU7441, orange = exclusive de-enrichment by CC-115, Red = enrichment by CC-115, purple = commonly de-enriched and green = commonly enriched. Commonly enriched and de-enriched pathways regulated by DNA-PK are represented using heat maps to the right.
    Figure Legend Snippet: A) Dose response proliferation assays using NU7441 (DNA-PK inhibitor) and CC-115 (dual DNA-PK/TOR kinase inhibitor) in HSPC and CRPC cell lines using Pico Green assay at 6 days post treatment compared to vehicle control. B) RNA-Seq schematic of C4-2 cell line treated with 1 μM of CC-115 in triplicate for 24 hours before RNA was harvested. MA plots was generated for CC-115 treatment compared to control showing gene expression modulation with the number of transcripts up-regulated (top) and down-regulated (bottom). C) GSEA using Hallmark geneset from MSigDB analysis was used to identify enriched and de-enriched pathways for NU7441 and CC-115 treated cells compared to control using FDR<0.25. Each pathway is depicted by a ribbon in the circos plot where blue ribbons identify pathways de-enriched exclusively by NU7441, dark blue = exclusive enrichment by NU7441, orange = exclusive de-enrichment by CC-115, Red = enrichment by CC-115, purple = commonly de-enriched and green = commonly enriched. Commonly enriched and de-enriched pathways regulated by DNA-PK are represented using heat maps to the right.

    Techniques Used: Control, RNA Sequencing, Generated, Gene Expression

    A) Combination Index determination in PC cell lines when using CC-115 at IC25, IC50 and IC75 in combination with varied concentrations of Enza. Experiments were performed in biological triplicates. B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene. Upon establishment of CRPC tumors, the AR axis was interrogated by measuring FKBP5 mRNA expression levels in tumors after treatments via qPCR (right). Data represented as mean ± SEM of biological triplicates. Student s’t-test statistical analyses were used where *p<0.05 compared to control (red) or as otherwise indicated by the brackets. C) Average tumor doubling time was calculated for each treatment cohort. D) The percentage of tumors reaching 1500 mm3 was calculated for each cohort. E) Tumor growth was monitored for 19 days after single agent or combination drug treatment. Relative tumor volume is shown for each treatment normalized to tumor volume at the start of treatment. Mouse data are presented as mean ± SEM and one-way ANOVA was used for statistical analysis where *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001 compared to control.
    Figure Legend Snippet: A) Combination Index determination in PC cell lines when using CC-115 at IC25, IC50 and IC75 in combination with varied concentrations of Enza. Experiments were performed in biological triplicates. B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene. Upon establishment of CRPC tumors, the AR axis was interrogated by measuring FKBP5 mRNA expression levels in tumors after treatments via qPCR (right). Data represented as mean ± SEM of biological triplicates. Student s’t-test statistical analyses were used where *p<0.05 compared to control (red) or as otherwise indicated by the brackets. C) Average tumor doubling time was calculated for each treatment cohort. D) The percentage of tumors reaching 1500 mm3 was calculated for each cohort. E) Tumor growth was monitored for 19 days after single agent or combination drug treatment. Relative tumor volume is shown for each treatment normalized to tumor volume at the start of treatment. Mouse data are presented as mean ± SEM and one-way ANOVA was used for statistical analysis where *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001 compared to control.

    Techniques Used: Expressing, Control

    A) Schematic of human Patient Derived Explant (PDE) model generation from human prostatectomy samples that are treated with single agent CC-115 (0.1, 0.5, 1 μM DNA-PK/TOR inhibitor) and Enza (1μM) and combination treatments (0.1, 0.5, 1 μM CC-115+ 1 μM Enza) for 6 days. B) Representative Ki67 IHC tissue staining after each treatment are shown at 40X magnification. C) Each PDE sample (each patient is represented by a different color) was scored by by Digital Imaging Analysis (Aperio System) and confirmed by a pathologist. Data is represented as Ki67 mean ± SD of each cohort of patient tissues treated with the same treatment. D) Schematic of the CC-115 and Enza clinical trial currently conducted in patients with CRPC. E) Model summarizing findings in this paper.
    Figure Legend Snippet: A) Schematic of human Patient Derived Explant (PDE) model generation from human prostatectomy samples that are treated with single agent CC-115 (0.1, 0.5, 1 μM DNA-PK/TOR inhibitor) and Enza (1μM) and combination treatments (0.1, 0.5, 1 μM CC-115+ 1 μM Enza) for 6 days. B) Representative Ki67 IHC tissue staining after each treatment are shown at 40X magnification. C) Each PDE sample (each patient is represented by a different color) was scored by by Digital Imaging Analysis (Aperio System) and confirmed by a pathologist. Data is represented as Ki67 mean ± SD of each cohort of patient tissues treated with the same treatment. D) Schematic of the CC-115 and Enza clinical trial currently conducted in patients with CRPC. E) Model summarizing findings in this paper.

