PPT-Adaptive Population Enrichment for Oncology Trials with Tim

Cyrus Mehta PhD President Cytel Inc Statistical research with Sebastien Irle and Helmut Schäfer Institute of Medical Biometry University of Marburg Germany Problem formulation based on collaborations with the Pfizer Inc and MD Anderson Cancer Center. Phil clin Psych students Elective international student teaching Public Cancer Awareness Programmes Dr Suraj Manjunath Associate Professor Head of Department Dr Shiva Kumar K Assistant Professor Dr Rakesh S R amesh Assistant Professor Dr Tanveer Huss Andy Grieve. SVP Clinical Trials Methodology, . Innovation Centre, Aptiv Solutions.. 1. Outline. Basic Principles of Adaptive . Designs. Why . adaptive trials?. Differences Between Early / Late Phase Adaptive Designs. Dream or Reality?. Michelle Ghert, MD, FRCSC. Associate Professor. Department of Surgery. McMaster University. 22 year-old male with sarcoma right femur. Deep infection in total joints. Approximately 1% risk. Acknowledgements to collaborators:. Steven . Julious. , Susan Todd, Jon Nicholl, and Jonathan . Boote. #ICTMC2015. Meandering journey towards routine trial adaptation: survey results on barriers to use of adaptive designs in confirmatory trials. Acknowledgements to collaborators:. Stevely. A, Todd S, . Julious. S, Nicholl J, Hind D, and Cooper C. . #ICTMC2015. 1. Investigation of the shortcomings of the CONSORT 2010 statement for the reporting of group sequential randomised controlled trials. Global Forum on Bioethics in Research. :. Emerging Epidemic Infections and Experimental Treatments. November 4, 2015. Lord Kelvin. I often say that when you can measure what you are speaking about and express it in numbers, you know something about it; but when you cannot measure it, when you cannot express it in numbers, your knowledge is of a meagre and unsatisfactory kind; it may be the beginning of knowledge, but you have scarcely in your thoughts advanced to the state of Science, whatever the matter may be.. Nick . Pavlakis. , MBBS, . MMed. (. Clin. Epi. ), . PhD. Royal North Shore Hospital. Sydney University. Outline. Aims of a Phase II study. Design aspects. Disease/population selection. Endpoint selection. Challenging Tradition. Chia-Chi (Josh) Lin, MD, PhD . 林家齊. Director of Phase I Center, Department of Oncology, National Taiwan University Hospital. Clinical Associate Professor, Graduate Institute of Oncology, National Taiwan University College of Medicine. Mahesh Parmar. MRC . Clinical Trials Unit at . UCL. Rationale . for adaptive trials. Our . adaptive trials and their setting. Discuss some broad practical and statistical challenges. Offer some solutions and thoughts. Robert A. Beckman, MD. Chair, ADWSG. Professor of Oncology and of Biostatistics, Bioinformatics, and Biomathematics. Georgetown University Medical Center. eniac1915@gmail.com. ADSWG . Membership: approximately . Elizabeth Garrett-Mayer, PhD. Director, Division of Biostatistics and . Research Data . Governance. Center for Research and Analytics (CENTRA). American Society of Clinical Oncology (ASCO). Alexandria, VA. D. esigns. 2. Steps in clinical . d. evelopment . p. rograms. Phase I:. . Studies on . dosing. Phase . III:. . Assess . therapeutic effect and benefit-risk in patients of candidate vs. standard of . What you should know about study design. Demonstrated on . Head of Statistics. nQuery. Lead Researcher. FDA Guest Speaker. Guest Lecturer. Webinar Host. HOSTED BY: . Ronan Fitzpatrick. AGENDA. Adaptive Designs in Confirmatory Trials. The PMN enrichment was carried out by double gradient centrifugation. A single cell suspension was (1x10^5 cells) stained with the following markers: CD15-BV421 (Pan-granulocyte), CD66b-FITC (Neutrophil maturity), CD16-APC (Neutrophil FC receptor), CCR3-APC-Cy7 (Eosinophil and basophil), and CD56-PerCP (NK cell). PMN population was gated based on the FSC-SSC scatter plot. The CD15+ and CD66b+ double positive cells were gated using a quadrant plot. This population indicated neutrophil enrichment, which was an average of 85.45% (± 6.20%). We also looked at contaminating eosinophil/basophil (CCR3) and NK-cell (CD56) populations by plotting against CD16 (neutrophil specific), and found them to be 1.14% (± 1.02%) and 1.9% (± 2.00 %) respectively. .