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Oceans of Opportunity of Oceans Grand Wailea Resort and Spa Wailea Hotel Grand ABSTRACTS Oceans of Opportunity Oceans of Opportunity 56th Annual Meeting Radiation Research Society 2010 ABSTRACTS Radiation Research Society 810 E. 10th St. Lawrence, KS 66044 Telephone (800) 627-0326 Fax (785) 843-6153 E-mail: [email protected] Website: www.radres.org Radiation Research Society September 25–29, 2010 Grand Wailea Resort Hotel and Spa Maui, Hawaii Abstracts 56th Annual Meeting of the Radiation Research Society Grand Wailea Resort Hotel and Spa Maui, Hawaii September 25th–September 29th, 2010 AWARD LECTURES Failla Lecture of radiation. As a complimentary approach, we are utilizing in vivo shRNA to reversibly knock down p53 to study radiation biology. Our results demonstrate that p53 is required in the GI epithelium to (AL01) Chasing free radicals in cells and tissues. James B. prevent the radiation-induced gastrointestinal (GI) syndrome and in Mitchell, National Cancer Institute, Bethesda, MD endothelial cells to prevent late effects of radiation. We have also In the context of ionizing radiation, it has long been known used these genetic tools to generate primary tumors in mice to study that free radicals, which exist over a very brief time scale, set into tumor response to radiation therapy. These advances in genetic Award Lectures motion a series of events that may lead to cell killing, mutation, and engineering provide a powerful model system to dissect mecha- untoward normal tissue effects (acute and late). Interestingly, from nisms of normal tissue injury and tumor cure by radiation. research conducted over the past 2-3 decades, it has become apparent that even under normal circumstances cells and tissues must cope with free radicals. Oxidative stress imposed by free radicals and reactive oxygen species have been identified in a Marie Curie Lecture number of normal processes including intracellular oxygen metabolism, immune-mediated attack of pathogens, inflammatory (AL03) Disabled DNA-PKcs phosphorylation impairs genomic responses, signal transduction/gene expression pathways, as well as stability in mice. Shichuan Zhang1, Hirihiko Yajima1, HoangDinh being present and contributing to an ever-increasing number of Huynh1, Junke Zheng1, Yu-Fen Lin1, Elsa Callen2, Hua-Tang human pathological conditions. A central theme of our research has Chen2, Andre Nussenzweig2, Cheng Cheng Zhang1, David J. been to better understand how cells and tissues cope with oxidative 1 1 1 Chen , Benjamin Chen , UT Southwestern Medical Center, Dallas, stress and how these responses can be modulated with the goal of TX, 2National Cancer Institute, National Institutes of Health, translating our findings into clinical trials for cancer patients. Bethesda, MD Various attempts to enhance tumor cell radiosensitivity or to protect normal tissue damage will be discussed along with our experiences The catalytic subunit of DNA dependent kinase (DNA-PKcs) with a unique class of compounds called nitroxides. Nitroxides is well known for its role in DNA double strand break repair. In possess antioxidant and radiation protective properties, despite the addition to its kinase activity, phosphorylation of DNA-PKcs is also fact that they are paradoxically stable free radicals. Nitroxides have indispensable for its proper functioning. We have previously shown become useful reagents to elucidate free radical mechanisms in that phosphorylation at the Thr2609 cluster (mouse equivalent biological systems. A number of practical and potentially Thr2605) is critical for DNA double strand break repair and this therapeutic applications of nitroxides have emerged encompassing phosphorylation is mediated by ataxia telangectasia mutated (ATM) ischemia/reperfusion injury, obesity, neurodegenerative disorders, and ATM and Rad3-related (ATR). To further understand the and cancer chemo-preventive agents. Because nitroxides are importance of phosphorylation of DNA-PKcs in DNA damage paramagnetic, they can also be used to interrogate the redox status response, we generated mice carrying DNA-PKcs with three alanine of tissue using MRI. Application of other free radical spin probes substitutions at Thr2605, Thr2634, and Thr2643 in the Thr2605 makes it now possible to non-invasively assess tissue oxygen cluster (3A mutant). Several lines of evidence from this newly- concentration. In this lecture I hope to highlight the thrill of the established mouse model strongly suggest an important role for chase. DNA-PKcs in maintenance of genomic integrity. First, mouse embryonic fibroblast derived from homozygotic mice showed high sensitivity toward both ionizing radiation and DNA crosslinking Michael Fry Lecture reagents. Profound chromosome aberrations were observed in these cells after DNA-damage treatment. Second and most