H
Hui Feng
Researcher at Boston University
Publications - 64
Citations - 2621
Hui Feng is an academic researcher from Boston University. The author has contributed to research in topics: Zebrafish & Medicine. The author has an hindex of 20, co-authored 49 publications receiving 2108 citations. Previous affiliations of Hui Feng include Harvard University & University of Georgia.
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CUL-4 ubiquitin ligase maintains genome stability by restraining DNA-replication licensing.
TL;DR: It is proposed that CUL-4 prevents aberrant re-initiation of DNA replication, at least in part, by facilitating the degradation of CDT-1, which is required for DNA replication in Caenorhabditis elegans.
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The emerging role and targetability of the TCA cycle in cancer metabolism.
TL;DR: Current knowledge about the fuels feeding the cycle, effects of oncogenes and tumor suppressors on fuel and cycle usage, common genetic alterations and deregulation of cycle enzymes, and potential therapeutic opportunities for targeting the TCA cycle in cancer cells are summarized.
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Activated ALK Collaborates with MYCN in Neuroblastoma Pathogenesis
Shizhen Zhu,Jeong-Soo Lee,Feng Guo,Jimann Shin,Antonio R. Perez-Atayde,Jeffery L. Kutok,Scott J. Rodig,Donna Neuberg,Daniel Helman,Hui Feng,Rodney A. Stewart,Wenchao Wang,Rani E. George,Rani E. George,John P. Kanki,A. Thomas Look,A. Thomas Look +16 more
TL;DR: A transgenic zebrafish model of neuroblastoma is generated in which MYCN-induced tumors arise from a subpopulation of neuroblasts that migrate into the adrenal medulla analog following organogenesis, and coexpression of activated ALK with MYCN in this model triples the disease penetrance and markedly accelerates tumor onset.
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Cre/lox-regulated transgenic zebrafish model with conditional myc-induced T cell acute lymphoblastic leukemia
TL;DR: It is shown that leukemias from this transgenic line are highly penetrant and render animals moribund by 80.7 ± 17.6 days of life, providing an essential step in preparing this model for chemical and genetic screens designed to identify modifiers of Myc-induced T-ALL.
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T-Lymphoblastic Lymphoma Cells Express High Levels of BCL2, S1P1, and ICAM1, Leading to a Blockade of Tumor Cell Intravasation
Hui Feng,David L. Stachura,Richard M. White,Alejandro Gutierrez,Alejandro Gutierrez,Lu Zhang,Takaomi Sanda,Cicely A. Jette,Joseph R. Testa,Donna Neuberg,David M. Langenau,Jeffery L. Kutok,Leonard I. Zon,David Traver,David Traver,Mark D. Fleming,John P. Kanki,A. Thomas Look,A. Thomas Look +18 more
TL;DR: Blockade of intravasation and hematologic dissemination in T-LBL is due to elevated S1P1 signaling, increased expression of ICAM1, and augmented homotypic cell-cell adhesion.