    Techniques Used: Derivative Assay, Staining, Imaging

    Related Articles

    Knockdown:

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies
    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    Inhibition:

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies
    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    Transfection:

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies
    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    Control:

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies
    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    BrdU Incorporation Assay:

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies
    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    RNA Sequencing:

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies
    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    Generated:

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies
    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    Gene Expression:

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies
    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    Expressing:

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies
    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    Derivative Assay:

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies
    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    Staining:

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies
    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    Imaging:

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies
    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.



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    schematic of castration resistant prostate cancer mouse model (crpc)  (Celgene)
    90
    Celgene schematic of castration resistant prostate cancer mouse model (crpc)
    A) Proliferation assays using DNA-PK knockdown (siDNA-PK) and pharmacological inhibition of DNA-PK (NU7441,1 μM) in <t>CRPC</t> cell lines using Trypan Blue(left) and Pico Green (right) assay respectively. Cell counts were obtained at 1, 4, and 6 days post transfection for knockdown experiments, and at day 0 (prior to treatment), 4, and 6 for inhibitor experiments. Relative cell number was calculated for each day normalizing to their appropriate controls. Data are represented as mean ± SD of biological triplicate. Student t-test statistical analyses were used where *p<0.05, ***p<0.001 compared to control. B) Representative FACS plots of BrdU incorporation after 24-hour treatment with 1 μM NU7441 and vehicle control (DMSO). Quantification of active S phase FACS data are presented as mean ± SD of biological triplicate. C) RNA-Seq schematic of C4-2 cell line treated with vehicle control (DMSO) and DNA-PK inhibitor (NU7441, 1 μM) in triplicate for 24 hours before RNA was harvested. MA plot was generated by comparing NU7441 treated cells to vehicle control showing gene expression modulation with the number of transcripts up-regulated (top) and down-regulated (bottom). GSEA using Hallmark geneset from MSigDB analysis was used to identify enriched and de-enriched pathways for DNA-PKi treated cells compared to vehicle control using FDR<0.25. Each pathway is depicted by a ribbon in the circos plot where blue ribbons identify pathways enriched exclusively by DNA-PKi and green ribbons identify pathways de-enriched by NU7441 treatment.
    Schematic Of Castration Resistant Prostate Cancer Mouse Model (Crpc), supplied by Celgene, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/schematic+of+castration+resistant+prostate+cancer+mouse+model+(crpc)/schematic+of+castration+resistant+prostate+cancer+mouse+model++crpc+/pmc06744985-401-3-12
    Average 90 stars, based on 1 article reviews
    schematic of castration resistant prostate cancer mouse model (crpc) - by Bioz Stars, 2026-09
    90/100 stars
    		  Buy from Supplier

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    A) Proliferation assays using DNA-PK knockdown (siDNA-PK) and pharmacological inhibition of DNA-PK (NU7441,1 μM) in CRPC cell lines using Trypan Blue(left) and Pico Green (right) assay respectively. Cell counts were obtained at 1, 4, and 6 days post transfection for knockdown experiments, and at day 0 (prior to treatment), 4, and 6 for inhibitor experiments. Relative cell number was calculated for each day normalizing to their appropriate controls. Data are represented as mean ± SD of biological triplicate. Student t-test statistical analyses were used where *p<0.05, ***p<0.001 compared to control. B) Representative FACS plots of BrdU incorporation after 24-hour treatment with 1 μM NU7441 and vehicle control (DMSO). Quantification of active S phase FACS data are presented as mean ± SD of biological triplicate. C) RNA-Seq schematic of C4-2 cell line treated with vehicle control (DMSO) and DNA-PK inhibitor (NU7441, 1 μM) in triplicate for 24 hours before RNA was harvested. MA plot was generated by comparing NU7441 treated cells to vehicle control showing gene expression modulation with the number of transcripts up-regulated (top) and down-regulated (bottom). GSEA using Hallmark geneset from MSigDB analysis was used to identify enriched and de-enriched pathways for DNA-PKi treated cells compared to vehicle control using FDR<0.25. Each pathway is depicted by a ribbon in the circos plot where blue ribbons identify pathways enriched exclusively by DNA-PKi and green ribbons identify pathways de-enriched by NU7441 treatment.

