Archive for the ‘Seminars Videos’ Category

Peter Kuhn – “The Fluid Phase of Solid Tumors: How does cancer spread?”

Friday, September 28th, 2012

Speaker: Peter Kuhn, PhD. founded the Scripps Physics Oncology Center with its core research program at the Kuhn Lab. He is a scientist and entrepreneur with a career long commitment in personalized healthcare and individualized cancer patient care. Dr. Kuhn is a physicist who trained at the Julius Maximilians Universität Würzburg, Germany, before receiving his Masters in Physics at the University of Albany, Albany, NY in 1993 and his Ph.D. in 1995. He then moved to Stanford University where he later joined the faculties of Medicine and Accelerator Physics. Since 2002 his primary faculty appointment is with Scripps Research in La Jolla, CA. Dr. Kuhn has co-authored of over 150 peer reviewed scientific publications and patents. Dr. Kuhn is a Director of the Scripps Physics Oncology Center where he is developing the concepts for lifelong diagnostic companions for cancer patients. Leveraging the fluid phase of solid tumors the Scripps Physics Oncology Center is advancing daily the forefront of both improving healthcare effectiveness by providing drug guidance and increasing our understanding of cancer as a disease in each individual patient.

Location: Biodesign Auditorium

Web Cast: View Web Cast Video

Date & Time: November 1st, 2012 12:00 p.m.

Title: The Fluid Phase of Solid Tumors: How does cancer spread?

Abstract: The fluid phase of solid tumors is a clinical tool in personalized cancer care and an emerging research tool in basic science cancer discoveries. The Scripps Physics Oncology Center developed a set of tools for probing the fluid phase. The leading tool is the HD-CTC assay with which we are undertaking a series of clinical studies investigating the metastatic pathways in cancer patients. We are now coupling the experimental data with a theoretical framework for a more complete description of the disease progression.
The fluid phase of solid tumors is a critical third microenvironment in the development and progression of carcinomas. Cells originating from primary or secondary sites travel through the blood circulatory system to either get cleared out or initiate new tumor growth. Translational research efforts are attempting to identify the various subtypes of circulating tumor cells (CTCs), their origins, their destinations and their impact on the disease. Understanding and characterizing CTCs is a first step towards utilizing them as both biopsy material and directly as a biomarker. It requires approaches of subtyping CTCs at the single cell level using molecular and cellular approaches.
Results will be presented that describe technical developments and validation, clinical validation and clinical utility of the HD-CTC Technology.

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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Landon Inge – “LKB1 and Non-Small Cell Lung Cancer: Can understanding the functions of the LKB1 tumor suppressor lead us to new treatments?”

Friday, September 28th, 2012

Speaker: Landon J. Inge, PhD. holds a B.S. in Cellular and Molecular Biology from the University of Arizona and a Ph.D. in Cellular Molecular Pathology from the University of California, Los Angeles. He is member of the Center for Thoracic Disease and Transplantation at St. Joseph’s Hospital and Medical Center, where he focused upon identifying new avenues for treating Non-small cell lung cancer and esophageal adenocarcinoma. He has a specific interest in characterizing how loss of the LKB1 tumor suppressor alters the cellular functions within lung cancer cells and utilizing this information to develop therapeutic treatments.

Location: Biodesign Auditorium

Web Cast: View Web Cast

Date & Time: November 15th, 2012 12:00 p.m.

Title: LKB1 and Non-Small Cell Lung Cancer: Can understanding the functions of the LKB1 tumor suppressor lead us to new treatments?

Abstract: Lung cancer, and more specifically non-small cell lung cancer (NSCLC), is the primary contributor to cancer related mortalities within the United States and accounts for the majority (~80%) of lung cancers compared to the other subtypes. Due to limited choices in treatment (surgical resection, chemotherapy and radiation), significant work has identified unique genetic alterations within NSCLC tumors in hopes of utilizing this information to develop improved treatment modalities. Genetic inactivation of the tumor suppressor gene, LKB1/STK11, is frequent in NSCLC and contributes to NSCLC disease progression. The unique regulatory functions of LKB1, combined with the increased frequency of inactivation in NSCLC, have resulted in considerable interest in developing therapies targeted towards LKB1 null NSCLC. In this talk, I will discuss the current understanding of LKB1’s regulatory functions and contribution of LKB1 loss to NSCLC progression, as well as our and others attempts to tailor treatments towards LKB1 null NSCLC.

