Bulletin of the American Physical Society
APS March Meeting 2010
Volume 55, Number 2
Monday–Friday, March 15–19, 2010; Portland, Oregon
Session Y7: Convergence of Physics and Life Sciences: Emerging Perspectives in Cancer |
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Sponsoring Units: DBP Chair: Larry Nagahara, National Cancer Institute Room: Portland Ballroom 254 |
Friday, March 19, 2010 8:00AM - 8:36AM |
Y7.00001: Mapping Epigenetic Changes One Molecule at a Time Invited Speaker: Gene expression, cell specialization, and, presumably, the progress to cancer, are controlled by a heritable, but environmentally modifiable code that ``lies on top of'' the genome. This is called the epigenetic code. Some known epigenetic markings consist of chemical modifications of amino acid residues in proteins. For example, a lysine residue on a histone protein (a protein that packages DNA) may have an amine group replaced ay an acetyl group. DNA itself is also modified. The most well-known modification of DNA is the addition of a methyl group at carbon 5 of the cytosine base. Epigentic modifications change with tissue type, and, presumably between healthy and normal tissues. Epigentic markings may even be dynamic, changing over the cell cycle. They could even be random, forming part of a combinatorial selection system (rather like the immune system). For this reason, these markings need to be mapped at the single molecule level. We are developing methods to simultaneously image molecular structure and the location of epigenetic markings using a method we call ``recognition imaging''. We are also developing a new single-molecule DNA sequencing technique that may prove sensitive to methylated cytosine bases. [Preview Abstract] |
Friday, March 19, 2010 8:36AM - 9:12AM |
Y7.00002: Complexity and Dynamic Heterogeneity of the Process of Cancer Metastasis Invited Speaker: Cancer metastasis -- the spread of cancer from a primary tumor to distant parts of the body -- is responsible for most cancer deaths. If cancer is detected early, before it has spread, it can often be treated with local therapies like surgery and radiation. If cancer is detected after it has already spread, it is much harder to treat successfully. Cancer cells may be distributed to many organs, may be present as tiny micrometastases that are hard to detect, and cancer cells can be in a dormant state that may be resistant to treatment that is directed against actively dividing cells. A better understanding of the process of metastasis thus is needed in order to improve survival from cancer. Cancer is not a static disease, but one that can undergo stepwise evolution and progression from early, treatable cancer to aggressive cancer that is harder to treat. Furthermore, cancers are made up of many cells, and there is considerable heterogeneity among the cells in a tumor. Thus, cancer is ``plastic,'' with heterogeneity among cancer cells and changes over time. Understanding this ``dynamic heterogeneity'' has proven to be difficult. Input from physical sciences disciplines may help to shed light on this complex aspect of cancer biology. Here the process of cancer metastasis will be discussed, and experimental models for imaging the process described. The concept of ``dynamic heterogeneity'' of the metastatic process will be discussed, and some of the questions that need to be addressed for better understanding of metastasis will be outlined. An evolving dialogue between cancer biologists and physical scientists may lead to new ways of studying and understanding this lethal aspect of cancer. [Preview Abstract] |
Friday, March 19, 2010 9:12AM - 9:48AM |
Y7.00003: Traction Stresses Exerted by Adherent Cells: From Angiogenesis to Metastasis Invited Speaker: Cells exert traction stresses against their substrate that mediate their ability to sense the mechanical properties of their microenvironment. These same forces mediate cell adhesion, migration and the formation of stable cell-cell contacts during tissue formation. In this talk, I will present our data on the traction stresses generated by endothelial cells and metastatic breast cancer cells focused on understanding the processes of angiogenesis and metastasis, respectively. In the context of capillary formation, our data indicate that the mechanics of the substrate play a critical role in establishing endothelial cell-cell contacts. On more compliant substrates, endothelial cell shape and traction stresses polarize and promote the formation of stable cell-cell contacts. On stiffer substrates, traction stresses are less polarized and cell connectivity is disrupted. These data indicate that the mechanical properties of the microenvironment may drive cell connectivity and the formation of stable cell-cell contacts through the reorientation of traction stresses. In our studies of metastatic cell migration, we have found that traction stresses increase with increasing metastatic potential. We investigated three lines of varying metastatic potential (MCF10A, MCF7 and MDAMB231). MDAMB231, which are the most invasive, exert the most significant forces as measured by Traction Force Microscopy. These data present the possibility that cellular traction stress generation aids in the ability of metastatic cells to migrate through the matrix-dense tumor microenvironment. Such measurements are integral to link the mechanical and chemical microenvironment with the resulting response of the cell in health and disease. [Preview Abstract] |
Friday, March 19, 2010 9:48AM - 10:24AM |
Y7.00004: Coordination of cell growth and division in normal and cancer cells Invited Speaker: The replication and segregation of the genome (the cell cycle) and the increase in bio-mass of individual cells (cell growth) must be coordinated in all cells, but the mechanism(s) underlying this coordination are poorly understood, particularly in mammalian cells. Many tumor suppressors and oncogenes can alter the normal balance between growth and division and some cancers are characterized by aberrant cell size. The relationship between the cell cycle and cell growth is fundamental to cell proliferation and needs to be understood if we are to fully understand how cell proliferation is altered in cancers. We are developing microfluidic approaches that will enable precise measurements of mass, volume and density to be correlated to molecular measurements during the cell cycle. In this talk, I will present recent progress towards achieving this goal and describe how such approaches are being used to investigate the coordination of cell growth and division in normal and cancer cells. [Preview Abstract] |
Friday, March 19, 2010 10:24AM - 11:00AM |
Y7.00005: Circulating Tumor Cells (CTCs): Emerging Technologies for Detection, Diagnosis and Treatment Invited Speaker: Circulating tumor cell enumeration and characterization have the potential of providing real-time access to epithelial cancers in patients. This fluid phase biopsy of solid phase tumors is crucial to the development of quantitative diagnostic aiding personalized medicine. Cancer is a highly heterogeneous disease over space and time. Our goal is to generate a mechanistic, yet comprehensive view of both the `FORCE-journey' of a cancer cell during the metastatic phase, and a `TIME-journey' of the disease as it progresses. The approach will correlate the `FORCE' and `TIME' journey with both the bio-clinical aspects and the genomics of this complex problem. Presented will be results from a case study in lung cancer patients for which CTC analysis is compared with clinical progression. Morphologic and molecular characterization at the single cell level will be discussed in the context of the data set and in the context of individual patient management. Preliminary data will be shown to guide a future research agenda to investigate the fluid phase of solid tumors. [Preview Abstract] |
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