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

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies

    doi: 10.1158/1078-0432.CCR-18-2207

    Figure Lengend Snippet: A) Proliferation assays using DNA-PK knockdown (siDNA-PK) and pharmacological inhibition of DNA-PK (NU7441,1 μM) in CRPC cell lines using Trypan Blue(left) and Pico Green (right) assay respectively. Cell counts were obtained at 1, 4, and 6 days post transfection for knockdown experiments, and at day 0 (prior to treatment), 4, and 6 for inhibitor experiments. Relative cell number was calculated for each day normalizing to their appropriate controls. Data are represented as mean ± SD of biological triplicate. Student t-test statistical analyses were used where *p<0.05, ***p<0.001 compared to control. B) Representative FACS plots of BrdU incorporation after 24-hour treatment with 1 μM NU7441 and vehicle control (DMSO). Quantification of active S phase FACS data are presented as mean ± SD of biological triplicate. C) RNA-Seq schematic of C4-2 cell line treated with vehicle control (DMSO) and DNA-PK inhibitor (NU7441, 1 μM) in triplicate for 24 hours before RNA was harvested. MA plot was generated by comparing NU7441 treated cells to vehicle control showing gene expression modulation with the number of transcripts up-regulated (top) and down-regulated (bottom). GSEA using Hallmark geneset from MSigDB analysis was used to identify enriched and de-enriched pathways for DNA-PKi treated cells compared to vehicle control using FDR<0.25. Each pathway is depicted by a ribbon in the circos plot where blue ribbons identify pathways enriched exclusively by DNA-PKi and green ribbons identify pathways de-enriched by NU7441 treatment.

    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    Techniques: Knockdown, Inhibition, Transfection, Control, BrdU Incorporation Assay, RNA Sequencing, Generated, Gene Expression

    A) Dose response proliferation assays using NU7441 (DNA-PK inhibitor) and CC-115 (dual DNA-PK/TOR kinase inhibitor) in HSPC and CRPC cell lines using Pico Green assay at 6 days post treatment compared to vehicle control. B) RNA-Seq schematic of C4-2 cell line treated with 1 μM of CC-115 in triplicate for 24 hours before RNA was harvested. MA plots was generated for CC-115 treatment compared to control showing gene expression modulation with the number of transcripts up-regulated (top) and down-regulated (bottom). C) GSEA using Hallmark geneset from MSigDB analysis was used to identify enriched and de-enriched pathways for NU7441 and CC-115 treated cells compared to control using FDR<0.25. Each pathway is depicted by a ribbon in the circos plot where blue ribbons identify pathways de-enriched exclusively by NU7441, dark blue = exclusive enrichment by NU7441, orange = exclusive de-enrichment by CC-115, Red = enrichment by CC-115, purple = commonly de-enriched and green = commonly enriched. Commonly enriched and de-enriched pathways regulated by DNA-PK are represented using heat maps to the right.

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

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies

    doi: 10.1158/1078-0432.CCR-18-2207

    Figure Lengend Snippet: A) Dose response proliferation assays using NU7441 (DNA-PK inhibitor) and CC-115 (dual DNA-PK/TOR kinase inhibitor) in HSPC and CRPC cell lines using Pico Green assay at 6 days post treatment compared to vehicle control. B) RNA-Seq schematic of C4-2 cell line treated with 1 μM of CC-115 in triplicate for 24 hours before RNA was harvested. MA plots was generated for CC-115 treatment compared to control showing gene expression modulation with the number of transcripts up-regulated (top) and down-regulated (bottom). C) GSEA using Hallmark geneset from MSigDB analysis was used to identify enriched and de-enriched pathways for NU7441 and CC-115 treated cells compared to control using FDR<0.25. Each pathway is depicted by a ribbon in the circos plot where blue ribbons identify pathways de-enriched exclusively by NU7441, dark blue = exclusive enrichment by NU7441, orange = exclusive de-enrichment by CC-115, Red = enrichment by CC-115, purple = commonly de-enriched and green = commonly enriched. Commonly enriched and de-enriched pathways regulated by DNA-PK are represented using heat maps to the right.

