Live Webinar: 7 October 2021, 4 pm CET
Organised by ECTS
Date & Time: 7 October 2021, 4 pm CET
Featuring Therasa Guise, and moderated by Jessica Pepe
Costs: Live webinar is free for ECTS members and non-members, but a registration is required. Recordings are accessible to ECTS members only.
Format:
- 5 min welcome & introductions
- 35 min presentation
- 20 min Q&A
Learning Objectives:
- To recognize states of pathologic bone destruction and learn to prevent the consequences locally and systemically.
- To understand how bone destruction could alter glucose metabolism
- To recognize that bone loss could have adverse consequences on metabolism and muscle function
The Cancer-Bone-muscle interactions, Brussels, Belgium, 07-10-2021 has been accredited by the European Accreditation Council for Continuing Medical Education (EACCME®) with 1 European CME credits (ECMEC®s).
Each medical specialist should claim only those hours of credit that he/she actually spent in the educational activity.”
Featuring Dr. Theresa Guise
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. She held the Zachery Chair for Translational Research at University of Texas, the Gerald D. Aurbach Chair of Endocrinology at the University of Virginia and the Jerry and Peggy Throgmartin Professor of Oncology and Professor of Medicine at the Indiana University School of Medicine. 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 American Society for Bone and Mineral Research (ASBMR), ASCI and International Bone and Mineral Society (IBMS), and as Associate Editor of the Journal of Bone and Mineral Research (JBMR), 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. Recognitions include the Fuller Albright, the Paula Stern Achievement and the Stephen M. Krane Awards (ASBMR), Philip S. Hench and Legacy Laureate Awards (University of Pittsburgh School of Medicine), Fellow of the ASBMR, 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. She has been continually funded by the NIH since 1992, has published over 190 articles and has trained over 50 postdoctoral fellows and students.
Moderated by Jessica Pepe
Abstract
Breast cancer cells frequently disseminate to the bone marrow, where they may either enter a dormant state or colonize the bone and induce osteolysis. The mechanisms that regulate tumor cell entry and exit from dormancy in the bone are not well understood, but several factors have been identified. Previous work from our group found that leukemia inhibitory factor receptor (LIFR) promotes tumor dormancy when expressed on bone-disseminated tumor cells and that loss of LIFR enables otherwise dormant tumor cells to colonize the bone. Our lab has therefore examined how LIFR expression is regulated in breast cancer cells, with the hope that understanding its regulation might provide novel avenues to therapeutically target dormant disseminated tumor cells. Through these efforts we have found that LIFR is epigenetically regulated, and that histone deacetylase (HDAC) inhibitors, which are FDA-approved for several blood cancers, stimulate LIFR expression on breast cancer cells from all subtypes. This finding presents an interesting therapeutic opportunity to explore whether HDAC inhibitors may be used to promote a chronic state of tumor dormancy and prevent recurrence in bone. Our findings suggest that this may be feasible, but that the effects of histone deacetylase inhibitors on bone remodeling profoundly impact tumor colonization and must be combined with appropriate anti-resorptive therapies.