Margaret A. Knowles
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View article: <i>CHP2</i> Modifies Chronic <i>Pseudomonas aeruginosa</i> Airway Infection Risk in Cystic Fibrosis
<i>CHP2</i> Modifies Chronic <i>Pseudomonas aeruginosa</i> Airway Infection Risk in Cystic Fibrosis Open
Rationale: Chronic Pseudomonas aeruginosa (Pa) airway infection is common and a key contributor to diminished lung function and early mortality in persons with cystic fibrosis (PwCF). Risk factors for chronic Pa…
View article: Modelling and breaking down the biophysical barriers to drug delivery in pancreatic cancer
Modelling and breaking down the biophysical barriers to drug delivery in pancreatic cancer Open
Developing tumour models that recapitulate the biophysical barriers that lead to drug resistance in cancer is critical in assessing new drugs and delivery mechanisms.
View article: Bladder cancer
Bladder cancer Open
View article: Affimer-mediated locking of p21-activated kinase 5 in an intermediate activation state results in kinase inhibition
Affimer-mediated locking of p21-activated kinase 5 in an intermediate activation state results in kinase inhibition Open
Kinases are important therapeutic targets, and their inhibitors are classified according to their mechanism of action, which range from blocking ATP binding to covalent inhibition. Here, a mechanism of inhibition is highlighted by capturin…
View article: Index
Index Open
This timely Research Handbook provides a comprehensive and transdisciplinary overview of current research in the field of health leadership. Emphasising diverse perspectives and under-explored issues, it calls for a sustainable future embr…
View article: Supplementary Figure 1 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Supplementary Figure 1 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Supplementary Figure 1 - PDF file 573K, Analysis of siRNA screen results
View article: Supplementary Tables S1-S2 from Genes Involved in Differentiation, Stem Cell Renewal, and Tumorigenesis Are Modulated in Telomerase-Immortalized Human Urothelial Cells
Supplementary Tables S1-S2 from Genes Involved in Differentiation, Stem Cell Renewal, and Tumorigenesis Are Modulated in Telomerase-Immortalized Human Urothelial Cells Open
Supplementary Tables S1-S2 from Genes Involved in Differentiation, Stem Cell Renewal, and Tumorigenesis Are Modulated in Telomerase-Immortalized Human Urothelial Cells
View article: Data from Genes Involved in Differentiation, Stem Cell Renewal, and Tumorigenesis Are Modulated in Telomerase-Immortalized Human Urothelial Cells
Data from Genes Involved in Differentiation, Stem Cell Renewal, and Tumorigenesis Are Modulated in Telomerase-Immortalized Human Urothelial Cells Open
The expression of hTERT, the catalytic subunit of telomerase, immortalizes normal human urothelial cells (NHUC). Expression of a modified hTERT, without the ability to act in telomere maintenance, did not immortalize NHUC, confirming that …
View article: Data from FGFR3 Translocations in Bladder Cancer: Differential Sensitivity to HSP90 Inhibition Based on Drug Metabolism
Data from FGFR3 Translocations in Bladder Cancer: Differential Sensitivity to HSP90 Inhibition Based on Drug Metabolism Open
Activating mutations and/or overexpression of FGFR3 are common in bladder cancer, making FGFR3 an attractive therapeutic target in this disease. In addition, FGFR3 gene rearrangements have recently been described that define a uniqu…
View article: Supplementary Figure Legends from FGFR3 Translocations in Bladder Cancer: Differential Sensitivity to HSP90 Inhibition Based on Drug Metabolism
Supplementary Figure Legends from FGFR3 Translocations in Bladder Cancer: Differential Sensitivity to HSP90 Inhibition Based on Drug Metabolism Open
PDF - 59K, Supplementary Figure Legends.
View article: Data from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Data from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Activation of fibroblast growth factor receptors (FGFR) is a common oncogenic event. Little is known about the determinants of sensitivity to FGFR inhibition and how these may vary between different oncogenic FGFRs. Using parallel RNA inte…
View article: Supplementary Figure Legends from FGFR3 Translocations in Bladder Cancer: Differential Sensitivity to HSP90 Inhibition Based on Drug Metabolism
Supplementary Figure Legends from FGFR3 Translocations in Bladder Cancer: Differential Sensitivity to HSP90 Inhibition Based on Drug Metabolism Open
PDF - 59K, Supplementary Figure Legends.
