maurice, ethel, and jane sokolow memorial cancer …cancer.ucsf.edu/_docs/2016_sokolow_flyer.pdf ·...

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John Dick, PhD, FRS Senior Scientist, Princess Margaret Cancer Centre, McEwen Centre for Regenerative Medicine, University Health Network Professor of Molecular Genetics, University of Toronto Maurice, Ethel, and Jane Sokolow Memorial Cancer Endowment Lectureship Clinical Lecture: Translating stemness concepts towards improved clinical management of AML Tuesday, June 21, 2016 | 12:00 - 1:00 pm Parnassus, HSW-300 | live stream | pizza served while supplies last Monday, June 20, 2016 | 4:00 - 5:00 pm Mission Bay, Byers Auditorium, Genentech Hall | live stream Sokolow Lecture: Towards unification of cancer stem cell and clonal evolution models of intratumoral heterogeneity cancer.ucsf.edu/sokolow Dr. Dick's research has been grounded in his pioneering quantitative in vivo assays for both normal hematopoietic stem cells (HSC) and leukemic stem cells (LSC). From the development of these functional assays, his studies have culminated in elucidating the developmental roadmap of early human hematopoietic development including the discovery of multilymphoid progenitors and the identification of human HSC at single cell resolution. In a parallel line of research on leukemia and colon cancer, his findings established, through prospective isolation and functional tumor initiation assays, that individual tumor cells are not functionally equal and that some cancer cells are endowed with stem cell properties. Collectively, his landmark papers on the first identification of LSC are recognized as altering our understanding of human cancer biology and ushering in the modern era of cancer stem cell (CSC) research. His recent research shows that LSC and CSC within an individual tumor are genetically diverse and related through complex evolutionary trajectories, thereby linking together the genetic and stem cell models of cancer, two models previously considered to be mutually exclusive. This research has stimulated burgeoning interest within the cancer research community to under- stand how functional diversity is driven by genetic and non-genetic determinants and how these together contribute to therapy failure resulting in disease progression and recurrence.

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John Dick, PhD, FRSSenior Scientist, Princess Margaret Cancer Centre,McEwen Centre for Regenerative Medicine, University Health NetworkProfessor of Molecular Genetics, University of Toronto

Maurice, Ethel, and Jane SokolowMemorial Cancer Endowment Lectureship

Clinical Lecture:Translating stemness concepts towards improved clinical management of AML

Tuesday, June 21, 2016 | 12:00 - 1:00 pmParnassus, HSW-300 | live stream | pizza served while supplies last

Monday, June 20, 2016 | 4:00 - 5:00 pmMission Bay, Byers Auditorium, Genentech Hall | live stream

Sokolow Lecture:Towards unification of cancer stem cell and clonal evolution models of intratumoral heterogeneity

cancer.ucsf.edu/sokolow

Dr. Dick's research has been grounded in his pioneering quantitative in vivo assays for both normal hematopoietic stem cells (HSC) and leukemic stem cells (LSC). From the development of these functional assays, his studies have culminated in elucidating the developmental roadmap of early human hematopoietic development including the discovery of multilymphoid progenitors and the identification of human HSC at single cell resolution. In a parallel line of research on leukemia and colon cancer, his findings established, through prospective isolation and functional tumor initiation assays, that individual tumor cells are not functionally equal and that some cancer cells are endowed with stem cell properties. Collectively, his landmark papers on the first identification of LSC are recognized as altering our understanding of human cancer biology and ushering in the modern era of cancer stem cell (CSC) research. His recent research shows that LSC and CSC within an individual tumor are genetically diverse and related through complex evolutionary trajectories, thereby linking together the genetic and stem cell models of cancer, two models previously considered to be mutually exclusive. This research has stimulated burgeoning interest within the cancer research community to under-stand how functional diversity is driven by genetic and non-genetic determinants and how these together contribute to therapy failure resulting in disease progression and recurrence.