FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2023001750> ?p ?o ?g. }

• W2023001750 abstract "Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CASmall,microscopic, avascular and therefore asymptomatic tumors can remain in their dormant stage for a considerable period of time depending on numerous processes. One crucial mechanism underlying the transformation from a dormant to a fast-growing phenotype is the ability of tumor cells to induce angiogenesis, a phenomenon termed “angiogenic switch”. We used the aggressive tumor-forming U-87 MG human glioblastoma cell line to identify and isolate a clone which generates dormant microscopic tumors (1). This clone was isolated using single-cell clone and identified by gene expression signature of dormant tumors (2). While both cell lines share a similar growth rate in vitro , we found profound differences in tumor growth patterns when injected into mice. Furthermore, both cell lines exhibit major differences in their angiogenic potential and in expression patterns of genes involved in angiogenesis regulation. Two of the major dissimilarities were found in thrombospondin-1 (TSP-1) and epidermal growth factor receptor (EGFR) expression levels. The dormant avascular tumor-generating cell line (U-87-D) expresses significantly higher levels of TSP-1 and lower levels of EGFR compared to the fast-growing angiogenic tumor-generating parental cell line (U-87-F). It has been previously demonstrated that TSP-1 is a key endogenous angiogenesis inhibitor, whose expression is lost during the malignant transformation. EGFR is a major modulator of tumorigenicity in glioblastoma and therefore, is considered an attractive potential target for glioblastoma therapy.Following the identification of a tumor dormancy gene signature, we induced the upregulation of TSP-1 signaling, using a TSP-1 peptidomimetic (TSP-1 PM), and the downregulation of EGFR, using a dendritic nanocarrier entrapping siRNA (polyglycerol amine (PG-NH2)-siEGFR). We evaluated the ability of this combination therapy to reverse the fast-growing angiogenic phenotype of U-87-F to the dormant avascular phenotype of U-87-D. Mice bearing established U-87-F tumors (50 mm3) received TSP-1 PM (50 mg/kg/day every day) and PG-NH2-siEGFR (2 mg/kg twice a week) for 14 days. This combination therapy exhibited anti-angiogenic and anti-tumorigenic activity. It remarkably decreased tumor volume by 99.5% compared with the control on day 25 post treatment initiation, to a volume of ∼1 mm3.Immunohistochemistry analysis of TSP-1 PM-treated tumors revealed reduced abnormal vasculature, increased αSMA expression and decreased VEGF expression. We concluded that TSP-1 PM in combination with EGFR-siRNA present a promising treatment for advanced glioblastoma promoting a dormant phenotype.References:1. Satchi-Fainaro*, Ferber*, et al., Prospective Identification of Glioblastoma Cells Generating Dormant Tumors, in press, PLoS One (2012). * Equal contribution.2. Almog et al., Transcriptional switch of dormant tumors to fast-growing angiogenic phenotype Cancer Res. 2009; 69(3):836-44.Citation Format: Shiran Ferber, Galia Tiram, Orit Amsalem, Eylon Yavin, Nava Almog, Jack Henkin, Marcelo Calderon, Rainer Haag, Ronit Satchi-Fainaro. Reverting the angiogenic switch of glioblastoma with a nanopolyplex based on the molecular fingerprint of tumor dormancy. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr LB-104. doi:10.1158/1538-7445.AM2014-LB-104" @default.
• W2023001750 created "2016-06-24" @default.
• W2023001750 creator A5000025451 @default.
• W2023001750 creator A5004129931 @default.
• W2023001750 creator A5010578630 @default.
• W2023001750 creator A5028902587 @default.
• W2023001750 creator A5034168883 @default.
• W2023001750 creator A5050764524 @default.
• W2023001750 creator A5061202040 @default.
• W2023001750 creator A5068440892 @default.
• W2023001750 creator A5087883720 @default.
• W2023001750 date "2014-09-30" @default.
• W2023001750 modified "2023-09-26" @default.
• W2023001750 title "Abstract LB-104: Reverting the angiogenic switch of glioblastoma with a nanopolyplex based on the molecular fingerprint of tumor dormancy" @default.
• W2023001750 doi "https://doi.org/10.1158/1538-7445.am2014-lb-104" @default.
• W2023001750 hasPublicationYear "2014" @default.
• W2023001750 type Work @default.