    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    Techniques: Control, RNA Sequencing, Generated, Gene Expression

    A) Combination Index determination in PC cell lines when using CC-115 at IC25, IC50 and IC75 in combination with varied concentrations of Enza. Experiments were performed in biological triplicates. B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene. Upon establishment of CRPC tumors, the AR axis was interrogated by measuring FKBP5 mRNA expression levels in tumors after treatments via qPCR (right). Data represented as mean ± SEM of biological triplicates. Student s’t-test statistical analyses were used where *p<0.05 compared to control (red) or as otherwise indicated by the brackets. C) Average tumor doubling time was calculated for each treatment cohort. D) The percentage of tumors reaching 1500 mm3 was calculated for each cohort. E) Tumor growth was monitored for 19 days after single agent or combination drug treatment. Relative tumor volume is shown for each treatment normalized to tumor volume at the start of treatment. Mouse data are presented as mean ± SEM and one-way ANOVA was used for statistical analysis where *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001 compared to control.

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

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies

    doi: 10.1158/1078-0432.CCR-18-2207

    Figure Lengend Snippet: A) Combination Index determination in PC cell lines when using CC-115 at IC25, IC50 and IC75 in combination with varied concentrations of Enza. Experiments were performed in biological triplicates. B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene. Upon establishment of CRPC tumors, the AR axis was interrogated by measuring FKBP5 mRNA expression levels in tumors after treatments via qPCR (right). Data represented as mean ± SEM of biological triplicates. Student s’t-test statistical analyses were used where *p<0.05 compared to control (red) or as otherwise indicated by the brackets. C) Average tumor doubling time was calculated for each treatment cohort. D) The percentage of tumors reaching 1500 mm3 was calculated for each cohort. E) Tumor growth was monitored for 19 days after single agent or combination drug treatment. Relative tumor volume is shown for each treatment normalized to tumor volume at the start of treatment. Mouse data are presented as mean ± SEM and one-way ANOVA was used for statistical analysis where *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001 compared to control.

    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    Techniques: Expressing, Control

    A) Schematic of human Patient Derived Explant (PDE) model generation from human prostatectomy samples that are treated with single agent CC-115 (0.1, 0.5, 1 μM DNA-PK/TOR inhibitor) and Enza (1μM) and combination treatments (0.1, 0.5, 1 μM CC-115+ 1 μM Enza) for 6 days. B) Representative Ki67 IHC tissue staining after each treatment are shown at 40X magnification. C) Each PDE sample (each patient is represented by a different color) was scored by by Digital Imaging Analysis (Aperio System) and confirmed by a pathologist. Data is represented as Ki67 mean ± SD of each cohort of patient tissues treated with the same treatment. D) Schematic of the CC-115 and Enza clinical trial currently conducted in patients with CRPC. E) Model summarizing findings in this paper.

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

    Article Title: Pleiotropic impact of DNA-PK in cancer and implications for therapeutic strategies

    doi: 10.1158/1078-0432.CCR-18-2207

    Figure Lengend Snippet: A) Schematic of human Patient Derived Explant (PDE) model generation from human prostatectomy samples that are treated with single agent CC-115 (0.1, 0.5, 1 μM DNA-PK/TOR inhibitor) and Enza (1μM) and combination treatments (0.1, 0.5, 1 μM CC-115+ 1 μM Enza) for 6 days. B) Representative Ki67 IHC tissue staining after each treatment are shown at 40X magnification. C) Each PDE sample (each patient is represented by a different color) was scored by by Digital Imaging Analysis (Aperio System) and confirmed by a pathologist. Data is represented as Ki67 mean ± SD of each cohort of patient tissues treated with the same treatment. D) Schematic of the CC-115 and Enza clinical trial currently conducted in patients with CRPC. E) Model summarizing findings in this paper.

    Article Snippet: B) Schematic of castration resistant prostate cancer mouse model (CRPC) developed by Celgene.

    Techniques: Derivative Assay, Staining, Imaging