Daygen L. Finch
BC Cancer Agency
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Featured researches published by Daygen L. Finch.
Urology | 2010
Michael M. Vickers; Toni K. Choueiri; Miranda Rogers; Andrew Percy; Daygen L. Finch; Ivan N. Zama; Tina Cheng; Scott North; Jennifer J. Knox; Christian Kollmannsberger; David F. McDermott; Brian I. Rini; Daniel Y.C. Heng
OBJECTIVES To characterize and evaluate the efficacy of second-line therapy in patients who had progressed on initial anti-vascular endothelial growth factor (VEGF) therapy. METHODS Between 2005 and 2007, patients with mRCC who received second-line therapy after 1st-line VEGF-targeted therapy were identified across 7 cancer centers. RESULTS A total of 645 mRCC patients received first-line VEGF-targeted therapy, of which 216 patients received second-line VEGF-targeted therapy (sunitinib, n = 93; sorafenib, n = 80; bevacizumab, n = 11; axitinib, n = 8) or mammalian target of rapamycin (mTOR)-inhibiting agents (temsirolimus, n = 21; everolimus, n = 3). On multivariate analysis, a higher baseline Karnofsky performance status score before first-line therapy predicted which patients were more likely to receive second-line therapy (P <.0001). The median time to treatment failure of second-line therapy was 4.9 months for anti-VEGF therapy and 2.5 months for mTOR inhibitors (P = .014) (HR: 0.52, CI: 0.29-0.91 and HR: 0.495, CI: 0.27-0.9 after adjusting for Memorial Sloan-Kettering Cancer Center prognostic factors and histology, respectively). Overall survival from start of second-line therapy was not significantly different (14.2 vs 10.6 months respectively; P = .38). CONCLUSIONS Baseline Karnofsky performance status is an independent predictor of receiving second-line targeted therapy. Patients who receive a second-line anti-VEGF drug appear to have a similar overall survival to those who receive a second-line anti-mTOR drug.
Cancer | 2015
Ethan Toumishey; Angeli Prasad; Greg Dueck; Neil Chua; Daygen L. Finch; James B. Johnston; Richard H. van der Jagt; D A Stewart; Darrell White; Andrew R. Belch; Tony Reiman
Patients with T‐cell lymphomas face a poorer prognosis compared with patients with B‐cell lymphomas. New therapeutic approaches need to be developed to improve outcomes for these patients.
Cancer Discovery | 2018
Matti Annala; Gillian Vandekerkhove; Daniel Khalaf; Sinja Taavitsainen; Kevin Beja; Evan W. Warner; Katherine Sunderland; Christian Kollmannsberger; Bernhard J. Eigl; Daygen L. Finch; Conrad D. Oja; Joanna Vergidis; Muhammad Zulfiqar; Arun Azad; Matti Nykter; Martin Gleave; Alexander W. Wyatt; Kim N. Chi
Primary resistance to androgen receptor (AR)-directed therapies in metastatic castration-resistant prostate cancer (mCRPC) is poorly understood. We randomized 202 patients with treatment-naïve mCRPC to abiraterone or enzalutamide and performed whole-exome and deep targeted 72-gene sequencing of plasma cell-free DNA prior to therapy. For these agents, which have never been directly compared, time to progression was similar. Defects in BRCA2 and ATM were strongly associated with poor clinical outcomes independently of clinical prognostic factors and circulating tumor DNA abundance. Somatic alterations in TP53, previously linked to reduced tumor dependency on AR signaling, were also independently associated with rapid resistance. Although detection of AR amplifications did not outperform standard prognostic biomarkers, AR gene structural rearrangements truncating the ligand binding domain were identified in several patients with primary resistance. These findings establish genomic drivers of resistance to first-line AR-directed therapy in mCRPC and identify potential minimally invasive biomarkers.Significance: Leveraging plasma specimens collected in a large randomized phase II trial, we report the relative impact of common circulating tumor DNA alterations on patient response to the most widely used therapies for advanced prostate cancer. Our findings suggest that liquid biopsy analysis can guide the use of AR-targeted therapy in general practice. Cancer Discov; 8(4); 444-57. ©2018 AACR.See related commentary by Jayaram et al., p. 392This article is highlighted in the In This Issue feature, p. 371.