View article: Supplementary Figure 3 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Supplementary Figure 3 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Supplementary Figure 3 - PDF file 87K, Analysis of cell cycle and apoptosis of FGFR and EGFR combination inhibition
View article: Supplementary Figure 6 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Supplementary Figure 6 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Supplementary Figure 6 - PDF file 123K, Mouse weights from xenograft experiments
View article: Data from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Data from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Activation of fibroblast growth factor receptors (FGFR) is a common oncogenic event. Little is known about the determinants of sensitivity to FGFR inhibition and how these may vary between different oncogenic FGFRs. Using parallel RNA inte…
View article: Supplementary Tables 1,2,3 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Supplementary Tables 1,2,3 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Supplementary Tables 1,2,3 - PDF file 283K, Details of cell lines included in siRNA screen and processed data from screen
View article: Supplementary Figure 2 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Supplementary Figure 2 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Supplementary Figure 2 - PDF file 649K, Efficacy of combined targeting of EGFR and FGFR3
View article: Supplementary Tables 1,2,3 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Supplementary Tables 1,2,3 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Supplementary Tables 1,2,3 - PDF file 283K, Details of cell lines included in siRNA screen and processed data from screen
View article: Supplementary Figure 4 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Supplementary Figure 4 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Supplementary Figure 4 - PDF file 354K, Analysis of the effects on combined EGFR and FGFR3 inhibition, and mechanism of EGFR upregulation by FGFR inhibitors
View article: Supplementary Figure 1 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Supplementary Figure 1 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Supplementary Figure 1 - PDF file 573K, Analysis of siRNA screen results
View article: Supplementary Figure 7 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Supplementary Figure 7 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Supplementary Figure 7 - PDF file 36K, Expression of EGFR and HGF from a publically available bladder cancer gene expression data set
View article: Supplementary Figure 2 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Supplementary Figure 2 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Supplementary Figure 2 - PDF file 649K, Efficacy of combined targeting of EGFR and FGFR3
View article: Supplementary Figure 5 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Supplementary Figure 5 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Supplementary Figure 5 - PDF file 243K, Analysis of FGFR3 mRNA and protein in 97-7 cells
View article: Supplementary Table 1 from FGFR3 Translocations in Bladder Cancer: Differential Sensitivity to HSP90 Inhibition Based on Drug Metabolism
Supplementary Table 1 from FGFR3 Translocations in Bladder Cancer: Differential Sensitivity to HSP90 Inhibition Based on Drug Metabolism Open
PDF - 67K, FGFR3 fusion-positive bladder cell line sensitivity and metabolism profiles of targeted anticancer compounds.
View article: Supplementary Figure 6 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Supplementary Figure 6 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Supplementary Figure 6 - PDF file 123K, Mouse weights from xenograft experiments
View article: Supplementary Table 1 from Alteration of Cell–Cell and Cell–Matrix Adhesion in Urothelial Cells: An Oncogenic Mechanism for Mutant FGFR3
Supplementary Table 1 from Alteration of Cell–Cell and Cell–Matrix Adhesion in Urothelial Cells: An Oncogenic Mechanism for Mutant FGFR3 Open
Supplementary Table 1. Clinico-pathological characteristics and FGFR3 mutation status of the tumours used for the mRNA study
View article: Supplementary Figure 3 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer
Supplementary Figure 3 from Parallel RNA Interference Screens Identify EGFR Activation as an Escape Mechanism in <i>FGFR3</i>-Mutant Cancer Open
Supplementary Figure 3 - PDF file 87K, Analysis of cell cycle and apoptosis of FGFR and EGFR combination inhibition
View article: Supplementary Figure 1 from FGFR3 Translocations in Bladder Cancer: Differential Sensitivity to HSP90 Inhibition Based on Drug Metabolism
Supplementary Figure 1 from FGFR3 Translocations in Bladder Cancer: Differential Sensitivity to HSP90 Inhibition Based on Drug Metabolism Open
PDF - 667K, Ganetespib treatment overcomes the FGFR inhibitor resistant phenotype in FGFR3 mutant bladder cancer cell lines.
View article: Data from Genes Involved in Differentiation, Stem Cell Renewal, and Tumorigenesis Are Modulated in Telomerase-Immortalized Human Urothelial Cells
Data from Genes Involved in Differentiation, Stem Cell Renewal, and Tumorigenesis Are Modulated in Telomerase-Immortalized Human Urothelial Cells Open
The expression of hTERT, the catalytic subunit of telomerase, immortalizes normal human urothelial cells (NHUC). Expression of a modified hTERT, without the ability to act in telomere maintenance, did not immortalize NHUC, confirming that …
View article: Supplementary Tables S1-S2 from Genes Involved in Differentiation, Stem Cell Renewal, and Tumorigenesis Are Modulated in Telomerase-Immortalized Human Urothelial Cells
Supplementary Tables S1-S2 from Genes Involved in Differentiation, Stem Cell Renewal, and Tumorigenesis Are Modulated in Telomerase-Immortalized Human Urothelial Cells Open
Supplementary Tables S1-S2 from Genes Involved in Differentiation, Stem Cell Renewal, and Tumorigenesis Are Modulated in Telomerase-Immortalized Human Urothelial Cells