• W2023001750 sameAs 2023001750 @default.
• W2023001750 citedByCount "0" @default.
• W2023001750 crossrefType "proceedings-article" @default.
• W2023001750 hasAuthorship W2023001750A5000025451 @default.
• W2023001750 hasAuthorship W2023001750A5004129931 @default.
• W2023001750 hasAuthorship W2023001750A5010578630 @default.
• W2023001750 hasAuthorship W2023001750A5028902587 @default.
• W2023001750 hasAuthorship W2023001750A5034168883 @default.
• W2023001750 hasAuthorship W2023001750A5050764524 @default.
• W2023001750 hasAuthorship W2023001750A5061202040 @default.
• W2023001750 hasAuthorship W2023001750A5068440892 @default.
• W2023001750 hasAuthorship W2023001750A5087883720 @default.
• W2023001750 hasConcept C100701293 @default.
• W2023001750 hasConcept C104317684 @default.
• W2023001750 hasConcept C121608353 @default.
• W2023001750 hasConcept C2779256057 @default.
• W2023001750 hasConcept C2780394083 @default.
• W2023001750 hasConcept C2993273003 @default.
• W2023001750 hasConcept C31033888 @default.
• W2023001750 hasConcept C3527866 @default.
• W2023001750 hasConcept C502942594 @default.
• W2023001750 hasConcept C54355233 @default.
• W2023001750 hasConcept C555283112 @default.
• W2023001750 hasConcept C59822182 @default.
• W2023001750 hasConcept C81089528 @default.
• W2023001750 hasConcept C81885089 @default.
• W2023001750 hasConcept C86803240 @default.
• W2023001750 hasConceptScore W2023001750C100701293 @default.
• W2023001750 hasConceptScore W2023001750C104317684 @default.
• W2023001750 hasConceptScore W2023001750C121608353 @default.
• W2023001750 hasConceptScore W2023001750C2779256057 @default.
• W2023001750 hasConceptScore W2023001750C2780394083 @default.
• W2023001750 hasConceptScore W2023001750C2993273003 @default.
• W2023001750 hasConceptScore W2023001750C31033888 @default.
• W2023001750 hasConceptScore W2023001750C3527866 @default.
• W2023001750 hasConceptScore W2023001750C502942594 @default.
• W2023001750 hasConceptScore W2023001750C54355233 @default.
• W2023001750 hasConceptScore W2023001750C555283112 @default.
• W2023001750 hasConceptScore W2023001750C59822182 @default.
• W2023001750 hasConceptScore W2023001750C81089528 @default.
• W2023001750 hasConceptScore W2023001750C81885089 @default.
• W2023001750 hasConceptScore W2023001750C86803240 @default.
• W2023001750 hasLocation W20230017501 @default.
• W2023001750 hasOpenAccess W2023001750 @default.
• W2023001750 hasPrimaryLocation W20230017501 @default.
• W2023001750 hasRelatedWork W1501705007 @default.
• W2023001750 hasRelatedWork W1559401050 @default.
• W2023001750 hasRelatedWork W1970716757 @default.
• W2023001750 hasRelatedWork W1972481147 @default.
• W2023001750 hasRelatedWork W2023564585 @default.
• W2023001750 hasRelatedWork W2069327529 @default.
• W2023001750 hasRelatedWork W2071820073 @default.
• W2023001750 hasRelatedWork W2087205099 @default.
• W2023001750 hasRelatedWork W2316323158 @default.
• W2023001750 hasRelatedWork W2317346400 @default.
• W2023001750 hasRelatedWork W2320223027 @default.
• W2023001750 hasRelatedWork W2321405133 @default.
• W2023001750 hasRelatedWork W2328410319 @default.
• W2023001750 hasRelatedWork W2329631058 @default.
• W2023001750 hasRelatedWork W2333021623 @default.
• W2023001750 hasRelatedWork W2480551763 @default.
• W2023001750 hasRelatedWork W2563426064 @default.
• W2023001750 hasRelatedWork W2953396691 @default.
• W2023001750 hasRelatedWork W3083152755 @default.
• W2023001750 hasRelatedWork W3193173701 @default.
• W2023001750 isParatext "false" @default.
• W2023001750 isRetracted "false" @default.
• W2023001750 magId "2023001750" @default.
• W2023001750 workType "article" @default.