[cid:image001.jpg@01DA6E2A.488EA280] Wednesday, March 6, 2024 9:30 - 10:20am, MJIS 1001 ZOOM LINK: https://purdue-edu.zoom.us/j/93407874576<https://nam04.safelinks.protection.outlook.com/?url=https%3A%2F%2Fpurdue-edu.zoom.us%2Fj%2F93407874576&data=05%7C02%7Cbmeroundtable-list%40ecn.purdue.edu%7Cdf30333ede5b435b623c08dc3c6b5499%7C4130bd397c53419cb1e58758d6d63f21%7C0%7C0%7C638451678875441124%7CUnknown%7CTWFpbGZsb3d8eyJWIjoiMC4wLjAwMDAiLCJQIjoiV2luMzIiLCJBTiI6Ik1haWwiLCJXVCI6Mn0%3D%7C0%7C%7C%7C&sdata=DZzqb0L4fsBVdgPNt%2FzokGonz5ZmcRG5yO%2BGq6BU8IA%3D&reserved=0> Students registered for the seminar are expected to attend in-person. "Redox systems biology: Computational strategies for predicting cancer therapeutic responses" \[cid:image002.jpg@01DA6E2A.488EA280] Melissa Lambeth Kemp, Ph.D. Carol Ann & David D. Flanagan Professor of Biomedical Engineering Wallace H. Coulter Department of Biomedical Engineering, Georgia Tech and Emory University Abstract: Despite the growing number of therapeutic options available for cancer patients, predicting which course of treatment will the best response for an individual is still a major challenge for precision medicine. In this talk, I will describe various computational systems biology strategies that we have developed to investigate heterogeneity of therapeutic responses among cancer patient populations. Our platforms range from genome-scale metabolic flux modeling to single cell kinetic models and agent-based simulations of tumor architecture. The common theme among these diverse approaches is exploring the role of redox systems in amplifying or suppressing cytotoxicity associated with oxidative damage induced by radiation or chemotherapeutics. Our genome-scale models have identified mitochondrial pan-cancer signatures implicated in radiation sensitivity. Single cell simulations reflected significant systems-level differences between the redox states of healthy and cancer cells, demonstrating in some patient samples a targetable cancer cell population or in others statistically indistinguishable effects between non-malignant and malignant cells and highlights the role of alternate antioxidant components in dictating drug-induced oxidative stress. Finally, spatial modeling has helped to identify organizational features of tumor required to fully realize the desired bystander effects of drug-induced reactive oxygen species formation that is observed in quinone-based cycling. Biography: Melissa Lambeth Kemp, Ph.D. is the Carol Ann & David D. Flanagan Professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University, where she has been a member of the faculty since 2006. Her research focuses on the development of computational systems biology methods to investigate two overarching themes in cancer, immunology, and regenerative medicine applications: i) the role of cellular redox metabolism in influencing information processing and cell fate decisions; and ii) modes of communication that drive self-organization in multicellular engineered living systems. Dr. Kemp is currently the research director of a multi-institutional NSF Engineering Research Center in Cell Manufacturing Technologies and is the former co-chair of the NCI Cancer Systems Biology Consortium. Dr. Kemp's career honors include Georgia Cancer Coalition Distinguished Scholar and NIH New Innovator. ~ BME Host: Elsje Pienaar ~ -- Bmeroundtable-list mailing list Bmeroundtable-list@ecn.purdue.edu https://engineering.purdue.edu/ECN/mailman/listinfo/bmeroundtable-list
