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View article: Biomarker analysis to unravel mechanisms of resistance to glofitamab monotherapy in large B cell lymphoma
Biomarker analysis to unravel mechanisms of resistance to glofitamab monotherapy in large B cell lymphoma Open
Background: Glofitamab, a CD20-CD3 T-cell bispecific, has demonstrated high and durable complete responses (CR) in patients (pts) with aggressive Non-Hodgkin Lymphoma (NHL). Glofitamab monotherapy is approved for relapsed or refractory dif…
View article: Supplementary Table 8 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Supplementary Table 8 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Supplementary Table 8. This table summarizes the results of PI3K-AKT pathway signature analysis across multiple single-cell datasets (both published and unpublished). The table reports median and mean Z-scores from GSEA (Gene Set Enrichmen…
View article: Supplementary Table 3 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Supplementary Table 3 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Supplementary Table 3. Table lists genes comprissing of prostate cancer relevant gene signatures curated from the literature.
View article: Supplementary Table 7 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Supplementary Table 7 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Supplementary Table 7. This table compares the frequency of altertations in AR, TP53 and PTEN in patients with mHSPC and mCRPC. Data are evaluated separately for ctDNA (liquid biopsy) and tumor biopsy cohorts.
View article: Supplementary Table 6 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Supplementary Table 6 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Supplementary Table 6. This table presents a comparison of genetic alteration prevalence between ctDNA (liquid biopsy) and tumor biopsy mCRPC cohorts.
View article: Data from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Data from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Purpose:Many preclinical hypotheses, including reciprocal feedback activation between the androgen receptor (AR)–PI3K pathway in PTEN loss and AR signaling inhibitor–induced “BRCAness” regardless of BRCA1/2 status, have struggled to transl…
View article: Supplementary Figure 1 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Supplementary Figure 1 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Supplementary Figure 1. Exploration of mHSPC and mCRPC cohort.
View article: Supplementary Figure 3 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Supplementary Figure 3 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Supplementary Figure 3. Evolution of PI3K-AKT and AR pathway.
View article: Supplementary Table 4 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Supplementary Table 4 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Supplementary Table 4. This table summarizes key demographic and geographic considerations for the prostate cancer cohort studied.
View article: Supplementary Figure 4 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Supplementary Figure 4 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Supplementary Figure 4. Investigation of reciprocal feedback regulation between AR and PI3K-AKT signaling in in vitro cell lines using AR inhibitors and AR degrader.
View article: Supplementary Table 5 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Supplementary Table 5 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Supplementary Table 5. This table presents a comparison of genetic alteration prevalence between ctDNA (liquid biopsy) and tumor biopsy mHSPC cohorts.
View article: Supplementary Figure 2 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Supplementary Figure 2 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Supplementary Figure 2. Exploration of PI3K-AKT genetic pathway alteration and gene signature in clinical and published single cell dataset.
View article: Supplementary Table 2 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Supplementary Table 2 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Supplementary Table 2. Following analysis details protein coding genes and their pearsons correlation with PTEN IHC amongst prostate tumor tissue collected from patients enrolled in the IPATential150 trial.
View article: Supplementary Table 1 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Supplementary Table 1 from Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Supplementary Table 1. This table contains the genes comprising the pathway gene signature used to evaluate genetic alterations in prostate cancer specimens.
View article: Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer
Clinical Context Shapes the Relationship between Genomic Alterations and Response to AR Inhibitors and Chemotherapy in Metastatic Prostate Cancer Open
Purpose: Many preclinical hypotheses, including reciprocal feedback activation between the androgen receptor (AR)–PI3K pathway in PTEN loss and AR signaling inhibitor–induced “BRCAness” regardless of BRCA1/2 status, have struggled to trans…
View article: Final Overall Survival and Molecular Data Associated with Clinical Outcomes in Patients Receiving Ipatasertib and Abiraterone in the Phase 3 IPATential150 Trial
Final Overall Survival and Molecular Data Associated with Clinical Outcomes in Patients Receiving Ipatasertib and Abiraterone in the Phase 3 IPATential150 Trial Open
Ipatasertib addition to abiraterone did not improve OS for men with mCRPC, regardless of PTEN status on IHC. Exploratory biomarker analyses identified additional genomic alterations of potential clinical relevance for AKT blockade in mCRPC…
View article: SPEX: A modular end-to-end platform for high-plex tissue spatial omics analysis
SPEX: A modular end-to-end platform for high-plex tissue spatial omics analysis Open
Recent advancements in transcriptomics and proteomics have opened the possibility for spatially resolved molecular characterization of tissue architecture with the promise of enabling a deeper understanding of tissue biology in either home…
