Suzanne Hector
YOU?
Author Swipe
View article: Supplementary Table 7 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 7 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 11K, Results from KEGG pathway analysis for p53 wild-type and p53 null basal comparison. The table shows the number of genes in each pathway and the p value associated with that pathway calculated using hypergeometric statistics…
View article: Supplementary Table 6 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 6 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 35K, Real-time PCR validation of HCT116 p53 null cells following treatment with 5nM SN38 for 6, 12 and 24h. This table shows the Pearson's correlation and p values for each individual gene
View article: Data from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Data from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
The topoisomerase I inhibitor irinotecan is used to treat advanced colorectal cancer and has been shown to have p53-independent anticancer activity. The aim of this study was to identify the p53-independent signaling mechanisms activated b…
View article: Supplementary Table 4 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 4 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 214K, List showing 2102 genes that are constitutively altered between isogenic HCT116 p53wild-type and HCT116 p53null cells. Genes have been normalised and filtered as stated in the materials and methods
View article: Supplementary Table 6 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 6 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 35K, Real-time PCR validation of HCT116 p53 null cells following treatment with 5nM SN38 for 6, 12 and 24h. This table shows the Pearson's correlation and p values for each individual gene
View article: Supplementary Table 2 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 2 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 321K, List showing 2544 genes that are uniquely altered following SN38 treatment over time in HCT116 p53wild-type cells only. Genes have been normalised and filtered as stated in the materials and methods
View article: Supplementary Table 7 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 7 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 11K, Results from KEGG pathway analysis for p53 wild-type and p53 null basal comparison. The table shows the number of genes in each pathway and the p value associated with that pathway calculated using hypergeometric statistics…
View article: Supplementary Table 3 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 3 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 261K, List showing 1986 genes that are uniquely altered following SN38 treatment over time in HCT116 p53null cells only. Genes have been normalised and filtered as stated in the materials and methods
View article: Supplementary Table 5 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 5 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 11K, Real-time PCR validation of genes basally altered between HCT116 p53 null cells and HCT116 p53 wild-type cells. This table shows the p53 null fold change by microarray and the p53 null fold change by real-time PCR, all comp…
View article: Supplementary Table 3 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 3 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 261K, List showing 1986 genes that are uniquely altered following SN38 treatment over time in HCT116 p53null cells only. Genes have been normalised and filtered as stated in the materials and methods
View article: Data from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Data from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
The topoisomerase I inhibitor irinotecan is used to treat advanced colorectal cancer and has been shown to have p53-independent anticancer activity. The aim of this study was to identify the p53-independent signaling mechanisms activated b…
View article: Supplementary Table 1 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 1 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 132K, List showing 752 genes that are commonly altered following SN38 treatment over time in isogenic HCT116 p53wild-type and HCT116 p53null cells. Genes have been normalised and filtered as stated in the materials and methods
View article: Supplementary Table 5 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 5 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 11K, Real-time PCR validation of genes basally altered between HCT116 p53 null cells and HCT116 p53 wild-type cells. This table shows the p53 null fold change by microarray and the p53 null fold change by real-time PCR, all comp…
View article: Supplementary Table 2 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 2 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 321K, List showing 2544 genes that are uniquely altered following SN38 treatment over time in HCT116 p53wild-type cells only. Genes have been normalised and filtered as stated in the materials and methods
View article: Supplementary Table 4 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 4 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 214K, List showing 2102 genes that are constitutively altered between isogenic HCT116 p53wild-type and HCT116 p53null cells. Genes have been normalised and filtered as stated in the materials and methods
View article: Supplementary Table 1 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells
Supplementary Table 1 from Pharmacogenomic Profiling and Pathway Analyses Identify MAPK-Dependent Migration as an Acute Response to SN38 in p53 Null and p53-Mutant Colorectal Cancer Cells Open
PDF file - 132K, List showing 752 genes that are commonly altered following SN38 treatment over time in isogenic HCT116 p53wild-type and HCT116 p53null cells. Genes have been normalised and filtered as stated in the materials and methods
View article: Supplementary Figure 3 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy
Supplementary Figure 3 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy Open
PDF file - 52K, Systems modeling can act as a clinical tool to determine therapeutic windows and to assess adjuvant treatments.
View article: Supplementary Figure 2 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy
Supplementary Figure 2 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy Open
PDF file - 53K, Temporal protein profiles for HCT-116 cells.
View article: Data from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy
Data from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy Open
Apoptotic desensitization is a hallmark of cancer cells, but present knowledge of molecular systems controlling apoptosis has yet to provide significant prognostic insights. Here, we report findings from a systems study of the intrinsic pa…
View article: Supplementary Methods, Figure Legends, Tables 1 - 9 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy
Supplementary Methods, Figure Legends, Tables 1 - 9 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy Open
PDF file - 237K, Supplementary Table 1: Translation of protein interactions into Ordinary Differential Equations. Supplementary Table 2: Pseudo-reactions for degradation and degradation rates as used in the model. Supplementary Table 3: Ps…
View article: Supplementary Methods, Figure Legends, Tables 1 - 9 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy
Supplementary Methods, Figure Legends, Tables 1 - 9 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy Open
PDF file - 237K, Supplementary Table 1: Translation of protein interactions into Ordinary Differential Equations. Supplementary Table 2: Pseudo-reactions for degradation and degradation rates as used in the model. Supplementary Table 3: Ps…
View article: Supplementary Figure 3 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy
Supplementary Figure 3 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy Open
PDF file - 52K, Systems modeling can act as a clinical tool to determine therapeutic windows and to assess adjuvant treatments.
View article: Data from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy
Data from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy Open
Apoptotic desensitization is a hallmark of cancer cells, but present knowledge of molecular systems controlling apoptosis has yet to provide significant prognostic insights. Here, we report findings from a systems study of the intrinsic pa…
View article: Supplementary Figure 1 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy
Supplementary Figure 1 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy Open
PDF file - 66K, Temporal protein profiles for HeLa cells.
View article: Supplementary Figure 1 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy
Supplementary Figure 1 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy Open
PDF file - 66K, Temporal protein profiles for HeLa cells.
View article: Supplementary Figure 2 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy
Supplementary Figure 2 from Systems Analysis of BCL2 Protein Family Interactions Establishes a Model to Predict Responses to Chemotherapy Open
PDF file - 53K, Temporal protein profiles for HCT-116 cells.
View article: A Novel Positron Emission Tomography (PET) Approach to Monitor Cardiac Metabolic Pathway Remodeling in Response to Sunitinib Malate
A Novel Positron Emission Tomography (PET) Approach to Monitor Cardiac Metabolic Pathway Remodeling in Response to Sunitinib Malate Open
Sunitinib is a tyrosine kinase inhibitor approved for the treatment of multiple solid tumors. However, cardiotoxicity is of increasing concern, with a need to develop rational mechanism driven approaches for the early detection of cardiac …
View article: Erratum to: Calnexin, an ER stress-induced protein, is a prognostic marker and potential therapeutic target in colorectal cancer
Erratum to: Calnexin, an ER stress-induced protein, is a prognostic marker and potential therapeutic target in colorectal cancer Open
View article: Calnexin, an ER-induced protein, is a prognostic marker and potential therapeutic target in colorectal cancer
Calnexin, an ER-induced protein, is a prognostic marker and potential therapeutic target in colorectal cancer Open