FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2896490565> ?p ?o ?g. }

• W2896490565 endingPage "35113" @default.
• W2896490565 startingPage "35100" @default.
• W2896490565 abstract "// Patricia D.B. Tiburcio 1, 2, * , Bing Xiao 1, 3, * , Yi Chai 1, 3 , Sydney Asper 1 , Sheryl R. Tripp 4 , David L. Gillespie 1 , Randy L. Jensen 1 and L. Eric Huang 1, 2 1 Department of Neurosurgery, Clinical Neurosciences Center, University of Utah, Salt Lake City, Utah, USA 2 Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, USA 3 Department of Neurosurgery, Nanchang University Second Affiliated Hospital, Nanchang, Jiangxi, People’s Republic of China 4 ARUP Institute for Clinical and Experimental Pathology, Salt Lake City, Utah, USA * These authors contributed equally to this work Correspondence to: L. Eric Huang, email: eric.huang@hsc.utah.edu Keywords: glioma; glutamate; isocitrate dehydrogenase 1; mouse model; RCAS Received: September 13, 2018      Accepted: September 21, 2018      Published: October 12, 2018 ABSTRACT Recurrent heterozygous mutation of isocitrate dehydrogenase 1 gene ( IDH1 ), predominantly resulting in histidine substitution at arginine 132, was first identified in glioma. The biological significance of IDH1 R132H , however, has been controversial, and its prevalent association with glioma remains enigmatic. Although recent studies indicate that IDH1 R132H is nonessential to tumor growth or even anti-tumor growth, whether IDH1 R132H initiates gliomagenesis remains obscure. In this study, we report that IDH1 R132H is intrinsically tumor-suppressive but the activity can be attenuated by glutamate—the cerebral neurotransmitter. We observed that IDH1 R132H was highly suppressive of subcutaneous tumor growth driven by platelet-derived growth factor B (PDGFB), but IDH1 R132H tumor growth and glioma penetrance were virtually indistinguishable from those of IDH1-wildtype tumors in orthotopic models. In vitro , addition of glutamate compromised IDH1 R132H inhibition of neurosphere genesis, indicating glutamate promotion of oncogenic dominance. Furthermore, we observed that IDH1 R132H expression was markedly decreased in tumors but became more permissible upon the deletion of tumor-suppressor gene Cdkn2a . To provide direct evidence for the opposing effect of IDH1 R132H on PDGFB-driven glioma development, we explored tandem expression of the two molecules from a single transcript to preclude selection against IDH1 R132H expression. Our results demonstrate that when juxtaposed with oncogenic PDGFB, IDH1 R132H overrides the oncogenic activity and obliterates neurosphere genesis and gliomagenesis even in the glutamate-rich microenvironment. We propose therefore that IDH1 R132H is intrinsically suppressive of glioma initiation and growth but such tumor-suppressive activity is compromised by the glutamate-rich cerebral cortex, thereby offering a unifying hypothesis for the perplexing role of IDH1 R132H in glioma initiation and growth." @default.
• W2896490565 created "2018-10-26" @default.
• W2896490565 creator A5023598061 @default.
• W2896490565 creator A5030232960 @default.
• W2896490565 creator A5030706523 @default.
• W2896490565 creator A5042024831 @default.
• W2896490565 creator A5047232406 @default.
• W2896490565 creator A5062051877 @default.
• W2896490565 creator A5085199354 @default.
• W2896490565 creator A5086175027 @default.
• W2896490565 date "2018-10-12" @default.
• W2896490565 modified "2023-10-01" @default.
• W2896490565 title "IDH1R132H is intrinsically tumor-suppressive but functionally attenuated by the glutamate-rich cerebral environment" @default.
• W2896490565 cites W1489145497 @default.
• W2896490565 cites W1524972015 @default.
• W2896490565 cites W1682346320 @default.
• W2896490565 cites W1812256879 @default.
• W2896490565 cites W1964001245 @default.
• W2896490565 cites W1978956991 @default.
• W2896490565 cites W1979240391 @default.
• W2896490565 cites W1983077588 @default.