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

Hans-Joachim Ziock – “A New Definition of Information: its Origins and Implications for Cancer”

Thursday, September 6th, 2012

***NEW LOCATION COMPUTING COMMONS 120

Speaker: Hans-Joachim Ziock, PhD. Reflecting his diverse interests, Dr. Ziock’s career covers a wide range of topics. He received his undergraduate and graduate degrees from the University of Virginia. His Ph.D. thesis was in the field of intermediate-energy physics. After joining Los Alamos National Laboratory (LANL) in the intermediate-energy physics group, Dr. Ziock began working in the field of elementary particle physics and became the lead LANL scientist investigating radiation tolerant solid state detectors for collider applications during which he discovered the ability of low temperatures to significantly increase the radiation tolerance and lifetime of these detectors. He was the chief LANL scientist for the high-energy physics Solenoid Detector Collaboration for the Superconducting Super Collider project and then the Large Hadron Collider project. This effort involved working closely with a mechanical engineering group and covered a diverse range of specialties including ultra-stable carbon composite structures, a heat pipe/evaporative cooling system development, and real-time television-based holography. Thereafter, he led the development of an extremely high speed imaging detector system (5 million frames per second) for a proton based radiography program. During this period, Dr. Ziock also became interested in the global issue of carbon management. Dr. Ziock organized and led the Cradle to Grave Carbon Management R&D and Zero Emission Coal programs at LANL. He is a co-inventor of the LANL Zero Emission Coal Technology. He has been the principal investigator at LANL for the CO 2 Mineral Sequestration effort, which involves the permanent disposal of CO 2 in solid mineral form and more recently helped develop the concept of directly extracting CO 2 from the atmosphere. He has most recently been one of the lead scientists on the Protocell Assembly project whose goal has been to produce an artificial self-replicating nanoscale system, where he has been examining the broader issues of self-regulation, information, and artificial intelligence. He continues to pursue efforts in carbon management, energy systems, origins of life, and artificial intelligence.

Location: Computing Commons 120

Web Cast: View Web Cast Video

Date & Time: October 4th, 2012 12:00 p.m.

Title: A New Definition of Information: its Origins and Implications for Cancer

Abstract: Definitions of information are often circular in nature. I present a new definition, rooted in the second law of thermodynamics, based on the requirements of replication and selection. The definition is remarkably simple, yet general enough to apply to both living and non-living systems. Crucially, it provides a scenario for the origin of information while predicting an increase of information with time. The underlying requirements for the continued existence and inevitable growth of information also imply that cancer is an inherent outcome of information’s existence. Much of this work was carried out in collaboration with Stirling Colgate.

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

Steve Henikoff – “Histone variants, nucleosome dynamics and epigenetics”

Thursday, August 9th, 2012

Speaker: Steve Henikoff, PhD, received a BS degree in Chemistry from the University of Chicago and a Ph.D. degree in Biochemistry and Molecular Biology from Harvard University, and carried out postdoctoral research at the University of Washington. He joined the Fred Hutchinson Cancer Research Center in Seattle in 1981, where he is a Member of the Basic Sciences Division and an Affiliate Professor of Genome Science at the University of Washington. He has been an Investigator of the Howard Hughes Medical Institute since 1990 and a Member of the US National Academy of Sciences since 2005. He is co-Editor-in-Chief of Epigenetics & Chromatin, a member of the Editorial Boards of Trends in Genetics, Current Opinion in Genetics and Development and Genome Biology, and a member of the Scientific Adisory Boards of Epizyme, Inc. and the Chicago Biomedical Consortium. His laboratory studies chromatin processes, epigenetic inheritance, centromere structure, function and evolution, and develops tools for epigenomics.

Location: Biodesign Auditorium

Web Cast: View Web Cast Video

Date & Time: September 6th, 2012 12:00 p.m.