View article: Evaluating the effectiveness of a mobile app-based self-guided psychological interventions to reduce relapse in substance use disorder: protocol for a randomized controlled trial
Evaluating the effectiveness of a mobile app-based self-guided psychological interventions to reduce relapse in substance use disorder: protocol for a randomized controlled trial Open
Background Substance Use Disorder (SUD) persists as a significant public health challenge worldwide, with an estimated prevalence of approximately 10-15% across the global populace. This condition is characterized by a notably high risk of…
View article: Primary results and characterization of patients with exceptional outcomes in a phase 1b study combining PARP and MEK inhibition, with or without anti–PD‐L1, for <i>BRCA</i> wild‐type, platinum‐sensitive, recurrent ovarian cancer
Primary results and characterization of patients with exceptional outcomes in a phase 1b study combining PARP and MEK inhibition, with or without anti–PD‐L1, for <i>BRCA</i> wild‐type, platinum‐sensitive, recurrent ovarian cancer Open
Background This phase 1b study (ClinicalTrials.gov identifier NCT03695380) evaluated regimens combining PARP and MEK inhibition, with or without PD‐L1 inhibition, for BRCA wild‐type, platinum‐sensitive, recurrent ovarian cancer (PSROC). Me…
View article: Automated rendering of multi-stranded DNA complexes with pseudoknots
Automated rendering of multi-stranded DNA complexes with pseudoknots Open
We present a general method for rendering representations of multi-stranded DNA complexes from textual descriptions into 2D diagrams. The complexes can be arbitrarily pseudoknotted, and if a planar rendering is possible, the method will de…
View article: Evaluating the effectiveness of mobile app-based self-guided psychological intervention to reduce craving and lapse risk in problematic substance use and behaviors: Protocol for a randomized control trial in the general population
Evaluating the effectiveness of mobile app-based self-guided psychological intervention to reduce craving and lapse risk in problematic substance use and behaviors: Protocol for a randomized control trial in the general population Open
[https://clinicaltrials.gov/], identifier [NCT054 34,429].
View article: 99P Exploratory analysis of differential gene expression (DGE) and non-negative matrix factorisation (NMF) clustering in KATHERINE: Adjuvant trastuzumab emtansine (T-DM1) vs trastuzumab (H) in patients with HER2-positive residual invasive breast cancer after neoadjuvant treatment (NAT)
99P Exploratory analysis of differential gene expression (DGE) and non-negative matrix factorisation (NMF) clustering in KATHERINE: Adjuvant trastuzumab emtansine (T-DM1) vs trastuzumab (H) in patients with HER2-positive residual invasive breast cancer after neoadjuvant treatment (NAT) Open
This exploratory biomarker analysis aimed to identify prognostic gene sets in the. T-DM1 and H arms of the phase III KATHERINE study (NCT01772472). RNA sequencing was performed on post-NAT surgical samples. Genes and pathways associated wi…
View article: Supplementary Figure S2 from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer
Supplementary Figure S2 from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer Open
Comparison of HER2 expression heterogeneity in paired pre-NAT (i.e., before surgery) and post-NAT surgical samples. Patients were categorized according to whether HER2 staining was focal (<30%), heterogeneous (30–79%), or homogeneous (≥80%…
View article: Supplementary Table S1 from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer
Supplementary Table S1 from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer Open
Comparison of baseline patient and disease characteristics assessed at eligibility in the ITT population versus in those with mRNA data derived from pre-NAT or post-NAT surgical samples (RNA-evaluable population). Note: the pre-NAT and pos…
View article: Data from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer
Data from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer Open
Purpose:In KATHERINE, adjuvant T-DM1 reduced risk of disease recurrence or death by 50% compared with trastuzumab in patients with residual invasive breast cancer after neoadjuvant therapy (NAT) comprised of HER2-targeted therapy and chemo…
View article: Supplementary Figure S1 from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer
Supplementary Figure S1 from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer Open
Comparison of HER2 expression intensity in paired pre-NAT (i.e., before surgery) and post-NAT surgical samples. HER2, human epidermal growth factor receptor 2; IHC, immunohistochemistry; NAT, neoadjuvant therapy.
View article: Supplementary Figure S3 from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer
Supplementary Figure S3 from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer Open
IDFS by HER2 IHC score at definitive surgery (derived from samples used for eligibility and exploratory purposes). IDFS, invasive disease-free survival; IHC, immunohistochemistry; T-DM1, trastuzumab emtansine.
View article: Supplementary Figure S3 from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer
Supplementary Figure S3 from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer Open
IDFS by HER2 IHC score at definitive surgery (derived from samples used for eligibility and exploratory purposes). IDFS, invasive disease-free survival; IHC, immunohistochemistry; T-DM1, trastuzumab emtansine.
View article: Supplementary Figure S5 from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer
Supplementary Figure S5 from Biomarker Data from the Phase III KATHERINE Study of Adjuvant T-DM1 versus Trastuzumab for Residual Invasive Disease after Neoadjuvant Therapy for HER2-Positive Breast Cancer Open
Comparison of pre-NAT and post-NAT surgical RNA-evaluable samples. (A) ERBB2 (i.e., HER2), CD274 (i.e., PD-L1), checkpoint inhibitor signature (i.e., PD-L1/PD-L2/IDO), CD8A (i.e., CD8), TEFF signature CD8/granzymeA/granzymeB/perforin/IFNγ)…