Vivek Nandakumar, a graduate student working withDeirdre Meldrum, presented a poster of his work to the Arizona Microscopy and Microanalysis Society (AIMS) annual meeting in March 2010.
Poster(Powerpoint): Single Cell Tomography for Early Cancer Detection
Poster (JPG): Single Cell Tomography for Early Cancer Detection
Poster(Powerpoint): Single Cell Tomography for Early Cancer Detection
Poster (JPG): Single Cell Tomography for Early Cancer Detection
Speaker: Kimberly J. Bussey, Ph.D., Associate Investigator in the Clinical Translational Research Division, Lead Investigator of the Adrenocortical Carcinoma (ACC) Research Program at TGen
Location: Biodesign Auditorium
Date & Time: March 25, 2010 12:00 p.m.
Title: The role of Bioinformatics in teasing apart epigenetics in cancer
Abstract:
The role of Bioinformatics in teasing apart epigenetics in cancer
The epigenome refers to heritable and reversible marks in the genome that do not result from changes in DNA sequence. These include modifications of DNA and/or histones such as methylation, acetylation, sumolation, and ubiquitination, as well as the region-specific incorporation of variant histone proteins. Recent work has highlighted the importance of the epigenome in regulating gene expression and contributing to phenotypic heterogeneity. The number and types of data being generated to look at various aspects of the epigenome is rapidly expanding and requires the adaptation of existing bioinformatics approaches or more commonly the development of new approaches. We will discuss where the field of epigenomics is currently, both experimentally and bioinformatically, and what questions need to be addressed, particularly as they relate to cancer.
Kim’s Biosketch: Dr. Bussey received her B.S. in general biology from the University of Arizona. She received her Ph.D. in Molecular and Medical Genetics from Oregon Health Sciences University where her dissertation research focused on the cytogenetic and molecular characterization of pediatric germ cell tumors, a group of rare tumors in children. Prior to coming to TGen as an Associate Investigator and Lead Investigator for the ACC Research Program, she did a post-doctoral fellowship and worked as a contract scientist with John Weinstein, M.D., Ph.D. and the Genomics and Bioinformatics lab in the Laboratory of Molecular Pharmacology at the NCI. Her work there focused on integrative analysis of array CGH data and expression data in the NCI60 and development of computational tools to facilitate such analyses.
Speaker: Carlo Maley, Ph.D., Assistant Professor, Molecular and Cellular Oncogenesis Program, Systems Biology Division, The Wistar Institute
Location: Biodesign Auditorium
Date & Time: March 31, 2010 7:30 p.m.
Title: Why we get cancer and why it has been so hard to cure.
Abstract: The story of cancer begins approximately 1 billion years ago, with the rise of multicellular organisms. Before that point, there was no cancer. Afterwards, cancer was the central problem threatening the integrity of the body. Cancer has become a particular problem in developed countries. In the U.S., men have a 45% and women a 38% lifetime risk of developing cancer. Despite the enormous progress we have made in technology and medicine in the last 50 years, we have made almost no progress reducing deaths from cancer, even when we take into account changes in lifespan.
Why is cancer such a difficult problem to solve? Because cells in tumors evolve. Tumor cells mutate a high rates and compete for space and resources like oxygen. Mutant cells that can reproduce or survive better than their competitors tend to spread in a tumor. Thus, tumors are microcosms of natural selection. By the time we detect a tumor in the clinic, it contains billions of cells carrying tens of thousands of mutations. By chance, some of those mutant cells are often resistant to the anti-cancer drugs we use. The result is temporary remission followed by relapse with a resistant tumor. Therapeutic resistance is so common that attention has recently switched to detecting cancer early in its development when it is still easy to cut out, or preventing cancer altogether.
Carlo’s Biosketch: Carlo Maley is an assistant professor in the systems biology division of the molecular and cellular oncogenesis program at the Wistar Institute and part of the Seattle Barrett’s Esophagus Research Program. He is a member of the University of Pennsylvania genomics and computational biology graduate program as well as the cellular and molecular biology graduate program. He received an M.Sc. degree from the University of Oxford, studying evolutionary biology with W.D. Hamilton. He earned his Ph.D. in computational biology from MIT, working with Rodney Brooks and Michael Donoghue, and then moved into cancer biology as a postdoc with Stephanie Forrest at the University of New Mexico and as a staff scientist with Brian Reid at the Fred Hutchinson Cancer Research Center. His research lies at the intersection of evolutionary biology, computational biology and cancer biology and includes both dry lab (computational) and wet lab (genetics of tumors and evolutionary tissue culture experiments) projects. He is interested in how cells evolve in neoplastic progression and in response to therapy with the goal of controlling that evolution to prevent cancer and therapeutic resistance.
No area of research better illustrates the constructive engagement of physics and cancer biology than the burgeoning field of cell mechanics. This workshop focused on the mechanical properties of healthy and cancer cells and the surrounding tissues. It covered topics such as changes in the elastic properties of cancer cells, the internal chemical and genetic changes triggered by the physical properties of the micro-environment (such as its hardness or surface adhesion) and the motility of cells, with special emphasis on metastasis. It brought together physicists, oncologists, cancer biologists, engineers and computer scientists, with the goal of determining whether cancer could be better understood and even controlled by manipulating the physical properties of the cancer cells’ environment.
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The seminar followed a 3 day conference at ASU on the mechanical properties of cancer. Don Coffey spoke to Pauline Davies from the Hugh Downs School of Human Communication about the conference. A transcript of the interview follows. (more…)
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Presentation online at: https://connect.asu.edu/p6whezlx0ff/
For more information on John D. Nagy please visit his website at: www.scottsdalecc.edu/nagy
Speaker: Jim Elser, Regents’ Professor in the School of Life Sciences, Arizona State University, Tempe, AZ
Location: Biodesign Auditorium
Date & Time: March 11, 2010 12:00 p.m.
Title: Are cancers phosphorus-limited “ecosystems” ?
Abstract: Phosphorus is vital to cell growth, and its supply can be a crucial limiting factor for organism growth in in many ecological situations, such as lakes and grasslands. What determines an organism’s demand for this important element? Work with plankton, bacteria, and fruit flies demonstrates a link between growth rates and the investment of P in RNA production, a result that may be understood within the framework of biological stoichiometry (the study of the balance of energy and multiple chemical elements in living systems). Here I’ll describe the application of these ideas to human cancer and present data that provide support for this “Growth Rate Hypothesis” in some types of tumors, including the possibility that tumor growth in the body may be limited by the supply of P.