Archive for the ‘Event Descriptions’ Category

Carlo Maley, Ph.D. Public Seminar- Evolution in Cancer: Lessons from Barrett’s Esophagus

Friday, February 17th, 2012

Speaker: Carlo Maley, Ph.D., is an Associate Professor in the Department of Surgery, a member of the Thoracic Oncology Program and a Principal Investigator in the Thoracic Oncology Lab and Maley Lab. The UCSF Helen Diller Family Comprehensive Cancer Center has also tapped Dr. Maley to lead a new Center for Evolution and Cancer.

Dr. Maley received his B.A. in computer science and psychology from Oberlin College in 1991 and his M.Sc. in Zoology (evolutionary theory) from University of Oxford in 1993 where he worked with William D. Hamilton. In 1998, Dr. Maley received a Ph.D. in Computer Science from MIT where he worked with Michael Donoghue and Rodney Brooks.

Dr. Maley did his postdoctoral training at the University of New Mexico, mentored by Professor Stephanie Forrest, and at the Fred Hutchinson Cancer Research Center by Dr. Brian Reid.

Prior to joining UCSF, Dr. Maley was an assistant professor at the Wistar Institute, and a member of two other graduate programs at the University of Pennsylvania: Genomics and Computational Biology, and Cellular and Molecular Biology.

Location: Biodesign Auditorium

Web Cast: View Web Cast

Date & Time: February 23rd, 2012 12:00 p.m.

Title: Evolution in Cancer: Lessons from Barrett’s Esophagus

Abstract: Neoplastic progression is a process of somatic evolution. Cells mutate and some mutations increase the fitness (survival or reproduction) of the clone, leading to a clonal expansion. The evolutionary theory of cancer is now 36 years old, but the dynamics of the process are still poorly understood. What are the mutation rates for the different kinds of genetic and epigenetic lesions in progression? How many clonal expansions (advantageous mutations) are involved in progression? Can we prevent cancer by slowing the rate of mutations? I will address all of these questions through a new longitudinal study of neoplastic progression in Barrett’s esophagus.

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
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Paul Davies, Ph.D. “Cancer as Metazoa 1.0”

Monday, January 23rd, 2012

Speaker: Paul Davies, Ph.D., is a theoretical physicist, cosmologist and astrobiologist. He is Director of The Beyond Center for Fundamental Concepts in Science, whose agenda encompasses foundational topics ranging from the origin of the universe to the origin of life and the nature of time. Davies is also Principal Investigator of the Center for the Convergence of Physical Science and Cancer Biology at ASU. Among his research accomplishments, Davies helped explain how black holes radiate energy, what caused the ripples in the cosmic afterglow of the big bang, and why life on Earth may have come from Mars. He has written about 30 books, most recently The Eerie Silence: Are We Alone in the Universe? His fearless championing of bold new ideas earned Davies the epithet of “The Disruptor” in a recent profile in Nature magazine.

Location: Biodesign Auditorium

Web Cast: Unavailable

Date & Time: January 26th, 2012 12:00 p.m.

Title: Cancer as Metazoa 1.0

Abstract: Cancer is widespread among eukaryotes, and can be successfully tackled only by understanding its place in the story of life itself – especially the evolution of multi-cellularity. In this seminar I will propose a new theory of cancer, drawing on insights from astrobiology. The central hypothesis is that cancer is an organized pre-programmed process driven by a cassette of highly conserved, deeply-evolved ancient genes – genes that are active in early-stage embryo development, and which become inappropriately re-awakened in the adult form. In effect, cancer tumors are atavisms, recapitulating an ancient life form – “Metazoa 1.0” – dating back to the dawn of multi-cellularity. This hypothesis differs fundamentally from the popular notion that cancers are deregulated rogue cells running amok, and explains cancer’s well-known robustness and resilience. It also offers a well-defined target for therapy.

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
email hidden; JavaScript is required

Sanjay Kumar, M.D., Ph.D., UC Berkeley – Mechanobiological control of tumor and stem cell behavior: Lessons from the brain

Tuesday, January 17th, 2012

Speaker: Sanjay Kumar, M.D., Ph.D., is Associate Professor of Bioengineering at the University of California, Berkeley. Dr. Kumar also holds appointments as a Faculty Scientist at Lawrence Berkeley National Laboratory and Supernumerary (Visiting) Professor at The University of Navarra in Spain. He earned a B.S. in chemical engineering from the University of Minnesota in 1996, and both a Ph.D. in molecular biophysics and an M.D. from Johns Hopkins University in 2003. From 2003-2005, he served as an NIH research fellow at Children’s Hospital Boston and Harvard Medical School. Since joining the faculty at UC Berkeley in 2005, Dr. Kumar has been recognized with the Presidential Early Career Award for Scientists and Engineers (PECASE) through the Department of Defense, The NSF CAREER Award, The NIH Director’s New Innovator Award, and The Arnold and Mabel Beckman Young Investigator Award.

