Matches in SemOpenAlex for { <https://semopenalex.org/work/W2242320280> ?p ?o ?g. }
Showing items 1 to 74 of
74
with 100 items per page.
- W2242320280 endingPage "1508" @default.
- W2242320280 startingPage "1508" @default.
- W2242320280 abstract "1508 Background: Resistance to chemotherapy is major impediment to the successful treatment of human glioblastomas. Methods: We used an integrated resistance model and genomics tools to globally explore molecular factors and cellular pathways mediating resistance to O 6 -alkylating agents in glioblastoma cells. Results: We identified a transcriptomic signature of 286 genes that predicts a common in vitro and in vivo resistance phenotype to these agents. This signature was significantly enriched for genes with functions in organismal survival (27.5%) and cell death (49.0%), both with P < 0.00001. Modularity was a predominant organizational principle of the signature, with functions being carried out by groups of interacting molecules in overlapping networks. A highly significant network was built around nuclear factor-κB (NF-κB), which included the persistent alterations of various NF-κB pathway elements. Tumor necrosis factor-α-induced protein 3 (TNFAIP3) was identified as a new endogenous regulatory component of a putative cytoplasmic signaling cascade that mediates NF-κB activation in response to DNA damage caused by O 6 -alkylating agents. Expression of the corresponding zinc finger protein A20 closely mirrored the expression of the TNFAIP3 transcript, and was inversely related to NF-κB activation status in the resistant cells. A prediction model based on the resistance signature enabled the subclassification of an independent, validation cohort of 31 glioblastomas into two outcome groups (P = .037). TNFAIP3 expression was a favorable factor in patient prognosis (P = .028), and was part of an optimized four-gene predictor (TNFAIP3, CD44 antigen, syndecan 1, and F-box protein 32) significantly associated with patient survival (P = .022). Conclusions: Our results offer strong evidence for TNFAIP3 as a key regulator of the cytoplasmic signaling to activate NF-κB en route to O 6 -alkylating agent resistance in glioblastoma cells. This gene may be an attractive target for therapeutic modulation of glioblastomas. No significant financial relationships to disclose." @default.
- W2242320280 created "2016-06-24" @default.
- W2242320280 creator A5019649110 @default.
- W2242320280 creator A5034768472 @default.
- W2242320280 creator A5049738459 @default.
- W2242320280 creator A5055115233 @default.
- W2242320280 creator A5055929035 @default.
- W2242320280 creator A5056495689 @default.
- W2242320280 creator A5068526964 @default.
- W2242320280 creator A5072887134 @default.
- W2242320280 creator A5074319945 @default.
- W2242320280 creator A5087308492 @default.
- W2242320280 date "2006-06-20" @default.
- W2242320280 modified "2023-10-18" @default.
- W2242320280 title "Tumor necrosis factor-α-induced protein 3 down-regulates nuclear factor-κB-mediated drug resistance in vitro and is a favorable clinical prognostic factor in human glioblastomas" @default.
- W2242320280 doi "https://doi.org/10.1200/jco.2006.24.18_suppl.1508" @default.
- W2242320280 hasPublicationYear "2006" @default.
- W2242320280 type Work @default.
- W2242320280 sameAs 2242320280 @default.
- W2242320280 citedByCount "0" @default.
- W2242320280 crossrefType "journal-article" @default.
- W2242320280 hasAuthorship W2242320280A5019649110 @default.
- W2242320280 hasAuthorship W2242320280A5034768472 @default.
- W2242320280 hasAuthorship W2242320280A5049738459 @default.
- W2242320280 hasAuthorship W2242320280A5055115233 @default.
- W2242320280 hasAuthorship W2242320280A5055929035 @default.
- W2242320280 hasAuthorship W2242320280A5056495689 @default.
- W2242320280 hasAuthorship W2242320280A5068526964 @default.
- W2242320280 hasAuthorship W2242320280A5072887134 @default.
- W2242320280 hasAuthorship W2242320280A5074319945 @default.
- W2242320280 hasAuthorship W2242320280A5087308492 @default.
- W2242320280 hasConcept C104317684 @default.
- W2242320280 hasConcept C150194340 @default.
- W2242320280 hasConcept C17991360 @default.
- W2242320280 hasConcept C202751555 @default.
- W2242320280 hasConcept C203014093 @default.
- W2242320280 hasConcept C2779733811 @default.
- W2242320280 hasConcept C2780932548 @default.
- W2242320280 hasConcept C502942594 @default.
- W2242320280 hasConcept C54355233 @default.
- W2242320280 hasConcept C71924100 @default.
- W2242320280 hasConcept C86803240 @default.
- W2242320280 hasConceptScore W2242320280C104317684 @default.
- W2242320280 hasConceptScore W2242320280C150194340 @default.
- W2242320280 hasConceptScore W2242320280C17991360 @default.
- W2242320280 hasConceptScore W2242320280C202751555 @default.
- W2242320280 hasConceptScore W2242320280C203014093 @default.
- W2242320280 hasConceptScore W2242320280C2779733811 @default.
- W2242320280 hasConceptScore W2242320280C2780932548 @default.
- W2242320280 hasConceptScore W2242320280C502942594 @default.
- W2242320280 hasConceptScore W2242320280C54355233 @default.
- W2242320280 hasConceptScore W2242320280C71924100 @default.
- W2242320280 hasConceptScore W2242320280C86803240 @default.
- W2242320280 hasIssue "18_suppl" @default.
- W2242320280 hasLocation W22423202801 @default.
- W2242320280 hasOpenAccess W2242320280 @default.
- W2242320280 hasPrimaryLocation W22423202801 @default.
- W2242320280 hasRelatedWork W2009966535 @default.
- W2242320280 hasRelatedWork W2067467096 @default.
- W2242320280 hasRelatedWork W2102289484 @default.
- W2242320280 hasRelatedWork W2143177291 @default.
- W2242320280 hasRelatedWork W2171277769 @default.
- W2242320280 hasRelatedWork W2410262319 @default.
- W2242320280 hasRelatedWork W2734999146 @default.
- W2242320280 hasRelatedWork W3211868871 @default.
- W2242320280 hasRelatedWork W4294954873 @default.
- W2242320280 hasRelatedWork W4363645812 @default.
- W2242320280 hasVolume "24" @default.
- W2242320280 isParatext "false" @default.
- W2242320280 isRetracted "false" @default.
- W2242320280 magId "2242320280" @default.
- W2242320280 workType "article" @default.