Bulletin of the American Physical Society
APS March Meeting 2014
Volume 59, Number 1
Monday–Friday, March 3–7, 2014; Denver, Colorado
Session F14: Invited Session: Delbrueck Prize Session: Chance and Necessity - Determinism in the Physics of Cancer |
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Sponsoring Units: DBIO Chair: Daniel Cox, University of California, Davis Room: 301-303 |
Tuesday, March 4, 2014 8:00AM - 8:36AM |
F14.00001: Delbrueck Prize Talk: ``I Don't Believe a Word of It'': My Struggles With Max Delbruck's Ghost Invited Speaker: Robert Austin I never meet Max Delbruck, but I have worked with similarly great biological physicists. Because of this, I am familiar with the expression ``I don't believe a word of it'' that Max Delbruck was known to say, and other great biological physicists have been known to say. Lately I have been working on evolution dynamics and how one might accelerate evolution of de novo mutations by standing on the shoulders of great theoretical evolution biologists such as Sewall Wright and Conrad Waddington and following their insights. I have found Delbruck's pronouncement ``I don't believe a word of it'' ringing in my ears. I will try to convince the ghost of Delbruck and his present day acolytes that Darwin did not have the final say on evolution, that biological organisms are quite creative when it comes to evolution of new traits, and that failure to understand this complexity in evolution has had a major impact on our struggles with the physics of cancer. [Preview Abstract] |
Tuesday, March 4, 2014 8:36AM - 9:12AM |
F14.00002: The Atavistic Model of Cancer: Evidence, Objections, Therapeutic Value Invited Speaker: Charles Lineweaver As cancer progresses tumor cells dedifferentiate. In the atavistic model this dedifferentiation is interpreted as a reversion to phylogenetically earlier capabilities (Davies {\&} Lineweaver 2011). Since there is an identifiable order to the evolution of capabilities, the more recently evolved capabilities are more likely to be compromised first during cancer progression. A loss of capabilities based on the phylogenetic order of evolution suggests a therapeutic strategy for targeting cancer -- design challenges that can only be met by the recently evolved capabilities still intact in normal cells, but lost in cancer cells. Such a target-the-weakness therapeutic strategy contrasts with most current therapies that target the main strength of cancer: cell proliferation. Here, we describe several examples of this target-the-weakness strategy. Our most detailed example involves the immune system. As cancer progresses, the atavistic model suggests that cancer cells lose contact with the more recently evolved adaptive immune system of the host (the basis of vaccination). The absence of adaptive immunity in immunosuppressed tumor environments is an irreversible weakness of cancer that can be exploited by creating a challenge that only the presence of adaptive immunity can meet. Thus, we propose the post-vaccination inoculation of disease at dosages that the recently evolved (and vaccination-primed) adaptive immune system will be able to destroy in normal cells, but not in the immunosuppressed microenvironment of tumor cells. [Preview Abstract] |
Tuesday, March 4, 2014 9:12AM - 9:48AM |
F14.00003: The Role of the Microenvironment in the Origins of Cancer Invited Speaker: Thea Tlsty |
Tuesday, March 4, 2014 9:48AM - 10:24AM |
F14.00004: Are biomechanical changes necessary for tumor progression? Invited Speaker: Josef A. Kas Already the Roman Celsus recognized rigid tissue as characteristic for solid tumors. Conversely, changes towards a weaker cytoskeleton have been described as a feature of cancer cells since the early days of tumor biology. It remains unclear if a carcinoma's rigid signature stems from more inflexible cells or is caused by the stroma. Despite that the importance of cell biomechanics for tumor progression becomes more and more evident the chicken-and-egg problem to what extent cancer cells already change their mechanical properties within the solid tumor in order to transgress its boundary or mechanical changes are induced by the microenvironment when the cell has left the tumor has been discussed highly controversial. Comprehensive clinical biomechanical measurements only exist from tumor tissue without the possibility to identify individual cells or from individual cancer cells from pleural effusions. Since the biomechanical properties of cells in carcinomas remain unknown measurements on individual cells that directly stem out of primary tumor samples are required, which we have conducted. We found in cervix and mammary carcinomas a distinctive increase of softer cells as well as contractile cells. A soft and contractile cell is like a strong elastic rope. The cell can generate a strong tensile tension to pull its self along and is soft against compression to avoid jamming. [Preview Abstract] |
Tuesday, March 4, 2014 10:24AM - 11:00AM |
F14.00005: Cancer: The beat of an ancient drum? Invited Speaker: Paul Davies |
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