Location: CPCOM 120

Web Cast: View Web Cast

Date & Time: March 8th, 2012 12:00 p.m.

Title: Mechanobiological control of tumor and stem cell behavior: Lessons from the brain

Abstract: One of the most exciting breakthroughs in cell biology over the past decade is the recognition that micromechanical inputs to cells from the solid-state extracellular matrix (ECM), such as those encoded in ECM geometry, topography, and elasticity, can influence cell and tissue physiology and pathology in profound and specific ways. This “physical microenvironment” bears direct relevance to the pathogenesis of diseases of the nervous system in which cells alter their structure, motility, or compliance, including neuronal and glial tumors and neurodegenerative disorders, and suggests that specific cell behaviors may be engineered by directly manipulating the underlying molecular systems. In this talk, I will discuss efforts my group has taken to elucidate the importance of the physical microenvironment in regulating tumor and stem cell biology in the central nervous system. This includes efforts to probe the molecular basis of the relationship between ECM mechanics, topology, and cellular motility and force generation in malignant glioma cells in two- and three-dimensional culture. In the case of adult neural stem cells, these approaches have enabled us to dissect and manipulate neurogenic commitment and maturation in vitro and in vivo by controlling both physical properties of the stem cell niche and the cellular signaling systems that interface with this niche. An important lesson from this work is that adult neural stem cells sense time-sensitive biomechanical signals from the microenvironment that are processed through Rho family GTPases, produce changes in cellular contractile signaling, and strongly influence neurogenic lineage commitment.

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
email hidden; JavaScript is required

John Pepper, National Cancer Institute – Cancer as a failure of multicellularity

Tuesday, January 17th, 2012

Speaker: John W. Pepper, Ph.D. received his Ph.D. in biology from the University of Michigan in 1966. He was a postdoctoral fellow at the Santa Fe Institute, where he now serves as a member of the External Research Faculty. He is also a biologist at the National Cancer
Institute. His research focuses on the theory of multilevel selection and evolution, and on applications of this theory. Currently, he is working primarily on applications of evolutionary theory to complex diseases, including cancer. His major goal is to bring scientific understanding of evolution to bear in understanding the role of somatic cell-level evolution in the origin and progression of cancer. Pepper’s 31 peer-reviewed publications in behavioral ecology, evolutionary theory and its applications, and in cancer biology have been cited an average of 25 times each.

Location: Biodesign Auditorium

Web Cast: View Web Cast

Date & Time: February 9th, 2012 12:00 p.m.

Title: Cancer as a failure of multicellularity

Abstract: Cancer results from a process of cellular evolution. Key cancer defenses and vulnerabilities
both arose from the ancient evolutionary transition from single-celled to multicellular
organisms. Because cellular evolution leads inexorably to cancer, organismal evolution has
led to adaptations that organize cell reproduction into patterns that are less subject to cellular
evolution. We used an agent-based computational model of evolution inside tissues to test the
hypothesis that cell differentiation is crucial to suppressing cellular evolution within the body.
The hypothesis was supported. If this most basic safeguard is compromised, all the obstacles
to cancer built by organismal evolution are quickly dismantled by cellular evolution within the
organism.

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
email hidden; JavaScript is required

John W. Pepper – Cancer as a failure of multicellularity

Friday, January 13th, 2012

Speaker: John W. Pepper, Ph.D. received his Ph.D. in biology from the University of Michigan in 1966. He was a postdoctoral fellow at the Santa Fe Institute, where he now serves as a member of the External Research Faculty. He is also a biologist at the National Cancer Institute. . His research focuses on the theory of multilevel selection and evolution, and on applications of this theory. Currently, he is working primarily on applications of evolutionary theory to complex diseases, including cancer. His major goal is to bring scientific understanding of evolution to bear in understanding the role of somatic cell-level evolution in the origin and progression of cancer. Pepper’s 31 peer-reviewed publications in behavioral ecology, evolutionary theory and its applications, and in cancer biology have been cited an average of 25 times each.

Location: Biodesign Auditorium

Web Cast: View Web Cast

Date & Time: February 9th, 2012 12:00 p.m.

Title: Cancer as a failure of multicellularity

Abstract: Cancer results from a process of cellular evolution. Key cancer defenses and vulnerabilities both arose from the ancient evolutionary transition from single-celled to multicellular organisms. Because cellular evolution leads inexorably to cancer, organismal evolution has led to adaptations that organize cell reproduction into patterns that are less subject to cellular evolution. We used an agent-based computational model of evolution inside tissues to test the hypothesis that cell differentiation is crucial to suppressing cellular evolution within the body. The hypothesis was supported. If this most basic safeguard is compromised, all the obstacles to cancer built by organismal evolution are quickly dismantled by cellular evolution within the organism.