Cuaj-canadian Urological Association Journal | 2017
Daniel Khalaf; Claudia M. Avilés; Arun Azad; Katherine Sunderland; Tilman Todenhöfer; Berhard J. Eigl; Daygen L. Finch; Lyly Le; Andrew Atwell; Bruce Keith; Christian Kollmannsberger; Kim N. Chi
INTRODUCTION Recently, a prognostic index including six risk factors (RFs) (unfavourable Eastern Cooperative Oncology Group performance status [ECOG PS], presence of liver metastases, short response to luteinizing hormone-releasing hormone [LHRH] agonists/antagonists, low albumin, increased alkaline phosphatase [ALP] and lactate dehydrogenase [LDH]) was developed from the COU-AA-301 trial in post-chemotherapy metastatic castration-resistant prostate cancer (mCRPC) patients treated with abiraterone acetate. Our primary objective was to evaluate this model in a cohort of chemotherapy-naive mCRPC patients receiving abiraterone. METHODS We identified 197 chemotherapy-naive patients who received abiraterone at six BC Cancer Agency centres and who had complete information on all six RFs. Study endpoints were prostate-specific antigen (PSA) response rate (RR), time to PSA progression, time on treatment, and overall survival (OS). PSA RR and survival outcomes were compared using Χ2 test and log-rank test. Multivariable Cox proportional hazard analysis was performed to identify RFs independently associated with OS. RESULTS Patients were classified into good (0-1 RFs), intermediate (2-3 RFs), and poor (4-6 RFs) prognostic groups (33%, 52%, and 15%, respectively). For good-, intermediate-, and poor-risk patients, PSA RR (≥50% decline) was 60% vs. 42% vs. 40% (p=0.05); median time to PSA progression was 7.3 vs. 5.3 vs. 5.0 months (p=0.02); and median OS was 29.4 vs. 13.8 vs. 8.7 months (p<0.0001). CONCLUSIONS The six-factor prognostic index model stratifies clinical outcomes in chemotherapy-naive mCRPC patients treated with abiraterone. Identifying patients at risk of poor outcome is important for informing clinical practice and clinical trial design.
Journal of Clinical Oncology | 2017
Kim N. Chi; Matti Annala; Katherine Sunderland; Daniel Khalaf; Daygen L. Finch; Conrad D. Oja; Joanna Vergidis; Muhammad Zulfiqar; Kevin Beja; Gillian Vandekerkhove; Martin Gleave; Alexander W. Wyatt
Blood | 2007
Tony Reiman; Daygen L. Finch; Neil Chua; Darrell White; Douglas A. Stewart; Richard H. van der Jagt; James B. Johnston; Angeli Prasad; Henry Schwarz; Jerome B. Zeldis; Andrew R. Belch
Journal of Clinical Oncology | 2016
Sunil Parimi; Bernhard J. Eigl; Katherine Sunderland; Muhammad Zulfiqar; Daygen L. Finch; Conrad D. Oja; Joanna Vergidis; Leanne Chung-Yan Seto; Arun Azad; Martin Gleave; Kim N. Chi
Journal of Clinical Oncology | 2017
Daniel Khalaf; Matti Annala; Kevin Beja; Gillian Vandekerkhove; Muhammad Zulfiqar; Daygen L. Finch; Conrad D. Oja; Joanna Vergidis; Martin Gleave; Alexander W. Wyatt; Kim N. Chi
Journal of Clinical Oncology | 2016
Alexander W. Wyatt; Matti Annala; Sunil Parimi; Muhammad Zulfiqar; Daygen L. Finch; Conrad D. Oja; Joanna Vergidis; Arun Azad; Martin Gleave; Kim N. Chi
Blood | 2013
Angeli Prasad; Gregory Scott Dueck; Neil Chua; Daygen L. Finch; Douglas A. Stewart; Darrell White; Richard H. van der Jagt; James B. Johnston; Andrew R. Belch; Tony Reiman