FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2000179703> ?p ?o ?g. }

• W2000179703 endingPage "e18709" @default.
• W2000179703 startingPage "e18709" @default.
• W2000179703 abstract "The Notch signaling pathway is essential for normal development due to its role in control of cell differentiation, proliferation and survival. It is also critically involved in tumorigenesis and cancer progression. A key enzyme in the activation of Notch signaling is the gamma-secretase protein complex and therefore, gamma-secretase inhibitors (GSIs)—originally developed for Alzheimer's disease—are now being evaluated in clinical trials for human malignancies. It is also clear that Notch plays an important role in angiogenesis driven by Vascular Endothelial Growth Factor A (VEGF-A)—a process instrumental for tumor growth and metastasis. The effect of GSIs on tumor vasculature has not been conclusively determined. Here we report that Compound X (CX), a GSI previously reported to potently inhibit Notch signaling in vitro and in vivo, promotes angiogenic sprouting in vitro and during developmental angiogenesis in mice. Furthermore, CX treatment suppresses tumor growth in a mouse model of renal carcinoma, leads to the formation of abnormal vessels and an increased tumor vascular density. Using a rabbit model of VEGF-A-driven angiogenesis in skeletal muscle, we demonstrate that CX treatment promotes abnormal blood vessel growth characterized by vessel occlusion, disrupted blood flow, and increased vascular leakage. Based on these findings, we propose a model for how GSIs and other Notch inhibitors disrupt tumor blood vessel perfusion, which might be useful for understanding this new class of anti-cancer agents." @default.
• W2000179703 created "2016-06-24" @default.
• W2000179703 creator A5008086583 @default.
• W2000179703 creator A5014220812 @default.
• W2000179703 creator A5020305163 @default.
• W2000179703 creator A5046873939 @default.
• W2000179703 creator A5069716647 @default.
• W2000179703 creator A5074736489 @default.
• W2000179703 creator A5076042483 @default.
• W2000179703 creator A5087086525 @default.
• W2000179703 date "2011-04-14" @default.
• W2000179703 modified "2023-10-17" @default.
• W2000179703 title "Gamma-Secretase Inhibitor Treatment Promotes VEGF-A-Driven Blood Vessel Growth and Vascular Leakage but Disrupts Neovascular Perfusion" @default.
• W2000179703 cites W1572225000 @default.
• W2000179703 cites W1835091344 @default.
• W2000179703 cites W1858310449 @default.
• W2000179703 cites W1971162717 @default.
• W2000179703 cites W1973333497 @default.
• W2000179703 cites W1979564603 @default.
• W2000179703 cites W1982023788 @default.
• W2000179703 cites W1987662957 @default.
• W2000179703 cites W1993428183 @default.
• W2000179703 cites W1996133370 @default.
• W2000179703 cites W1997801717 @default.
• W2000179703 cites W2000589976 @default.
• W2000179703 cites W2004757799 @default.
• W2000179703 cites W2011582582 @default.
• W2000179703 cites W2014253046 @default.
• W2000179703 cites W2015425841 @default.
• W2000179703 cites W2017253762 @default.
• W2000179703 cites W2018527149 @default.
• W2000179703 cites W2027092108 @default.
• W2000179703 cites W2030370645 @default.
• W2000179703 cites W2040827891 @default.
• W2000179703 cites W2052565988 @default.
• W2000179703 cites W2062069005 @default.
• W2000179703 cites W2062240872 @default.
• W2000179703 cites W2066628372 @default.
• W2000179703 cites W2075503331 @default.
• W2000179703 cites W2075773133 @default.
• W2000179703 cites W2081887573 @default.
• W2000179703 cites W2083483697 @default.
• W2000179703 cites W2084293525 @default.
• W2000179703 cites W2097705657 @default.
• W2000179703 cites W2098456531 @default.
• W2000179703 cites W2103046899 @default.
• W2000179703 cites W2106933841 @default.
• W2000179703 cites W2111458469 @default.
• W2000179703 cites W2112180572 @default.
• W2000179703 cites W2113337076 @default.
• W2000179703 cites W2116036875 @default.
• W2000179703 cites W2119937633 @default.
• W2000179703 cites W2133660369 @default.
• W2000179703 cites W2140857987 @default.
• W2000179703 cites W2143958554 @default.
• W2000179703 cites W2149131291 @default.
• W2000179703 cites W2154861644 @default.
• W2000179703 cites W2157930949 @default.
• W2000179703 cites W2160947862 @default.
• W2000179703 cites W2166630455 @default.
• W2000179703 cites W2166807613 @default.
• W2000179703 cites W2167133646 @default.
• W2000179703 doi "https://doi.org/10.1371/journal.pone.0018709" @default.
• W2000179703 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3077402" @default.
• W2000179703 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21533193" @default.
• W2000179703 hasPublicationYear "2011" @default.
• W2000179703 type Work @default.
• W2000179703 sameAs 2000179703 @default.
• W2000179703 citedByCount "33" @default.
• W2000179703 countsByYear W20001797032012 @default.
• W2000179703 countsByYear W20001797032013 @default.
• W2000179703 countsByYear W20001797032014 @default.
• W2000179703 countsByYear W20001797032015 @default.
• W2000179703 countsByYear W20001797032017 @default.
• W2000179703 countsByYear W20001797032018 @default.
• W2000179703 countsByYear W20001797032019 @default.
• W2000179703 countsByYear W20001797032020 @default.
• W2000179703 crossrefType "journal-article" @default.
• W2000179703 hasAuthorship W2000179703A5008086583 @default.
• W2000179703 hasAuthorship W2000179703A5014220812 @default.
• W2000179703 hasAuthorship W2000179703A5020305163 @default.
• W2000179703 hasAuthorship W2000179703A5046873939 @default.
• W2000179703 hasAuthorship W2000179703A5069716647 @default.
• W2000179703 hasAuthorship W2000179703A5074736489 @default.
• W2000179703 hasAuthorship W2000179703A5076042483 @default.
• W2000179703 hasAuthorship W2000179703A5087086525 @default.
• W2000179703 hasBestOaLocation W20001797031 @default.
• W2000179703 hasConcept C121608353 @default.
• W2000179703 hasConcept C126322002 @default.
• W2000179703 hasConcept C134018914 @default.
• W2000179703 hasConcept C142724271 @default.
• W2000179703 hasConcept C161879069 @default.
• W2000179703 hasConcept C167734588 @default.
• W2000179703 hasConcept C2777025900 @default.
• W2000179703 hasConcept C2777663904 @default.
• W2000179703 hasConcept C2778271429 @default.
• W2000179703 hasConcept C2779013556 @default.
• W2000179703 hasConcept C2779395532 @default.

• next