OCT 11, 2018 7:30 AM PDT

Keynote Presentation: In Advanced Cancers Curative Therapies Must Target All Cancer Cells

C.E. Credits: P.A.C.E. CE Florida CE
Speaker
  • Program Director, National Science Foundation
    Biography
      Dr. Blagoev completed his first MS degree in Nuclear and Elementary Particle Physics at Sofia University in 1990 and a second MS degree at the Physics Department at Florida Atlantic University in 1992. He received a PhD from the Physics Department at Boston College in 1998 and continued his research on superconductivity and magnetism at University of Cambridge as a postdoctoral fellow. In 1999 he moved to Harvard University Medical School working on mathematical models of ultrasound propagation in the brain. In 2002 he joined the Theoretical Division of Los Alamos National Laboratory as a staff member working on condensed matter physics as well as mathematical models of telomere dynamics and its influence on aging and cancer. Dr. Blagoev moved to the National Science Foundation as a Program Director in the Division of Physics in 2007, where he currently directs the Physics of Living Systems program. Since 2015 he is an Associate Research Scientist at the Department of Biophysics at Johns Hopkins University. His research interests focus on understanding the mechanisms of tumor growth during cancer progression and analysis of cancer clinical trials. He is also interested in the non-equilibrium phyical processes in mammalian cells and their role in DNA repair.

    Abstract

    In the past two decades a small number of infrequently dividing cells have been proposed as the source of multi-drug resistance during cancer treatment. These cells identified by their expression of stem cell markers have been shown to proliferate when grafted in animals and have been called cancer stem cells in analogy to adult stem cells maintaining organ homeostasis. In this talk different kinetic models of tumor proliferation are presented and compared to tumor kinetics in large number of patients with metastatic disease obtained from cancer clinical trials. The conclusion from this analysis is that almost all analyzed tumors after initial volume decrease begin to grow exponentially, inconsistent with the hypothesis that small number of self-renewing, drug resistance cells drive this growth. Cell proliferation resembles the proliferation of embryonic stem cells early in embryogenesis and not of adult stem cells. Our data is consistent with exponential cell proliferation with fixed growth rate, implying that the number of proliferating cells in these cancers is very large and divide symmetrically. The main implication of this work is that cancer therapies must target all cells and not just a small subset of cells in a tumor. 

    Learning Objectives: 

    1. To present current models of tumor growth and evidence that in advanced cancers, although rare stem-like cancer cells might exist, the majority of cells drive tumor growth.
    2. For a therapy to be curative it has to target all cancer cells, because most cells are the source of drug resistance. 


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