Title: Histone variants, nucleosome dynamics and epigenetics

Abstract: Dr. Henikoff will talk about histone variants, nucleosome dynamics and epigenetics.

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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Karen Anderson – “Designing Cancer Vaccines: From Antigen Identification to Targeting Tumor Dormancy”

Friday, April 6th, 2012

Speaker: Karen Anderson, MD, PhD, Dr. Anderson graduated from the University of Virginia with a BA in Chemistry. She then completed a combined MD and PhD program at Duke University, where she studied immunology under Dr. Peter Cresswell, a National Academy member and HHMI investigator now at Yale University. She completed internal medicine residency at the Brigham and Women’s Hospital in Boston, and hematology/oncology fellowship training at the Dana Farber Cancer Institute in Boston, where she remained for 11 years as faculty, until she came here to ASU in late 2011. Her laboratory focuses on understanding how the immune response can be harnessed to detect and alter cancer development.

Location: Biodesign Auditorium

Web Cast: View Web Cast

Date & Time: April 19th, 2012 12:00 p.m.

Title: Designing Cancer Vaccines: From Antigen Identification to Targeting Tumor Dormancy

Abstract: Cancer does not exist in a vacuum: the host immune system continuously monitors cells for alterations in protein content and structure. Several key questions in cancer immunology are the identification of antigens associated with tumor destruction, optimal timing and method of antigen delivery, and the identification of the regulatory pathways and tumor heterogeneity that limit effective immunity. The design of future vaccines requires understanding both the targets and the biology of effective anti-tumor immune responses. To determine if tumor cells can induce effective immune responses, we conducted first-in-human clinical trials of autologous breast cancer vaccination with tumor cells engineered to secrete granulocyte-macrophage colony stimulating factor (GM-CSF), a potent cytokine that stimulates immune activation. These studies demonstrated that autologous vaccination induces both antibody and T-cell immunity to tumor-derived proteins with minimal toxicity. Using proteomic monitoring of immune responses, the breadth and specificity of the immune response was determined. However, the timing of immune activation is critical; immunotherapy is likely to be most effective at eradicating minimal residual disease before the immune system is too impaired from the burden of disease. For breast and prostate cancers, tumor cells may disseminate early, and are frequently found dormant for years in the bone marrow prior to reactivation. The design of future immunotherapies that target both primary and disseminated tumor cells in the bone marrow 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

Barbara Hempstead, MD, PhD, Weill Cornell Medical College – “The Impact of Genomic Evolution on Clinical Challenges”

Monday, March 26th, 2012

Speaker: Barbara Hempstead, MD, PhD, is the Senior Co-investigator and Center Co-Director, the O. Wayne Isom Professor of Medicine, and Co-Chief of the Division of Hematology and Medical Oncology at Weill Cornell Medical College, New York. Dr. Hempstead is a practicing board-certified medical oncologist and hematologist and the principal investigator for numerous NIH research grants. Her research effort focuses on the study of growth factors, neurotrophins. She is evaluating the role of neurotrophins in regulating vessel growth, stabilization and regression, in models of vascular development and in tumors. Dr. Hempstead administratively oversees with Co-Division Chief, Dr. David Nanus, a faculty of 43 academic clinical researchers, translational scientists and basic scientists focused on cancer. These include clinical investigators with more than 100 ongoing clinical trials, most with translational components. She is a member of the Internal Advisory Board for the New York-Presbyterian-Weill Cornell Cancer Center, and has chaired international meetings in her area of research interest.

Location: Biodesign Auditorium

Web Cast: View Web Cast

Date & Time: April 5th, 2012 12:00 p.m.

Title: The Impact of Genomic Evolution on Clinical Challenges

Abstract: The major recent advances in genomic sequencing provide unparalleled opportunities to identify novel mechanisms that regulate susceptibility to human diseases, as well as disease pathogenesis and progression. However, the heterogeneity of human populations leads to complexity that complicates these analyses. Here, we will discuss clinical conundrums of human adaptation to extreme environments, and the impact of tumor heterogeneity on clinical prognoses, for which genetic profiling has uncovered unique and targetable pathways to improve patient outcomes.

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

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
email hidden; JavaScript is required

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
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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