Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.16/2179
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degois.publication.firstPage39795pt_PT
degois.publication.issue24pt_PT
degois.publication.lastPage39804pt_PT
degois.publication.locationUnited States of Americapt_PT
degois.publication.titleOncotargetpt_PT
dc.relation.publisherversionhttp://www.impactjournals.com/oncotarget/index.php?journal=oncotarget&page=article&op=view&path[]=7794&pubmed-linkout=1pt_PT
dc.contributor.authorCoelho, A.-
dc.contributor.authorGomes, M.-
dc.contributor.authorCatarino, R.-
dc.contributor.authorRolfo, C.-
dc.contributor.authorLopes, A.-
dc.contributor.authorMedeiros, R.-
dc.contributor.authorAraújo, A.-
dc.date.accessioned2017-09-04T16:59:38Z-
dc.date.available2017-09-04T16:59:38Z-
dc.date.issued2017-06-13-
dc.identifier.citationOncotarget. 2017 Jun 13;8(24):39795-39804pt_PT
dc.identifier.issn1949-2553-
dc.identifier.urihttp://hdl.handle.net/10400.16/2179-
dc.description.abstractThe 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.pt_PT
dc.language.isoengpt_PT
dc.publisherImpact Journalspt_PT
dc.rightsopenAccesspt_PT
dc.subjectNSCLCpt_PT
dc.subjectangiogenesispt_PT
dc.subjectangiopoietin-2pt_PT
dc.subjectanti-angiogenic strategiespt_PT
dc.subjectvessel co-optionpt_PT
dc.titleAngiogenesis in NSCLC: is vessel co-option the trunk that sustains the branches?pt_PT
dc.typearticlept_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.peerreviewedyespt_PT
degois.publication.volume8pt_PT
dc.identifier.doi10.18632/oncotarget.7794pt_PT
Aparece nas colecções:SOnc - Artigos publicados em revistas indexadas na Medline

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