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Browsing by Author "Park, Eugene"
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Item Rethinking Global Health Education in Plastic Surgery Residency(American Society of Plastic Surgeons, 2021-09-22) Christie, Brian M.; Kurnik, Nicole M.; Park, Eugene; Ranganathan, Kavitha; Smith, Anthony A.; Medicine, School of MedicineSurgical disease is now among the most common, preventable, and growing contributors to the global burden of disease. The attitudes of trainees toward global surgery and the viability of a global surgery as an academic track have blossomed. More optimized experiences within residency education are necessary, however, to prepare the next generation of global surgeons. The field of plastic surgery is thus at an important crossroads in the effort to incorporate global surgery into training programs in a uniform fashion across the country. The recent American Council of Academic Plastic Surgeons meeting in February 2020 was dedicated to identifying strategies that will enhance the adoption of global surgery practices within plastic surgery. In this article, we discuss the principles, themes, and ideas that emerged from this session, and further develop concrete initiatives believed to be potentially fruitful. Some have been discussed in other surgical disciplines or presented in isolation to the plastic surgery community, but never as a cohesive set of recommendations that take into account the background and shortfalls of the current model for global health education in the 21st century. We then introduce five recommendations to optimize learner education: (1) clarification of learner expectations and roles; (2) domestic teaching for optimization of field experiences; (3) expansion of longitudinal, formal rotations; (4) strengthening of the role of research; and (5) integration of program financing.Item Small molecule inhibition of CBP/catenin interactions eliminates drug resistant clones in acute lymphoblastic leukemia(NPG - Nature Publishing Group, 2014-04-24) Gang, Eun Ji; Hsieh, Yao-Te; Pham, Jennifer; Zhao, Yi; Nguyen, Cu; Huantes, Sandra; Park, Eugene; Naing, Khatija; Klemm, Lars; Swaminathan, Srividya; Conway, Edward M.; Pelus, Louis M.; Crispino, John; Mullighan, Charles; McMillan, Michael; Müschen, Markus; Kahn, Michael; Kim, Yong-Mi; Department of Microbiology & Immunology, School of MedicineDrug resistance in acute lymphoblastic leukemia (ALL) remains a major problem warranting new treatment strategies. Wnt/catenin signaling is critical for the self-renewal of normal hematopoietic progenitor cells. Deregulated Wnt signaling is evident in chronic and acute myeloid leukemia, however little is known about ALL. Differential interaction of catenin with either the Kat3 coactivator CREBBP (CBP) or the highly homologous EP300 (p300) is critical to determine divergent cellular responses and provides a rationale for the regulation of both proliferation and differentiation by the Wnt signaling pathway. Usage of the coactivator CBP by catenin leads to transcriptional activation of cassettes of genes that are involved in maintenance of progenitor cell self-renewal. However, the use of the coactivator p300, leads to activation of genes involved in the initiation of differentiation. ICG-001 is a novel small molecule modulator of Wnt/catenin signaling, which specifically binds to the N-terminus of CBP and not p300, within amino acids 1–110, thereby disrupting the interaction between CBP and catenin. Here, we report that selective disruption of the CBP/β- and γ-catenin interactions using ICG-001 leads to differentiation of pre-B ALL cells and loss of self-renewal capacity. Survivin, an inhibitor-of-apoptosis protein, was also downregulated in primary ALL after treatment with ICG-001. Using ChIP assay, we demonstrate occupancy by CBP of the survivin promoter, which is decreased by ICG-001 in primary ALL. CBP-mutations have been recently identified in a significant percentage of ALL patients, however, almost all of the identified mutations reported occur C-terminal to the binding site for ICG-001. Importantly, ICG-001, regardless of CBP mutational status and chromosomal aberration, leads to eradication of drug-resistant primary leukemia in combination with conventional therapy in vitro and significantly prolongs the survival of NOD/SCID mice engrafted with primary ALL. Therefore, specifically inhibiting CBP/catenin transcription represents a novel approach to overcome relapse in ALL.