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
email hidden; JavaScript is required

Rodger P McEver, M.D. Oklahoma Medical Research Foundation – ‘Force-regulated Adhesion of Leukocytes to Vascular Surfaces’

Monday, January 9th, 2012

Speaker: Rodger P McEver, M.D. is Chair, Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation. He studies how circulating blood cells attach to blood vessel surfaces at sites of tissue injury or infection.

Location: Biodesign Auditorium

Web Cast: View Web Cast

Date & Time: TBA, 2012 12:00 p.m.

Title: Force-regulated Adhesion of Leukocytes to Vascular Surfaces

Abstract: During inflammation, flowing leukocytes tether to and roll on activated endothelial cells, then decelerate and arrest before they emigrate into the underlying tissues. Interactions of selectins with glycosylated ligands mediate leukocyte rolling, a prerequisite for integrin-mediated deceleration and arrest. Counterintuitively, rolling requires a minimal flow rate, or shear threshold. As flow drops below this threshold, rolling becomes more rapid and irregular until the cells detach. Shear stress applies force to bonds between selectins and their ligands, which affects their lifetimes. As flow increases from suboptimal levels, force first prolongs bond lifetimes (catch bonds) until they reach a maximal level. Further increases in force shorten bond lifetimes (slip bonds). Catch bonds between selectins and ligands enable flow-enhanced adhesion of leukocytes to vascular surfaces and may prevent inappropriate agglutination of circulating cells. Recent data indicate that the mechanical environment of blood flow influences the functions of other adhesion receptors on leukocytes and platelets during infection or tissue injury. Mechanical forces might also regulate migration of tumor cells in extravascular tissues and metastasis of tumor cells through the blood stream.

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
email hidden; JavaScript is required

Geoffrey West, Santa Fe Institute ‘Towards a Quantitative, Predictive Theory of Tumor Growth, Metabolic Rate and Vascular Structure’

Wednesday, January 4th, 2012

Speaker: Geoffrey West, PhD. is a theoretical physicist whose primary interests have been in fundamental questions in physics, especially those concerning the elementary particles, their interactions and cosmological implications. West served as SFI President from July 2005 through July 2009. Prior to joining the Santa Fe Institute as a Distinguished Professor in 2003, he was the leader, and founder, of the high energy physics group at Los Alamos National Laboratory, where he is one of only approximately ten Senior Fellows. His long-term fascination in general scaling phenomena evolved into a highly productive collaboration on the origin of universal scaling laws that pervade biology from the molecular genomic scale up through mitochondria and cells to whole organisms and ecosystems. This led to the development of realistic quantitative models for the structural and functional design of organisms based on underlying universal principles. This work, begun at the Institute, has received much attention in both the scientific and popular press, and provides a framework for quantitative understanding of problems ranging from fundamental issues in biology (such as cell size, growth, metabolic rate, DNA nucleotide substitution rates, and the structure and dynamics of ecosystems) to questions at the forefront of medical research (such as aging, sleep, and cancer). Among his current interests is the extension of these ideas to understand quantitatively the structure and dynamics of social organizations, such as cities and corporations, including the relationships between economies of scale, growth, innovation and wealth creation and their implications for long-term survivability and sustainability.

Location: Biodesign Auditorium

Web Cast: View Web Cast Video

Date & Time: January 12, 2012 12:00 p.m.

Title: Towards a Quantitative, Predictive Theory of Tumor Growth, Metabolic Rate and Vascular Structure

Abstract: A conceptual framework successfully developed for quantitatively understanding and predicting many physiological and dynamical properties of mammals and plants, including metabolic rates, ontogenetic growth trajectories and vascular structure, is extended to tumors. The theory presumes that life at all scales from intra- to multi-cellular levels is sustained by space-filling, fractal-like, hierarchical branching networks whose “universal” geometric and dynamical properties provide a mathematical framework that captures the essential features of these diverse systems. When applied to tumors (and their interface with host tissue) the theory yields extensive quantitative predictions for many of their properties, including growth rates, metabolic rates, degree of necrosis, blood flow rates, capillary density and vessel sizes, in good agreement with data. In addition, it shows how these properties depend on both tumor and host size thereby explaining why similar tumors grow systematically slower and occur less frequently in larger animals, shedding light on Peto’s paradox. The role of damage (and consequent entropy production) due to dissipative forces in host networks as a generator of tumors and its relationship to aging, mortality and sleep will be explored. Possible implications for potential therapeutic strategies will be discussed.

