Stephen P. Finn
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View article: The role of TRPA1 in lung cancer
The role of TRPA1 in lung cancer Open
Lung cancer is the leading cause of cancer related death worldwide and is typically categorised as either small cell lung carcinoma (SCLC) or non-small cell lung carcinoma (NSCLC). SCLC accounts for 15% of all lung cancer diagnoses while N…
View article: Process Development of a Model Solvate for Drying Research
Process Development of a Model Solvate for Drying Research Open
Drying of organic solvates remains hard to scale down and fully understand, as (a) residual solvent is typically hard to remove due to high solid-phase transport resistances, and (b) precise control over crystal properties is challenging. …
View article: ETOP 25-23 ADOPT-lung: An international, multicentre, open-label randomised phase III trial to evaluate the benefit of adding adjuvant durvalumab after neoadjuvant chemotherapy plus durvalumab in patients with stage IIB-IIIB (N2) resectable NSCLC
ETOP 25-23 ADOPT-lung: An international, multicentre, open-label randomised phase III trial to evaluate the benefit of adding adjuvant durvalumab after neoadjuvant chemotherapy plus durvalumab in patients with stage IIB-IIIB (N2) resectable NSCLC Open
View article: Editorial: Tools for assessing family relationships
Editorial: Tools for assessing family relationships Open
View article: Supplementary Table 1 from Prevalence of Mismatch Repair Deficiency in Primary Prostate Cancer in a Large Prospective Cohort
Supplementary Table 1 from Prevalence of Mismatch Repair Deficiency in Primary Prostate Cancer in a Large Prospective Cohort Open
Supplementary Table 1. All validation results and evaluation of intratumoral heterogeneity.
View article: Data from Prevalence of Mismatch Repair Deficiency in Primary Prostate Cancer in a Large Prospective Cohort
Data from Prevalence of Mismatch Repair Deficiency in Primary Prostate Cancer in a Large Prospective Cohort Open
Purpose:Mismatch repair (MMR) deficiency and microsatellite instability are predictive biomarkers for immunotherapy response. The best approach to identify patients with such tumors is unclear in prostate cancer.Experimental Design:This st…
View article: Data from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Data from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression Open
Background:Vigorous physical activity has been associated with lower risk of fatal prostate cancer. However, mechanisms contributing to this relationship are not understood.Methods:We studied 117 men with prostate cancer in the University …
View article: Supplementary Table S2 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Supplementary Table S2 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression Open
Supplementary Table S2. Associations between physical activity and odds of histological inflammation in prostate tumor core and tumor adjacent compartments.
View article: Supplementary Figure S2 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Supplementary Figure S2 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression Open
Supplementary Figure S2. Concordance between QuPath algorithm and pathologist and reproducibility across times. A-D, Bland-Altman plots showing differences in TILs% between QuPath algorithm and manual counting in (A) stroma of tumor core, …
View article: Supplementary Table S6 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Supplementary Table S6 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression Open
Supplementary Table S6. Hazard ratios and 95% confidence intervals for associations between histologic inflammation and risk of prostate cancer progression in the pooled study, overall and stratified by ERG expression.
View article: Supplementary Figure S1 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Supplementary Figure S1 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression Open
Supplementary Figure S1. Correlation plot for the relationship of gene expression-based with histological measures of immune infiltrate in prostate cancer. Gene expression-based measures include B cells, T cells, Th cells, Tfh, Treg, exhau…
View article: Supplementary Table S7 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Supplementary Table S7 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression Open
Supplementary Table S7. Hazard ratios and 95% confidence intervals for associations between immune cell types and risk of prostate cancer progression in the UNC CSC, overall and stratified by ERG expression.
View article: Supplementary Table S1 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Supplementary Table S1 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression Open
Supplementary Table S1. Gene list of immune signature.
View article: Supplementary Figure S4 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Supplementary Figure S4 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression Open
Supplementary Figure S4. Boxplots comparing gene expression-based immune cell types in men with high tumor aggressiveness reporting any vs. no vigorous recreational activity. A. Gleason score ≥4 + 3. B. Clinical stage III-IV.
