Aaron Cranston
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USP7 inhibitors suppress tumour neoangiogenesis and promote synergy with immune checkpoint inhibitors by downregulating fibroblast VEGF Open
Background Understanding how to modulate the microenvironment of tumors that are resistant to immune checkpoint inhibitors represents a major challenge in oncology.Here we investigate the ability of USP7 inhibitors to reprogram the tumor m…
View article: Supplementary Figure Legends 1-10 from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors
Supplementary Figure Legends 1-10 from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors Open
PDF file - 86K
View article: Supplementary Tables 1-2 from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors
Supplementary Tables 1-2 from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors Open
PDF file - 28K, Information on all antibodies and primers that were used in this study
View article: Supplementary Tables 1-2 from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors
Supplementary Tables 1-2 from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors Open
PDF file - 28K, Information on all antibodies and primers that were used in this study
View article: Supplementary Figures 1-10 from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors
Supplementary Figures 1-10 from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors Open
PDF file - 1.2MB, This file contains additional data on tumor responses to olaparib treatment (Fig. S1 and S2), pH2AX stainings on treated and untreated tumors (Fig. S3), analysis of mutations in 53BP1 (Fig. S4 and S7B), characterization o…
View article: Data from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors
Data from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors Open
Inhibition of PARP is a promising therapeutic strategy for homologous recombination–deficient tumors, such as BRCA1-associated cancers. We previously reported that BRCA1-deficient mouse mammary tumors may acquire resistance to the clinical…
View article: Data from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors
Data from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors Open
Inhibition of PARP is a promising therapeutic strategy for homologous recombination–deficient tumors, such as BRCA1-associated cancers. We previously reported that BRCA1-deficient mouse mammary tumors may acquire resistance to the clinical…
View article: Supplementary Figure Legends 1-10 from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors
Supplementary Figure Legends 1-10 from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors Open
PDF file - 86K
View article: Supplementary Figures 1-10 from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors
Supplementary Figures 1-10 from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors Open
PDF file - 1.2MB, This file contains additional data on tumor responses to olaparib treatment (Fig. S1 and S2), pH2AX stainings on treated and untreated tumors (Fig. S3), analysis of mutations in 53BP1 (Fig. S4 and S7B), characterization o…
Data from Tumor Growth Inhibition by Olaparib in <i>BRCA2</i> Germline-Mutated Patient-Derived Ovarian Cancer Tissue Xenografts Open
Purpose: Most patients with ovarian carcinomas succumb to their disease and there is a critical need for improved therapeutic approaches. Carcinomas arising in BRCA mutation carriers display defective DNA double-strand break repair that ca…
Supplementary Figure S1 from Tumor Growth Inhibition by Olaparib in <i>BRCA2</i> Germline-Mutated Patient-Derived Ovarian Cancer Tissue Xenografts Open
Supplementary Figure S1.
Supplementary Figure S1 from Tumor Growth Inhibition by Olaparib in <i>BRCA2</i> Germline-Mutated Patient-Derived Ovarian Cancer Tissue Xenografts Open
Supplementary Figure S1.
Supplementary Materials and Methods, Supplementary Tables 1 through 3, and Supplementary Figure 1 from The PARP Inhibitor AZD2461 Provides Insights into the Role of PARP3 Inhibition for Both Synthetic Lethality and Tolerability with Chemotherapy in Preclinical Models Open
Supplementary materials and methods. Suppl Table 1. MMS combination PF50 cell line assays. Concentration-dependent potentiation of MMS (PF50 ratios). Suppl Table 2. Permeability of AZD2461 and olaparib were assessed. Suppl Table 3. Activit…
Data from Tumor Growth Inhibition by Olaparib in <i>BRCA2</i> Germline-Mutated Patient-Derived Ovarian Cancer Tissue Xenografts Open
Purpose: Most patients with ovarian carcinomas succumb to their disease and there is a critical need for improved therapeutic approaches. Carcinomas arising in BRCA mutation carriers display defective DNA double-strand break repair that ca…
Data from The PARP Inhibitor AZD2461 Provides Insights into the Role of PARP3 Inhibition for Both Synthetic Lethality and Tolerability with Chemotherapy in Preclinical Models Open
The PARP inhibitor AZD2461 was developed as a next-generation agent following olaparib, the first PARP inhibitor approved for cancer therapy. In BRCA1-deficient mouse models, olaparib resistance predominantly involves overexpression of P-g…