interesting, in sharp contrast to the normal life span of DNA-PKcs knockout mice, (AL02) Using Genetically Engineered Mice for Radiation all homozygotic 3A mutant mice died of hematopoietic stem cell Research. David G. Kirsch, Duke University Medical Center, (HSC) failure at a premature age. Importantly, loss of HSCs Durham, NC happens between embryonic day 12.5 and 16.5 when HSCs are fast The laboratory mouse has been utilized for many decades as a cycling, suggesting a pivotal role of DNA-PKcs phosphorylation in model system for radiation research. Recent advances in genetic replication associated stress response for stem/progenitor cells. In engineering allow scientists to delete genes in specific cell types at addition to early and acute loss of HSCs, mice surviving anemia by different stages of development. The ability to manipulate genes in bone marrow transplantation developed varied kinds of tumors the mouse with spatial and temporal control opens new opportu- including lymphoma, skin cancer, and breast cancer. The high nities to investigate the role of genes in regulating the response of tumor incidence and broad spectrum of tumor type suggested that normal tissues and tumors to radiation. We are using the Cre-loxP phosphorylation of the Thr2609 cluster is critical in modulating system to delete genes, such as p53, in a cell-type specific manner in DNA repair pathways and thus maintaining the mammalian mice to study mechanisms of acute radiation injury and late effects genome. 3 PLENARY SESSIONS CANCER COMPLEXITY: radiation-induced single-strand breaks at every nucleotide in the yeast INSIGHTS FROM SYSTEMS ANALYSIS genome. We thus have come full circle, to study the damaging effects OF TUMOUR SUSCEPTIBILITY of radiation-produced hydroxyl radical on an entire genome. (P001) Cancer Complexity: insights from systems analysis of CLINICAL IMPLICATIONS OF THE CANCER tumour susceptibility. Alan Balmain, UCSF Helen Diller Family STEM CELL HYPOTHESIS Comprehensive Cancer Center, San Francisco, CA Quantitative genetics has identified polymorphisms within gene (P003) Clinical implications of the cancer stem cell hypothesis. regulatory factors or their target genes which cause variation in Max S. Wicha, University of Michigan Comprehensive Cancer phenotypes, such as inflammation and obesity, or responses to Center, Ann Arbor, MI exogenous perturbation by carcinogens or radiation. Expression There is accumulating evidence that many cancers are organized levels of individual genes can also be regarded as ‘‘phenotypes’’ under in a hierarchical fashion in which a cellular sub component displaying genetic control, some of which may influence susceptibility to cancers stem cell properties drives tumorigenesis. These stem cell properties induced by environmental agents. Applying expression Quantitative include self renewal which drives tumorigenesis and differentiation Trait Locus (eQTL) approaches to mouse strains with differing which generates cellular heterogeneity . Cancer stem cells were first susceptibility to diseases, such as obesity and cancer, has identified described in human leukemias and more recently in a variety of solid signaling hubs that may be important targets for drug development. malignancies. These cancer stem cells have been shown to be We used network construction methods to analyze the genetic relatively resistant to both radiation and chemotherapy. A number of architecture of gene expression in normal mouse skin in a cross mechanisms have been proposed to account for the relative radio between tumor-susceptible Mus musculus and tumor-resistant Mus resistance of a cancer stem cells. These include more efficient DNA spretus. The data showed that gene expression motifs representing repair, lower level of oxidants and changes in cell cycle kinetics. In different constituent cell types within the skin such as hair follicle addition cancer stem cells may express increased levels of anti cells, haematopoietic cells, and melanocytes are under separate apoptotic proteins. These mechanisms may also account for Plenary Sessions genetic control. Motifs associated with inflammation, epidermal chemotherapy resistance. In addition cancer stem cells express barrier function, cell cycle control and proliferation are differentially increased levels of cellular transporters and metabolizing enzymes regulated in mice susceptible or resistant to tumor development. The which may also contribute to their chemotherapy resistance. Both in intestinal stem cell marker Lgr5 is identified as a candidate master vitro and mouse studies suggest that stem cells mediate a tumor regulator of hair follicle gene expression, and the Vitamin D receptor invasion and metastasis. Since these cells contribute to treatment (Vdr) links epidermal barrier function, inflammation,
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