Ashley Frith
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View article: Supplementary Table 1 from Neoadjuvant BMS-813160, Nivolumab, Gemcitabine, and Nab-Paclitaxel for Patients with Pancreatic Cancer
Supplementary Table 1 from Neoadjuvant BMS-813160, Nivolumab, Gemcitabine, and Nab-Paclitaxel for Patients with Pancreatic Cancer Open
Supplementary Table 1. Antibodies used in flow cytometry.
View article: Data from Neoadjuvant BMS-813160, Nivolumab, Gemcitabine, and Nab-Paclitaxel for Patients with Pancreatic Cancer
Data from Neoadjuvant BMS-813160, Nivolumab, Gemcitabine, and Nab-Paclitaxel for Patients with Pancreatic Cancer Open
Purpose:Targeting tumor-associated macrophages through C–C chemokine receptor type 2 (CCR) in pancreatic ductal adenocarcinoma (PDAC) improves the efficacy of chemotherapy and restores T-cell immunity in preclinical models.Patients and Met…
View article: Supplementary Table 2 from Neoadjuvant BMS-813160, Nivolumab, Gemcitabine, and Nab-Paclitaxel for Patients with Pancreatic Cancer
Supplementary Table 2 from Neoadjuvant BMS-813160, Nivolumab, Gemcitabine, and Nab-Paclitaxel for Patients with Pancreatic Cancer Open
Supplementary Table 2. Representativeness of study participants.
View article: Supplementary Figure 1 from Neoadjuvant BMS-813160, Nivolumab, Gemcitabine, and Nab-Paclitaxel for Patients with Pancreatic Cancer
Supplementary Figure 1 from Neoadjuvant BMS-813160, Nivolumab, Gemcitabine, and Nab-Paclitaxel for Patients with Pancreatic Cancer Open
Supplementary Figure 1. Data supporting correlative analyses.
View article: Data from Detection of Circulating Tumor DNA Using a Tissue-Free Epigenomic Assay Is a Highly Prognostic Biomarker in Early-Stage Triple-Negative Breast Cancer
Data from Detection of Circulating Tumor DNA Using a Tissue-Free Epigenomic Assay Is a Highly Prognostic Biomarker in Early-Stage Triple-Negative Breast Cancer Open
Purpose:Clinical tools to monitor treatment response and metastatic risk could improve early-stage triple-negative breast cancer (TNBC) care. Although molecular residual disease assays show promise, their use in the neoadjuvant setting req…
View article: Supplementary Data 1 from Detection of Circulating Tumor DNA Using a Tissue-Free Epigenomic Assay Is a Highly Prognostic Biomarker in Early-Stage Triple-Negative Breast Cancer
Supplementary Data 1 from Detection of Circulating Tumor DNA Using a Tissue-Free Epigenomic Assay Is a Highly Prognostic Biomarker in Early-Stage Triple-Negative Breast Cancer Open
Supplementary Figures S1-S5
View article: Supplemental Table S1 from Detection of Circulating Tumor DNA Using a Tissue-Free Epigenomic Assay Is a Highly Prognostic Biomarker in Early-Stage Triple-Negative Breast Cancer
Supplemental Table S1 from Detection of Circulating Tumor DNA Using a Tissue-Free Epigenomic Assay Is a Highly Prognostic Biomarker in Early-Stage Triple-Negative Breast Cancer Open
Details of patient-level evaluable samples
View article: Neoadjuvant BMS-813160, Nivolumab, Gemcitabine, and Nab-Paclitaxel for Patients with Pancreatic Cancer
Neoadjuvant BMS-813160, Nivolumab, Gemcitabine, and Nab-Paclitaxel for Patients with Pancreatic Cancer Open
Purpose: Targeting tumor-associated macrophages through C–C chemokine receptor type 2 (CCR) in pancreatic ductal adenocarcinoma (PDAC) improves the efficacy of chemotherapy and restores T-cell immunity in preclinical models. Patients and M…
View article: Supplementary Data S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Data S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
DNA sequencing data summary.
View article: Supplementary Table 2 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Table 2 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Patient demographics.
View article: Supplementary Methods S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Methods S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Supplementary Methods
View article: Supplementary Table 1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Table 1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
PredicineATLAS gene panel.
View article: Supplementary Figures S1-S15 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Figures S1-S15 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Supplementary Figure S1. High bTMB is associated with the presence of specific mutations.Supplementary Figure S2. ROC analysis to determine optimal bTMB cutoff.Supplementary Figure S3. High correlation between bTMB determined from WES and …
View article: Supplementary Table 3 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Table 3 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Gene alterations associated with shorter PFS.
View article: Supplementary Table 1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Table 1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
PredicineATLAS gene panel.
View article: Supplementary Table 2 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Table 2 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Patient demographics.
View article: Supplementary Data S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Data S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
DNA sequencing data summary.
View article: Supplementary Methods S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Methods S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Supplementary Methods
View article: Supplementary Table 3 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Table 3 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Gene alterations associated with shorter PFS.
View article: Supplementary Figures S1-S15 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Figures S1-S15 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Supplementary Figure S1. High bTMB is associated with the presence of specific mutations.Supplementary Figure S2. ROC analysis to determine optimal bTMB cutoff.Supplementary Figure S3. High correlation between bTMB determined from WES and …
View article: Supplementary Methods S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Methods S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Supplementary Methods
View article: Supplementary Table 2 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Table 2 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Patient demographics.
View article: Supplementary Table 1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Table 1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
PredicineATLAS gene panel.
View article: Supplementary Table 3 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Table 3 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Gene alterations associated with shorter PFS.
View article: Supplementary Data S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Data S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
DNA sequencing data summary.
View article: Supplementary Table 1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Table 1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
PredicineATLAS gene panel.
View article: Supplementary Figures S1-S15 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Figures S1-S15 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Supplementary Figure S1. High bTMB is associated with the presence of specific mutations.Supplementary Figure S2. ROC analysis to determine optimal bTMB cutoff.Supplementary Figure S3. High correlation between bTMB determined from WES and …
View article: Data from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Data from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Purpose:Clinical biomarkers to identify patients unlikely to benefit from CDK4/6 inhibition (CDK4/6i) in combination with endocrine therapy (ET) are lacking. We implemented a comprehensive circulating tumor DNA (ctDNA) analysis to identify…
View article: Supplementary Figures S1-S15 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Figures S1-S15 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Supplementary Figure S1. High bTMB is associated with the presence of specific mutations.Supplementary Figure S2. ROC analysis to determine optimal bTMB cutoff.Supplementary Figure S3. High correlation between bTMB determined from WES and …
View article: Supplementary Methods S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Supplementary Methods S1 from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer Open
Supplementary Methods