model schematics Search Results


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
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schematic diagram of stretching model  (COMSOL Inc)
90
COMSOL Inc schematic diagram of stretching model
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 Diagram Of Stretching Model, supplied by COMSOL Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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2d schematic geometric model  (COMSOL Inc)
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COMSOL Inc 2d schematic geometric model
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.
2d Schematic Geometric Model, supplied by COMSOL Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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schematic structure model of the influenza a virion  (Nature Biotechnology)
90
Nature Biotechnology schematic structure model of the influenza a virion
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 Structure Model Of The Influenza A Virion, supplied by Nature Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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schematic diagram of the model plant immune system  (Biomodels LLC)
90
Biomodels LLC schematic diagram of the model plant immune system
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 Diagram Of The Model Plant Immune System, supplied by Biomodels LLC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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modified schematic model  (Abbott Laboratories)
90
Abbott Laboratories modified schematic model
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.
Modified Schematic Model, supplied by Abbott Laboratories, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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modified schematic model - by Bioz Stars, 2026-04
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one-dimensional schematic of this material model  (Abaqus Inc)
90
Abaqus Inc one-dimensional schematic of this material model
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.
One Dimensional Schematic Of This Material Model, supplied by Abaqus Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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one-dimensional schematic of this material model - by Bioz Stars, 2026-04
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polans schematic eye model  (ZEMAX Development Corporation)
90
ZEMAX Development Corporation polans schematic eye model
<t>ZEMAX</t> ray trace model of individual subject where above descried parameters were adjusted A) Retinal imaging path of a single scan position with subject eye modeled using previously calculated subject position and axial length. A script moves the beam within the model and the chief ray vector position and angle at the retina is calculated and stored. B) Zoom of modified <t>Polans</t> eye model using axial length of the subject.
Polans Schematic Eye Model, supplied by ZEMAX Development Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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polans schematic eye model - by Bioz Stars, 2026-04
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schematic patient phantom model  (Fotofinder Systems GmbH)
90
Fotofinder Systems GmbH schematic patient phantom model
<t>ZEMAX</t> ray trace model of individual subject where above descried parameters were adjusted A) Retinal imaging path of a single scan position with subject eye modeled using previously calculated subject position and axial length. A script moves the beam within the model and the chief ray vector position and angle at the retina is calculated and stored. B) Zoom of modified <t>Polans</t> eye model using axial length of the subject.
Schematic Patient Phantom Model, supplied by Fotofinder Systems GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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schematic patient phantom model - by Bioz Stars, 2026-04
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schematic biomimetic model  (BioMimetic Therapeutics)
90
BioMimetic Therapeutics schematic biomimetic model
<t>ZEMAX</t> ray trace model of individual subject where above descried parameters were adjusted A) Retinal imaging path of a single scan position with subject eye modeled using previously calculated subject position and axial length. A script moves the beam within the model and the chief ray vector position and angle at the retina is calculated and stored. B) Zoom of modified <t>Polans</t> eye model using axial length of the subject.
Schematic Biomimetic Model, supplied by BioMimetic Therapeutics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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numerical model a) schematic b  (Abaqus Inc)
90
Abaqus Inc numerical model a) schematic b
<t>ZEMAX</t> ray trace model of individual subject where above descried parameters were adjusted A) Retinal imaging path of a single scan position with subject eye modeled using previously calculated subject position and axial length. A script moves the beam within the model and the chief ray vector position and angle at the retina is calculated and stored. B) Zoom of modified <t>Polans</t> eye model using axial length of the subject.
Numerical Model A) Schematic B, supplied by Abaqus Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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numerical model a) schematic b - by Bioz Stars, 2026-04
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schematic model for the evolution of the kvc  (Compex Inc)
90
Compex Inc schematic model for the evolution of the kvc
<t>ZEMAX</t> ray trace model of individual subject where above descried parameters were adjusted A) Retinal imaging path of a single scan position with subject eye modeled using previously calculated subject position and axial length. A script moves the beam within the model and the chief ray vector position and angle at the retina is calculated and stored. B) Zoom of modified <t>Polans</t> eye model using axial length of the subject.
Schematic Model For The Evolution Of The Kvc, supplied by Compex Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


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

ZEMAX ray trace model of individual subject where above descried parameters were adjusted A) Retinal imaging path of a single scan position with subject eye modeled using previously calculated subject position and axial length. A script moves the beam within the model and the chief ray vector position and angle at the retina is calculated and stored. B) Zoom of modified Polans eye model using axial length of the subject.

Journal: Biomedical Optics Express

Article Title: Wide-field whole eye OCT system with demonstration of quantitative retinal curvature estimation

doi: 10.1364/BOE.10.000338

Figure Lengend Snippet: ZEMAX ray trace model of individual subject where above descried parameters were adjusted A) Retinal imaging path of a single scan position with subject eye modeled using previously calculated subject position and axial length. A script moves the beam within the model and the chief ray vector position and angle at the retina is calculated and stored. B) Zoom of modified Polans eye model using axial length of the subject.

Article Snippet: Additionally, we utilized the Polans schematic eye model in our optical design [ 38 , 39 ] (ZEMAX model available in [ 39 ]).

Techniques: Imaging, Plasmid Preparation, Modification