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dc.contributor.authorCastro Ponce, Marioes-ES
dc.contributor.authorMolina París, Carmenes-ES
dc.contributor.authorDeisboeck, T.S.es-ES
dc.date.accessioned2016-05-23T03:06:50Z
dc.date.available2016-05-23T03:06:50Z
dc.date.issued2005-10-01es_ES
dc.identifier.issn1539-3755es_ES
dc.identifier.urihttps:doi.org10.1103PhysRevE.72.041907es_ES
dc.descriptionArtículos en revistases_ES
dc.description.abstractes-ES
dc.description.abstractMotivated by experimental observations, we develop a mathematical model of chemotactically directed tumor growth. We present an analytical study of the model as well as a numerical one. The mathematical analysis shows that: (i) tumor cell proliferation by itself cannot generate the invasive branching behavior observed experimentally, (ii) heterotype chemotaxis provides an instability mechanism that leads to the onset of tumor invasion, and (iii) homotype chemotaxis does not provide such an instability mechanism but enhances the mean speed of the tumor surface. The numerical results not only support the assumptions needed to perform the mathematical analysis but they also provide evidence of (i), (ii), and (iii). Finally, both the analytical study and the numerical work agree with the experimental phenomena.en-GB
dc.format.mimetypeapplication/pdfes_ES
dc.language.isoen-GBes_ES
dc.rightses_ES
dc.rights.uries_ES
dc.sourceRevista: Physical Review E, Periodo: 1, Volumen: online, Número: 4, Página inicial: 041907.1, Página final: 041907.12es_ES
dc.subject.otherInstituto de Investigación Tecnológica (IIT)es_ES
dc.titleTumor growth instability and the onset of invasiones_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.description.versioninfo:eu-repo/semantics/publishedVersiones_ES
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccesses_ES
dc.keywordses-ES
dc.keywordsimmune system competition, multicellular spheroids, theoretical-analysis, capillary formation, factor expression, cell motility, human gliomas, fielden-GB


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