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
email hidden; JavaScript is required

William Muller – How Endothelial Cells Regulate Leukocyte Transmigration: Application to Cancer Metastasis

Thursday, November 3rd, 2011

Speaker: William Muller, MD, PhD. received his A.B. degree summa cum laude from Harvard University in 1975. He earned his PhD degree from The Rockefeller University in 1981 under the mentorship of Dr. Ralph Steinman and the late Dr. Zanvil Cohn. He received his MD degree in 1982 from Cornell University Medical College as part of the combined MD/PhD program. In 2007 he was recruited to Northwestern University Feinberg School of Medicine as the Magerstadt Professor and Chairman of the Department of Pathology. Dr. Muller’s research focuses on the cellular and molecular basis of the inflammation, and in particular the interactions of leukocytes and endothelial cells in the inflammatory response. Dr. Muller’s research has been well funded by the National Institutes of Health, the American Heart Association, and several biotech companies. He is the recipient of the prestigious MERIT Award from the NIH. He is one of the Editors of The Journal of Experimental Medicine and Annual Reviews of Pathology: Mechanisms of Disease and serves on the editorial boards of several other journals. He has served in many official capacities over the years for the American Society for Investigative Pathology as well as for the North American Vascular Biology Organization (NAVBO) and was elected President of NAVBO in 2004. He was elected a Fellow of the AAAS in 2010.

Location: Biodesign Auditorium

Web Cast: View Web Cast Video

Date & Time: November 3rd, 2011 12:00 p.m.

Title: How Endothelial Cells Regulate Leukocyte Transmigration: Application to Cancer Metastasis

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
email hidden; JavaScript is required

Ernst-Ludwig Florin – Microtubules: A prototype for biological and manmade fiber bundles

Monday, October 24th, 2011

Speaker: Ernst-Ludwig Florin, PhD.
Location: Goldwater 487

Date & Time: October 26th, 2011 4:00 p.m.

Title: Microtubules: A prototype for biological and manmade fiber bundles

Abstract: Microtubules are part of the cytoskeleton and are involved in a large number of fundamental cellular processes such as cell division or intracellular transport. Due to their essential role in cell division, they are among the most successful targets for anticancer therapy. Individual microtubules are 25 nm thin and up to 100 µm long tube-like biopolymers built from even smaller fibers called protofilmaments. The protofilament architecture leads to unusual mechanical properties, such as a length dependence of the persistence length, not found in any manmade material. In my presentation, I will describe recent experimental results and present a model that explains how the length dependence of the persistence length arises from the protofilament architecture and local interactions between adjacent filaments. Implications for the regulation ofmicrotubule stiffness in cells and possible evolutionary advantages of thiscontrol will be discussed. Finally, I will show that the model can be used to describe the mechanical response of a wide range of biopolymer bundles and may help for instance in the efficient design of new multifunctional materials based on carbon nanotubes.

To schedule a meeting with the speaker click here

If you have any questions, please contact Jill Kolp, email hidden; JavaScript is required, Series Coordinator

Thai Tran – Discovery of Prolactin Signaling Pathway in Breast Cancer

Monday, October 10th, 2011

Speaker: Thai Tran, PhD. received his Ph.D. in molecular biology from Purdue University and was trained a as a postdoctoral fellow with Dr. Hallgeir Rui at the Kimmel Cancer Center, Thomas Jefferson University. Dr. Tran has background in molecular and cellular biology of cancer. His research focus is to investigate the molecular functions that govern cancer cell development and progression. Specifically, his research has centered on identifying molecular biomarkers in breast, pancreatic and esophagus cancers using the combined approaches of high throughput immunohistochemistry, molecular and cellular technologies. More recently, he has focused more on dissecting intratumoral heterogeneity at the single-cell level by analyzing gene expression profiles of individual cells freshly isolated from true human clinical samples. The primary goal of this study is to identify minute populations of cells that potentially play major roles in cancer progression and metastasis.

Location: Biodesign Auditorium

Web Cast: View Web Cast Video

Date & Time: October 20th, 2011 12:00 p.m.

Title: Discovery of Prolactin Signaling Pathway in Breast Cancer

Abstract: Breast cancer is the second leading cause of deaths among women. In the United States, an estimated 230,480 are diagnosed with breast cancer each year and, of these, 39,520 are expected to die from the disease. This devastating consequence is partly due our inability to detect and provide treatments while the tumor is localized to the breast. As a result, numerous efforts have been made to identify early breast cancer biomarkers. In my talk I will discuss the implications of a number of potential breast cancer biomarkers specifically focusing on the functions of prolactin and its downstream target, Stat5. Unraveling the details of this new mechanism illustrates the complexity of signaling pathways and the formidable challenge of designing chemical intervention.

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
email hidden; JavaScript is required