Data from The PARP Inhibitor AZD2461 Provides Insights into the Role of PARP3 Inhibition for Both Synthetic Lethality and Tolerability with Chemotherapy in Preclinical Models Open
The PARP inhibitor AZD2461 was developed as a next-generation agent following olaparib, the first PARP inhibitor approved for cancer therapy. In BRCA1-deficient mouse models, olaparib resistance predominantly involves overexpression of P-g…
Supplementary Materials and Methods, Supplementary Tables 1 through 3, and Supplementary Figure 1 from The PARP Inhibitor AZD2461 Provides Insights into the Role of PARP3 Inhibition for Both Synthetic Lethality and Tolerability with Chemotherapy in Preclinical Models Open
Supplementary materials and methods. Suppl Table 1. MMS combination PF50 cell line assays. Concentration-dependent potentiation of MMS (PF50 ratios). Suppl Table 2. Permeability of AZD2461 and olaparib were assessed. Suppl Table 3. Activit…
Data from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous <i>Brca2/p53</i>-Mutant Mammary Tumors <i>In vivo</i> and Delays Tumor Relapse in Combination with Carboplatin Open
Germ-line heterozygosity of the BRCA2 gene in women predisposes to breast and ovarian cancers. Successful therapies targeted specifically at these neoplasms have thus far remained elusive. Recent studies in mice have shown that inhibition …
Supplementary Table 2 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous <i>Brca2/p53</i>-Mutant Mammary Tumors <i>In vivo</i> and Delays Tumor Relapse in Combination with Carboplatin Open
Supplementary Table 2 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous Brca2/p53-Mutant Mammary Tumors In vivo and Delays Tumor Relapse in Combination with Carboplatin
Supplementary Figure 1 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous <i>Brca2/p53</i>-Mutant Mammary Tumors <i>In vivo</i> and Delays Tumor Relapse in Combination with Carboplatin Open
Supplementary Figure 1 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous Brca2/p53-Mutant Mammary Tumors In vivo and Delays Tumor Relapse in Combination with Carboplatin
Supplementary Figure 2 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous <i>Brca2/p53</i>-Mutant Mammary Tumors <i>In vivo</i> and Delays Tumor Relapse in Combination with Carboplatin Open
Supplementary Figure 2 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous Brca2/p53-Mutant Mammary Tumors In vivo and Delays Tumor Relapse in Combination with Carboplatin
Supplementary Table 1 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous <i>Brca2/p53</i>-Mutant Mammary Tumors <i>In vivo</i> and Delays Tumor Relapse in Combination with Carboplatin Open
Supplementary Table 1 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous Brca2/p53-Mutant Mammary Tumors In vivo and Delays Tumor Relapse in Combination with Carboplatin
Data from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous <i>Brca2/p53</i>-Mutant Mammary Tumors <i>In vivo</i> and Delays Tumor Relapse in Combination with Carboplatin Open
Germ-line heterozygosity of the BRCA2 gene in women predisposes to breast and ovarian cancers. Successful therapies targeted specifically at these neoplasms have thus far remained elusive. Recent studies in mice have shown that inhibition …
Supplementary Table 2 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous <i>Brca2/p53</i>-Mutant Mammary Tumors <i>In vivo</i> and Delays Tumor Relapse in Combination with Carboplatin Open
Supplementary Table 2 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous Brca2/p53-Mutant Mammary Tumors In vivo and Delays Tumor Relapse in Combination with Carboplatin
Supplementary Figure 2 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous <i>Brca2/p53</i>-Mutant Mammary Tumors <i>In vivo</i> and Delays Tumor Relapse in Combination with Carboplatin Open
Supplementary Figure 2 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous Brca2/p53-Mutant Mammary Tumors In vivo and Delays Tumor Relapse in Combination with Carboplatin
Supplementary Table 1 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous <i>Brca2/p53</i>-Mutant Mammary Tumors <i>In vivo</i> and Delays Tumor Relapse in Combination with Carboplatin Open
Supplementary Table 1 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous Brca2/p53-Mutant Mammary Tumors In vivo and Delays Tumor Relapse in Combination with Carboplatin
Supplementary Figure 1 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous <i>Brca2/p53</i>-Mutant Mammary Tumors <i>In vivo</i> and Delays Tumor Relapse in Combination with Carboplatin Open
Supplementary Figure 1 from Poly(ADP-Ribose) Polymerase-1 Inhibitor Treatment Regresses Autochthonous Brca2/p53-Mutant Mammary Tumors In vivo and Delays Tumor Relapse in Combination with Carboplatin
A Three-Dimensional <i>In Vitro</i> Coculture Model to Quantify Breast Epithelial Cell Adhesion to Endothelial Cells Open
Three-dimensional (3D) in vitro culture models better recapitulate the tissue microenvironment, and therefore may provide a better platform to evaluate therapeutic effects on adhesive cell-cell interactions. The objective of this study was…