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https://hdl.handle.net/10216/112887
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DC Field | Value | Language |
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dc.creator | Antonio Araújo | |
dc.date.accessioned | 2019-04-20T23:07:53Z | - |
dc.date.available | 2019-04-20T23:07:53Z | - |
dc.date.issued | 2017 | |
dc.identifier.issn | 1949-2553 | |
dc.identifier.other | sigarra:273364 | |
dc.identifier.uri | https://hdl.handle.net/10216/112887 | - |
dc.description.abstract | The critical role of angiogenesis in tumor development makes its inhibition a valuable new approach in therapy, rapidly making anti-angiogenesis a major focus in research. While the VEGF/VEGFR pathway is the main target of the approved anti-angiogenic molecules in NSCLC treatment, the results obtained are still modest, especially due to resistance mechanisms. Accumulating scientific data show that vessel co-option is an alternative mechanism to angiogenesis during tumor development in well-vascularized organs such as the lungs, where tumor cells highjack the existing vasculature to obtain its blood supply in a non-angiogenic fashion. This can explain the low/lack of response to current anti-angiogenic strategies. The same principle applies to lung metastases of other primary tumors. The exact mechanisms of vessel co-option need to be further elucidated, but it is known that the co-opted vessels regress by the action of Angiopoietin-2 (Ang-2), a vessel destabilizing cytokine expressed by the endothelial cells of the pre-existing mature vessels. In the absence of VEGF, vessel regression leads to tumor cell loss and hypoxia, with a subsequent switch to a neoangiogenic phenotype by the remaining tumor cells. Unravelling the vessel co-option mechanisms and involved players may be fruitful for numerous reasons, and the particularities of this form of vascularization should be carefully considered when planning anti-angiogenic interventions or designing clinical trials for this purpose. In view of the current knowledge, rationale for therapeutic approaches of dual inhibition of Ang-2 and VEGF are swiftly gaining strength and may serve as a launchpad to more successful NSCLC anti-vascular treatments. | |
dc.language.iso | eng | |
dc.rights | openAccess | |
dc.title | Angiogenesis in NSCLC: is vessel co-option the trunk that sustains the branches? | |
dc.type | Outra Publicação em Revista Científica Internacional | |
dc.contributor.uporto | Instituto de Ciências Biomédicas Abel Salazar | |
dc.identifier.doi | 10.18632/oncotarget.7794 | |
dc.identifier.authenticus | P-00Q-6QQ | |
Appears in Collections: | ICBAS - Outra Publicação em Revista Científica Internacional |
Files in This Item:
File | Description | Size | Format | |
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273364.pdf | 1.01 MB | Adobe PDF | View/Open |
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