View article: Supplementary Figure S3 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Supplementary Figure S3 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression Open
Supplementary Figure S3. Boxplots comparing gene expression-based immune cell types in men with low tumor aggressiveness reporting any vs. no vigorous recreational activity. A. Gleason score ≤3 + 4. B. Clinical stage I-II.
View article: Supplementary Table S8 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Supplementary Table S8 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression Open
Supplementary Table S8. Hazard ratios and 95% confidence intervals for associations between immune cell types and risk of prostate cancer progression in the FASTMAN, overall and stratified by ERG expression.
View article: Supplementary Table S5 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Supplementary Table S5 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression Open
Supplementary Table S5. Associations between immune cell types and disease aggressiveness in the pooled study, overall and stratified by ERG expression.
View article: Supplementary Table S3 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Supplementary Table S3 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression Open
Supplementary Table S3. Associations of physical activity and TILs in prostate cancer stratified by ERG status in the UNC CSC.
View article: Supplementary Table S4 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression
Supplementary Table S4 from Associations of Prostate Tumor Immune Landscape with Vigorous Physical Activity and Prostate Cancer Progression Open
Supplementary Table S4. Associations between histologic inflammation and disease aggressiveness in the pooled study, overall and stratified by ERG expression.
View article: Supplementary Figure S11 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial
Supplementary Figure S11 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial Open
Supplementary Figure S11. Overall survival by EGFR del19/L858R mutational status at week 9 (N=107) - landmark analysis (post 9-week time).
View article: Supplementary Figure S9 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial
Supplementary Figure S9 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial Open
Supplementary Figure S9. Overall survival for the N=136 patients constituting the biomarker analysis cohort, by baseline mutational status of (A) EGFR T790M (B) TP53.
View article: Supplementary Figure S3 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial
Supplementary Figure S3 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial Open
Supplementary Figure S3. EGFR T790M mutational status (MD/MND) by treatment arm at baseline (N=136), week 9 (N=110) and progression (N=65).
View article: Supplementary Figure S8 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial
Supplementary Figure S8 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial Open
Supplementary Figure S8. Progression-free survival by EGFR del19/L858R mutational status at week 9 (N=105) - landmark analysis (post 9-week time).
View article: Supplementary Appendix S1 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial
Supplementary Appendix S1 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial Open
List of ETOP 10-16 BOOSTER collaborators
View article: Supplementary Figure S6 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial
Supplementary Figure S6 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial Open
Supplementary Figure S6. Association of EGFR T790M MAF with time, based on N=136 baseline, N=110 week 9 and N=65 progression samples.
View article: Supplementary Figure S10 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial
Supplementary Figure S10 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial Open
Supplementary Figure S10. Overall survival by EGFR T790M mutational status at week 9 (N=106) - landmark analysis (post 9-week time).
View article: Supplementary Figure S7 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial
Supplementary Figure S7 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial Open
Supplementary Figure S7. Progression-free survival by treatment arm and smoking status for patients (A) with EGFR T790M mutation (n=97) (B) without EGFR T790M mutation (n=39) at baseline.
View article: Supplementary Tables S1-S14 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial
Supplementary Tables S1-S14 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial Open
Supplementary Tables S1-S14
View article: Supplementary Figure S4 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial
Supplementary Figure S4 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial Open
Supplementary Figure S4. Evolution of EGFR T790M mutational status across time for the N=45 patients with available samples at all 3 timepoints.
View article: Supplementary Figure S2 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial
Supplementary Figure S2 from ctDNA Dynamics and Mechanisms of Acquired Resistance in Patients Treated with Osimertinib with or without Bevacizumab from the Randomized Phase II ETOP-BOOSTER Trial Open
Supplementary Figure S2. Baseline genomic profile for the N=136 patients constituting the biomarker analysis cohort.