Howard I. Scher
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View article: Genomic alterations in the YAP/TAZ pathway are associated with stem cell-like castration-resistant prostate cancer
Genomic alterations in the YAP/TAZ pathway are associated with stem cell-like castration-resistant prostate cancer Open
Castration-resistant prostate cancer (CRPC) is an aggressive disease exhibiting multiple epigenomic subtypes: androgen receptor-dependent CRPC-AR, and lineage plastic subtypes CRPC-SCL (stem cell-like), CRPC-WNT (Wnt-dependent), and CRPC-N…
View article: Molecular Imaging of Androgen Receptor Expression and Glycolysis as Biomarkers for Clinical Outcome for Metastatic Castration–Resistant Prostate Cancer
Molecular Imaging of Androgen Receptor Expression and Glycolysis as Biomarkers for Clinical Outcome for Metastatic Castration–Resistant Prostate Cancer Open
Purpose Patients with metastatic castration–resistant prostate cancer (mCRPC) with tumors that display disease heterogeneity, including features of androgen receptor (AR)–independence and/or lineage plasticity, have particularly poor outco…
View article: Recommended Clinical Context and Patient Context Data Elements for Liquid Biopsy Data Submitted to Data Repositories and Data Commons
Recommended Clinical Context and Patient Context Data Elements for Liquid Biopsy Data Submitted to Data Repositories and Data Commons Open
In 2020, BLOODPAC recommended 11 pre‐analytical minimal technical data elements for collection and submission of liquid biopsy data to public databases. This article expands on that work by recommending 22 clinical context and 10 patient c…
View article: Data from Advancing Global Health Equity in Oncology Clinical Trial Access
Data from Advancing Global Health Equity in Oncology Clinical Trial Access Open
Summary:Despite exponentially increased industry investment in oncology research and development with more than $80 billion spent annually, patient enrollment in clinical trials remains below 5% globally. Our multistakeholder international…
View article: Supplementary Figure 2 from Advancing Global Health Equity in Oncology Clinical Trial Access
Supplementary Figure 2 from Advancing Global Health Equity in Oncology Clinical Trial Access Open
Supplementary Figure 2: Number of cancer cases and deaths across geography in 2020, Millions
View article: Supplementary Table 1 from Advancing Global Health Equity in Oncology Clinical Trial Access
Supplementary Table 1 from Advancing Global Health Equity in Oncology Clinical Trial Access Open
Supplementary Table 1: Authors and affiliations
View article: Supplementary Figure 1 from Advancing Global Health Equity in Oncology Clinical Trial Access
Supplementary Figure 1 from Advancing Global Health Equity in Oncology Clinical Trial Access Open
Supplementary Figure 1: Number of cancer cases and deaths across indications in 2020, Millions
View article: Supplemental Figure S5 from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer
Supplemental Figure S5 from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer Open
Supplemental Figure S5. Top differentially expressed genes by expression level and statistical significance.
View article: Supplemental Figure S3 from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer
Supplemental Figure S3 from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer Open
Supplemental Figure S3. Top differentially activated GO pathways with ADT.
View article: Supplemental Figure S4 from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer
Supplemental Figure S4 from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer Open
Supplemental Figure S4. GO Activated Immune Response Genes.
View article: Supplemental Figure S1 from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer
Supplemental Figure S1 from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer Open
Supplemental Figure S1. Sample clustering by RNAseq and top differentially expressed genes by treatment group.
View article: Supplemental Figure S6 from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer
Supplemental Figure S6 from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer Open
Supplemental Figure S6. Spatial proximity between immune cells and tumor cells.
View article: Data from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer
Data from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer Open
Purpose:Androgen deprivation therapy (ADT) remains the backbone of prostate cancer treatment. Beyond the suppression of testosterone and tumor cell growth, emerging evidence suggests that ADT also modulates the immune tumor microenvironmen…
View article: Supplemental Figure S2 from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer
Supplemental Figure S2 from Androgen Deprivation Therapy Drives a Distinct Immune Phenotype in Localized Prostate Cancer Open
Supplemental Figure S2. Differential expression of androgen-related genes with or without degarelix.
View article: Automated real-world data integration improves cancer outcome prediction
Automated real-world data integration improves cancer outcome prediction Open
The digitization of health records and growing availability of tumour DNA sequencing provide an opportunity to study the determinants of cancer outcomes with unprecedented richness. Patient data are often stored in unstructured text and si…
View article: Fc-enhanced anti-CTLA-4 depletes tumor-infiltrating regulatory T cells to augment immune effects of androgen ablation in high-risk prostate cancer
Fc-enhanced anti-CTLA-4 depletes tumor-infiltrating regulatory T cells to augment immune effects of androgen ablation in high-risk prostate cancer Open
Despite high rates of post-surgical recurrence in men with high-risk localized prostate cancer (PCa), there is currently no role for neoadjuvant therapy. Tumor infiltrating regulatory T cells (TI-Tregs) limit the antitumor effects of presu…
View article: Supplemental Figure 1 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer
Supplemental Figure 1 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer Open
Supplemental Figure 1
View article: Supplemental Table 1 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer
Supplemental Table 1 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer Open
Supplemental Table 1
View article: Supplemental Figure 4 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer
Supplemental Figure 4 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer Open
Supplemental Figure 4
View article: Supplemental Table 3 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer
Supplemental Table 3 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer Open
Supplemental Table 3
View article: Supplemental Table 2 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer
Supplemental Table 2 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer Open
Supplemental Table 2
View article: Supplemental Figure 2 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer
Supplemental Figure 2 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer Open
Supplemental Figure 2
View article: Supplemental Table 1 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer
Supplemental Table 1 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer Open
Supplemental Table 1
View article: Supplemental Figure 2 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer
Supplemental Figure 2 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer Open
Supplemental Figure 2
View article: Supplemental Table 3 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer
Supplemental Table 3 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer Open
Supplemental Table 3
View article: Supplemental Figure 3 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer
Supplemental Figure 3 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer Open
Supplemental Figure 3
View article: Data from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer
Data from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer Open
Purpose:Patients with microsatellite instability–high/mismatch repair-deficient (MSI-H/dMMR) and high tumor mutational burden (TMB-H) prostate cancers are candidates for pembrolizumab. We define the genomic features, clinical course, and r…
View article: Supplemental Figure 4 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer
Supplemental Figure 4 from Microsatellite Instability, Tumor Mutational Burden, and Response to Immune Checkpoint Blockade in Patients with Prostate Cancer Open
Supplemental Figure 4