Bulletin of the American Physical Society
APS March Meeting 2013
Volume 58, Number 1
Monday–Friday, March 18–22, 2013; Baltimore, Maryland
Session W47: Invited Session: The Spread of Cancer and the Tumor Microenvironment |
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Sponsoring Units: DBIO Chair: Herb Levine, Rice University Room: Hilton Baltimore Holiday Ballroom 6 |
Thursday, March 21, 2013 2:30PM - 3:06PM |
W47.00001: Modeling invasion of brain tissue by glioblastoma cells: ECM alignment and motility Invited Speaker: L.M. Sander A key stage in the development of highly malignant brain tumors (Glioblastoma Multiforme) is invasion of normal brain tissue by motile cells moving through a crowded, complex environment. Evidence from \emph{in vitro} experiments suggests the cell motion is accompanied by considerable deformation and alignment of the extra-cellular matrix (ECM) of the brain. In the case of breast cancer, alignment effects of this sort have been seen \emph{in vivo}. We have modeled features of this system including stress confinement in the non-linear elasticity of the ECM and contact guidance of the cell motion. [Preview Abstract] |
Thursday, March 21, 2013 3:06PM - 3:42PM |
W47.00002: The interplay between invasion and proliferation in tumor cell navigation Invited Speaker: Eshel Ben-Jacob Tumor cells can employ different cellular and molecular modes of invasion. The two main phenotypic mechanisms are: 1. \textit{Amoeboid} (or ``path finder'') cells that can squeeze through small gaps in the ECM (extracellular matrix). 2. \textit{Mesenchymal} (or ``path generator'') cells that are more rigid and can decompose the ECM to pass through. In addition there is interplay between energy directed to more rapid motility vs. energy used for proliferation. Understanding the relative contributions of these distinct mechanisms and the balance between motility and proliferation to the efficiency of metastatic cancer migration is fundamental to the therapeutic targeting of cancer. We present a conceptual and modeling framework for the analysis and assessment of the success rate, time-to-target, and survival probability of amoeboid vs. mesenchymal modes. Similarly, we contrast invasion with and without proliferation. We treat the complex ECM geometry as a maze and employ semi-realistic modeling of cell motility. Our approach includes metabolic and timing degrees of freedom. The theoretical studies were compared with experimental efforts of cell navigation in specially designed microfluidic devices. [Preview Abstract] |
Thursday, March 21, 2013 3:42PM - 4:18PM |
W47.00003: The Interplay between Signaling and Metabolism in Breast Cancer Cell Motility and Metastasis Invited Speaker: Ilan Tsarfaty The initiation and growth of tumor metastases require tumor cells go through a transition between collective-to-individual cell migration. Understanding the molecular, cellular and physical mechanisms of these different migration modes is limited. We focus on the tumor cell migration induced by Hepatocyte Growth Factor / Scatter Factor (HGF/SF) - Met-signaling, a master regulator of cell motility in normal and malignant processes. Met has been implicated in tumorigenesis and metastasis and several Met targeting agents have been introduced into the clinic, and are currently in all phases of clinical trials Our analysis demonstrates that Met signaling dramatically alter the morpho-kinetic dynamics of collective migration of tumor cells. It induce a ``wave'' of increasing velocities that propagates back from the leading edge, increases cells' orientation and cooperation capabilities. In parallel Met signaling induces amoeboid cell motility that increased cell individuality. The decision making regarding the motility mode is dependent on the extent of activation of unique signal and metabolic cues. We present a combination of molecular imaging, conceptual and modeling framework for the analysis and assessment of the collective mesenchymal to epithelial versus amoeboid motility. Combined together our analysis can contribute to the understanding of metastasis and personalizing anti Met targeted therapy. [Preview Abstract] |
Thursday, March 21, 2013 4:18PM - 4:54PM |
W47.00004: The biology of tumor cell invasion in the brain and its therapy Invited Speaker: E Antonio Chiocca |
Thursday, March 21, 2013 4:54PM - 5:30PM |
W47.00005: The interplay between cell motility and tissue architecture Invited Speaker: Kandice Tanner Glandular tissue form arboreal networks comprised of acini and tubes. Loss of structure is concomitant with the in vivo pathologic state. \textit{In vitro} models have been shown to recapitulate the functional units of the mammary gland and other organs. Despite our much improved understanding gleaned from both in vitro and in vivo interrogation, the mechanisms by which cells are able to achieve the correct tissue organization remain elusive. How do single mammary epithelial cells form polarized acini when cultured in a surrogate basement membrane gel but not on 2D surfaces? Simply put, how does a cell know which way is up? Why do malignant breast cells show a differential response in that they form non-polarized aggregates? Recently, it was determined that non-malignant cells undergo multiple rotations to establish acini while tumor cells are randomly motile during tumor formation. Can it be that a tumor cell has simply lost its way. [Preview Abstract] |
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