ASBMR 2020 Gerald D. Aurbach Lecture: Communicating Clocks: Circadian Metabolism and Epigenetics
Paolo Sassone-Corsi, Ph.D., University of California, USA
Friday, September 11 | 8:30 a.m. – 9:30 a.m.
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Dr. Paolo Sassone-Corsi is the Director of the Center for Epigenetics and Metabolism and a Donald Bren Professor at the University of California, Irvine. After receiving his PhD in Genetics in Italy and completing post-doctoral studies in France and US, he established his research team in Strasbourg, France, with the position of Directeur de Recherche between 1989-2006. Dr. Sassone-Corsi joined the University of California, Irvine as a Distinguished Professor and Chair of the Department of Pharmacology in 2006. As of 2011, Dr. Sassone-Corsi has been the Director of the Center for Epigenetics and Metabolism and a Donald Bren Professor. In addition, Dr. Sassone-Corsi is an External Professor of the Max-Planck Institute of Germany. During the past three decades, Dr. Sassone-Corsi’s research has focused on the molecular mechanisms of transcriptional regulation and chromatin remodeling, specifically in response to changes in signaling transduction and cellular metabolism. In the past three decades, his team has uncovered the specific role of transcriptional and epigenetic regulators in circadian clock function and deciphered how metabolic circuits intimately connect to the circadian system. For these studies he has received many high-profile international awards and prizes.Research conducted in the Sassone-Corsi Laboratory has significantly impacted the fields of transcription, epigenetics, metabolism and endocrinology. The high impact of his team’s research is witnessed by the numerous high-profile publications, invitations as plenary speaker at high-profile conferences, and by an h-index of 128. Some of Dr. Sassone-Corsi’s most notable research has revealed how nutritional challenge reprogram circadian homeostasis, explored the molecular mechanisms that involve the NAD+-dependent class of deacetylases, and revealed previously unforeseen pathways of circadian control-dependent metabolic sensors that connect to nutrition, cancer and aging. These studies provide new leads towards therapeutic strategies for metabolic disorders.
The circadian clock is responsible for biological timekeeping on a systemic level. The mammalian central pacemaker is localized in the hypothalamus, in a paired neuronal structure called the suprachiasmatic nucleus (SCN). The discovery that all tissues and virtually all cells contain an intrinsic circadian clock revolutionized the field, providing a conceptual framework towards the understanding of organismal homeostasis and physiological tissue-to-tissue communications. The circadian clock controls a remarkable array of physiological and metabolic functions through governing a significant portion of the genome. Furthermore, the clock drives cyclic chromatin remodeling associated to circadian transcription, including spatial nuclear organization. The circadian epigenome shares intimate links with cellular metabolic processes and has remarkable plasticity showing reprogramming during aging and in response to nutritional challenges. We will present findings that reveal specific molecular connections between chromatin remodelers, metabolic pathways and the circadian clock.
ASBMR 2020 Louis V. Avioli Lecture: Cancer, Bone and Beyond: An Integrated View of the Bone Microenvironment
Theresa A. Guise, M.D., Indiana University School of Medicine, USA
Saturday, September 12 | 8:30 a.m. – 9:30 a.m.
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Dr. Theresa A. Guise is Professor, Department of Endocrine Neoplasia and Hormonal Disorders, Chief, Section of Bone and Mineral Disorders at The University of Texas MD Anderson Cancer Center, Cancer Prevention Research Institute of Texas (CPRIT) Scholar and Co-Director of the Rolanette and Berdon Lawrence Bone Disease Program of Texas. She directs a basic, translational and clinical research program on the effects of cancer and cancer treatment on bone, muscle and metabolism. Dr. Guise obtained her M.D. and Internal Medicine Residency Training from the University of Pittsburgh and completed an Endocrinology Fellowship at the University of Texas. Dr. Guise held the Jerry and Peggy Throgmartin Professor of Oncology at the Indiana School of Medicine, the Gerald D. Aurbach Professor of Endocrinology, at the University of Virginia and the Zachry Chair for Translational Research at the University of Texas. She was elected to the American Society for Clinical Investigation (ASCI), the Association of American Physicians (AAP) and chaired the NIH study section of Skeletal Biology, Structure and Regeneration. Dr. Guise served on the Council of ASBMR, ASCI and International Bone and Mineral Society (IBMS), and as Associate Editor of the Journal of Bone and Mineral Research of ASBMR, Treasurer of ASCI, President of IBMS and Scholar of Susan Komen Foundation. She currently Chairs the Tumor Microenvironment Steering Committee of the American Association for Cancer Research (AACR). Recognitions include the Fuller Albright Award and the Paula Stern Achievement Award from the ASBMR, the Outstanding Investigator Award from the International Bone and Calcium Institute, election to the ASCI and the AAP, Philip S. Hench Award Distinguished Alumnus Award and Legacy Laureate Award from the University of Pittsburgh School of Medicine and Established Investigator and Scholar of CPRIT. Dr. Guise is currently principal investigator in several grant-funded research projects from the NIH, the Department of Defense and CPRIT. Her laboratory has been consistently funded by the NIH, DOD (breast cancer, prostate cancer and neurofibromatosis) as well as by Susan G. Komen, Prostate Cancer Foundation, V-Foundation, Mary K. Ash, pharmaceutical companies and philanthropy.
Bone metastases are common in advanced cancers of breast, prostate, lung, renal, and cause significant morbidity such as bone pain, fracture, hypercalcemia, nerve compression syndromes and muscle weakness. Tumor-bone interactions which result in pathologic bone destruction mediate these well-recognized morbidities. Local events in the bone microenvironment due to cancer and cancer treatment which result in pathologic bone destruction may have wide-spread systemic consequences that further increase morbidity and mortality. Potential mechanisms and therapy will be discussed.