J
Jean Francois H. Geschwind
Researcher at Johns Hopkins University
Publications - 44
Citations - 5909
Jean Francois H. Geschwind is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Transcatheter arterial chemoembolization & Cancer. The author has an hindex of 28, co-authored 44 publications receiving 5235 citations. Previous affiliations of Jean Francois H. Geschwind include Johns Hopkins University School of Medicine & Yale University.
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Journal ArticleDOI
Tumor glycolysis as a target for cancer therapy: progress and prospects.
TL;DR: The objective of this review is to present the most recent research on the cancer-specific role of glycolysis including their non-glycolytic functions in order to explore the potential for therapeutic opportunities.
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Lipiodol transarterial chemoembolization for hepatocellular carcinoma: A systematic review of efficacy and safety data.
Riccardo Lencioni,Thierry de Baere,Michael C. Soulen,William S. Rilling,Jean Francois H. Geschwind +4 more
TL;DR: In a systematic literature review, survival figures of HCC patients undergoing lipiodol TACE appear to be in line with those reported in previous RCTs, and no new or unexpected safety concerns were identified.
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MRI guidance of focused ultrasound therapy of uterine fibroids: early results
Jonathan T. Hindley,Wladyslaw Gedroyc,Lesley Regan,Elizabeth A. Stewart,Clare M. Tempany,Kullervo Hynnen,Nathan Macdanold,Yael Inbar,Yacov Itzchak,Jaron Rabinovici,Kevin Kim,Jean Francois H. Geschwind,Gina K. Hesley,Brian Gostout,Tillman Ehrenstein,Sylvia Hengst,Miri Sklair-Levy,Asher Shushan,Ferenc A. Jolesz +18 more
TL;DR: This early description of MRI-guided focused ultrasound therapy treatment of fibroids shows that, although the volume reduction is moderate, it correlates with treatment volume and the symptomatic response to this treatment is encouraging.
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Mitochondrial bound type II hexokinase: a key player in the growth and survival of many cancers and an ideal prospect for therapeutic intervention.
TL;DR: The authors now have a much better molecular understanding of the high glycolytic phenotype of many cancers, the pivotal roles that Type II hexokinase-mitochondrial interactions play in this process to promote tumor cell growth and survival, and how this new knowledge can lead to improved therapies that may ultimately turn the tide on their losing war on cancer.
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Glucose catabolism in the rabbit VX2 tumor model for liver cancer: characterization and targeting hexokinase.
TL;DR: Results of a limited screen show that the glycolytic rate is inhibited best by 2-deoxyglucose (2DOG) and 3-bromopyruvate (3BrPA), the former compound of which is phosphorylated by hexokinase but not further metabolized, while the latter directly inhibits Hexokinase.