Bulletin of the American Physical Society
APS March Meeting 2016
Volume 61, Number 2
Monday–Friday, March 14–18, 2016; Baltimore, Maryland
Session K55: Physics of Cancer MetastasisInvited
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Sponsoring Units: DBIO GSOFT Chair: Michael Espey, National Institute of Health Room: Hilton Baltimore Holiday Ballroom 6 |
Wednesday, March 16, 2016 8:00AM - 8:36AM |
K55.00001: Why do tumor cells spread? Invited Speaker: Kenneth Pienta |
Wednesday, March 16, 2016 8:36AM - 9:12AM |
K55.00002: Mechanical induction of transitions into mesenchymal and amoeboid states Invited Speaker: Jan Liphardt One of the fundamental mysteries of biology lies in the ability of cells to convert from one phenotype to another in response to external control inputs. We have been studying the Epithelial-to-Mesenchymal Transition (EMT), which allows organized assemblies of epithelial cells to scatter into lone mesenchymal cells. EMT is critical for normal development and wound healing, and may be important for cancer metastasis. I’ll present recent data on disorganizing mammary epithelial structures. We have used CRISPR to insert fluorescent tags directly into eight EMT-related genes (such as E-cadherin and Vimentin), which allows us to monitor the dynamics of the transition in real time, subject only to delays imposed by fluorophore folding/maturation times. With this information, we can begin to order events in time (temporal resolution ~ 30 minutes), starting with external signal inputs and proceeding through a secession of intracellular changes of gene expression on the path to the mesenchymal state. [Preview Abstract] |
Wednesday, March 16, 2016 9:12AM - 9:48AM |
K55.00003: The Genetics and Biophysics of the Epithelial-Mesenchymal Transition (EMT): Can Theoretical Physics Help Cancer Biology Invited Speaker: Herbert Levine In order to spread from the primary tumor to distant sites, cancer cells must undergo a coordinated change in their phenotypic properties referred to as the "epithelial-to-mesenchymal" transition. ~We have studied the~nonlinear genetic circuits that are responsible for this cellular decision-making progress and propose that the transition actually goes through a series of intermediate states. At the same time, we have formulated motility models which allow for the correlation of the state of this network and the cell's biophysical capabilities. Hopefully, these thereby efforts will help us better understand the transition to metastatic disease and possible treatments thereof. ~ [Preview Abstract] |
Wednesday, March 16, 2016 9:48AM - 10:24AM |
K55.00004: Critical high-dimensional state transitions in cell populations or why cancers follow the principle "What does not kill me makes me stronger" Invited Speaker: Sui Huang Transitions between high-dimensional attractor states in the quasi-potential landscape of the gene regulatory network, induced by environmental perturbations and/or facilitated by mutational rewiring of the network, underlie cell phenotype switching in development as well as in cancer progression, including acquisition of drug-resistant phenotypes. Considering heterogeneous cell populations as statistical ensembles of cells, and single-cell resolution gene expression profiling of cell populations undergoing a cell phenotype shift allow us now to map the topography of the landscape and its distortion. From snapshots of single-cell expression patterns of a cell population measured during major transitions we compute a quantity that identifies symmetry-breaking destabilization of attractors (bifurcation) and concomitant dimension-reduction of the state space manifold (landscape distortion) which precede critical transitions to new attractor states. The model predicts, and we show experimentally, the almost inevitable generation of aberrant cells associated with such critical transitions in multi-attractor landscapes: therapeutic perturbations which seek to push cancer cells to the apoptotic state, almost always produce ``rebellious'' cells which move in the ``opposite direction'': instead of dying they become more stem-cell-like and malignant. We show experimentally that the inadvertent generation of more malignant cancer cells by therapy indeed results from transition of surviving (but stressed) cells into unforeseen attractor states and not simply from selection of inherently more resistant cells. Thus, cancer cells follow not so much Darwin, as generally thought (survival of the fittest), but rather Nietzsche (What does not kill me makes me stronger). [Preview Abstract] |
Wednesday, March 16, 2016 10:24AM - 11:00AM |
K55.00005: Cell-ECM Interactions During Cancer Invasion Invited Speaker: Yi Jiang The extracellular matrix (ECM), a fibrous material that forms a network in a tissue, significantly affects many aspects of cellular behavior, including cell movement and proliferation. Transgenic mouse tumor studies indicate that excess collagen, a major component of ECM, enhances tumor formation and invasiveness. Clinically, tumor associated collagen signatures are strong markers for breast cancer survival. However, the underlying mechanisms are unclear since the properties of ECM are complex, with diverse structural and mechanical properties depending on various biophysical parameters. We have developed a three-dimensional elastic fiber network model, and parameterized it with~in vitro~collagen mechanics. Using this model, we study ECM remodeling as a result of local deformation and cell migration through the ECM as a network percolation problem. We have also developed a three-dimensional, multiscale model of cell migration and interaction with ECM. Our model reproduces quantitative single cell migration experiments. This model is a first step toward a fully biomechanical cell-matrix interaction model and may shed light on tumor associated collagen signatures in breast cancer. [Preview Abstract] |
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