Publication
Angiogenesis in NSCLC: is vessel co-option the trunk that sustains the branches?
| dc.contributor.author | Coelho, A. | |
| dc.contributor.author | Gomes, M. | |
| dc.contributor.author | Catarino, R. | |
| dc.contributor.author | Rolfo, C. | |
| dc.contributor.author | Lopes, A. | |
| dc.contributor.author | Medeiros, R. | |
| dc.contributor.author | Araújo, A. | |
| dc.date.accessioned | 2017-09-04T16:59:38Z | |
| dc.date.available | 2017-09-04T16:59:38Z | |
| dc.date.issued | 2017-06-13 | |
| 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. | pt_PT |
| dc.description.version | info:eu-repo/semantics/publishedVersion | pt_PT |
| dc.identifier.citation | Oncotarget. 2017 Jun 13;8(24):39795-39804 | pt_PT |
| dc.identifier.doi | 10.18632/oncotarget.7794 | pt_PT |
| dc.identifier.issn | 1949-2553 | |
| dc.identifier.uri | http://hdl.handle.net/10400.16/2179 | |
| dc.language.iso | eng | pt_PT |
| dc.peerreviewed | yes | pt_PT |
| dc.publisher | Impact Journals | pt_PT |
| dc.relation.publisherversion | http://www.impactjournals.com/oncotarget/index.php?journal=oncotarget&page=article&op=view&path[]=7794&pubmed-linkout=1 | pt_PT |
| dc.subject | NSCLC | pt_PT |
| dc.subject | angiogenesis | pt_PT |
| dc.subject | angiopoietin-2 | pt_PT |
| dc.subject | anti-angiogenic strategies | pt_PT |
| dc.subject | vessel co-option | pt_PT |
| dc.title | Angiogenesis in NSCLC: is vessel co-option the trunk that sustains the branches? | pt_PT |
| dc.type | journal article | |
| dspace.entity.type | Publication | |
| oaire.citation.conferencePlace | United States of America | pt_PT |
| oaire.citation.endPage | 39804 | pt_PT |
| oaire.citation.issue | 24 | pt_PT |
| oaire.citation.startPage | 39795 | pt_PT |
| oaire.citation.title | Oncotarget | pt_PT |
| oaire.citation.volume | 8 | pt_PT |
| rcaap.rights | openAccess | pt_PT |
| rcaap.type | article | pt_PT |