• W2896490565 cites W1994674360 @default.
• W2896490565 cites W2027559073 @default.
• W2896490565 cites W2027834197 @default.
• W2896490565 cites W2035409103 @default.
• W2896490565 cites W2039945243 @default.
• W2896490565 cites W2040827479 @default.
• W2896490565 cites W2047867594 @default.
• W2896490565 cites W2051207198 @default.
• W2896490565 cites W2070655255 @default.
• W2896490565 cites W2087431503 @default.
• W2896490565 cites W2088682928 @default.
• W2896490565 cites W2092527265 @default.
• W2896490565 cites W2101246344 @default.
• W2896490565 cites W2104917184 @default.
• W2896490565 cites W2111163869 @default.
• W2896490565 cites W2115276344 @default.
• W2896490565 cites W2115338756 @default.
• W2896490565 cites W2120963683 @default.
• W2896490565 cites W2126665584 @default.
• W2896490565 cites W2126817554 @default.
• W2896490565 cites W2128083719 @default.
• W2896490565 cites W2132555177 @default.
• W2896490565 cites W2137361994 @default.
• W2896490565 cites W2149363397 @default.
• W2896490565 cites W2155214429 @default.
• W2896490565 cites W2158900087 @default.
• W2896490565 cites W2160300695 @default.
• W2896490565 cites W2161289668 @default.
• W2896490565 cites W2165027097 @default.
• W2896490565 cites W2165307233 @default.
• W2896490565 cites W2184483246 @default.
• W2896490565 cites W2192221936 @default.
• W2896490565 cites W2222531233 @default.
• W2896490565 cites W2263206910 @default.
• W2896490565 cites W2496785181 @default.
• W2896490565 cites W2526865897 @default.
• W2896490565 cites W2552186867 @default.
• W2896490565 cites W2582446241 @default.
• W2896490565 cites W2584285792 @default.
• W2896490565 cites W2606667746 @default.
• W2896490565 cites W2611222875 @default.
• W2896490565 cites W2620446315 @default.
• W2896490565 cites W2755660258 @default.
• W2896490565 cites W2760885207 @default.
• W2896490565 cites W2766649068 @default.
• W2896490565 cites W2772792536 @default.
• W2896490565 cites W2780559017 @default.
• W2896490565 cites W2783323773 @default.
• W2896490565 cites W2793046629 @default.
• W2896490565 cites W2843800587 @default.
• W2896490565 doi "https://doi.org/10.18632/oncotarget.26203" @default.
• W2896490565 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6205547" @default.
• W2896490565 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30416682" @default.
• W2896490565 hasPublicationYear "2018" @default.
• W2896490565 type Work @default.
• W2896490565 sameAs 2896490565 @default.
• W2896490565 citedByCount "8" @default.
• W2896490565 countsByYear W28964905652019 @default.
• W2896490565 countsByYear W28964905652020 @default.
• W2896490565 countsByYear W28964905652021 @default.
• W2896490565 countsByYear W28964905652022 @default.
• W2896490565 countsByYear W28964905652023 @default.
• W2896490565 crossrefType "journal-article" @default.
• W2896490565 hasAuthorship W2896490565A5023598061 @default.
• W2896490565 hasAuthorship W2896490565A5030232960 @default.
• W2896490565 hasAuthorship W2896490565A5030706523 @default.
• W2896490565 hasAuthorship W2896490565A5042024831 @default.
• W2896490565 hasAuthorship W2896490565A5047232406 @default.
• W2896490565 hasAuthorship W2896490565A5062051877 @default.
• W2896490565 hasAuthorship W2896490565A5085199354 @default.
• W2896490565 hasAuthorship W2896490565A5086175027 @default.
• W2896490565 hasBestOaLocation W28964905651 @default.
• W2896490565 hasConcept C104317684 @default.
• W2896490565 hasConcept C109007969 @default.
• W2896490565 hasConcept C126322002 @default.
• W2896490565 hasConcept C127848430 @default.
• W2896490565 hasConcept C143998085 @default.

• next