{"database":"BioModels","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Txt":["https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000771?filename=curation_notes.txt"],"Owl":["https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000771?filename=Bazjer2008-biopax3.owl","https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000771?filename=Bazjer2008-biopax2.owl"],"Xml":["https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000771?filename=manifest.xml","https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000771?filename=Bazjer2008.xml"],"Other":["https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000771?filename=Bazjer2008.ode","https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000771?filename=Bazjer2008.sedml","https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000771?filename=metadata.rdf","https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000771?filename=Bazjer2008-octave.m","https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000771?filename=curation_image.png","https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000771?filename=Bazjer2008-matlab.m","https://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000771?filename=Bazjer2008.cps"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"submitter":["Johannes Meyer"],"curationStatus":["Manually curated"],"modellingApproach":["ordinary differential equation model"],"levelVersion":["L2V4"],"submitter_keywords":["Oncology"],"full_dataset_link":["https://www.ebi.ac.uk/biomodels/BIOMD0000000771"],"publication_pubmed":["18316099"],"isPrivate":["false"],"repository":["BioModels"],"omics_type":["Models"],"modelFormat":["SBML"],"tokenised_name":["Bajzer2008   Modeling of cancer virotherapy with recombinant measles viruses"],"publication_year":["2008"],"submissionId":["MODEL1907310005"],"first_author":["Zeljko Bajzer"],"publication_authors":["Zeljko Bajzer, Thomas Carr, Kresimir Josić, Stephen J Russell, David Dingli"],"publication":["18316099,\n                            The Edmonston vaccine strain of measles virus has potent and selective activity against a wide range of tumors. Tumor cells infected by this virus or genetically modified strains express viral proteins that allow them to fuse with neighboring cells to form syncytia that ultimately die. Moreover, infected cells may produce new virus particles that proceed to infect additional tumor cells. We present a model of tumor and virus interactions based on established biology and with proper accounting of the free virus population. The range of model parameters is estimated by fitting to available experimental data. The stability of equilibrium states corresponding to complete tumor eradication, therapy failure and partial tumor reduction is discussed. We use numerical simulations to explore conditions for which the model predicts successful therapy and tumor eradication. The model exhibits damped, as well as stable oscillations in a range of parameter values. These oscillatory states are organized by a Hopf bifurcation.. 1, 252.\n                            Biomathematics Resource and Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Guggenheim 1611b, Rochester, MN 55905, USA. bajzer@mayo.edu"],"submitter_mail":["johannes.p.meyer@gmail.com"],"submitter_affiliation":["EMBL-EBI"],"publicationId":["BIOMD0000000771"],"pubmed_abstract":["The Edmonston vaccine strain of measles virus has potent and selective activity against a wide range of tumors. Tumor cells infected by this virus or genetically modified strains express viral proteins that allow them to fuse with neighboring cells to form syncytia that ultimately die. Moreover, infected cells may produce new virus particles that proceed to infect additional tumor cells. We present a model of tumor and virus interactions based on established biology and with proper accounting of the free virus population. The range of model parameters is estimated by fitting to available experimental data. The stability of equilibrium states corresponding to complete tumor eradication, therapy failure and partial tumor reduction is discussed. We use numerical simulations to explore conditions for which the model predicts successful therapy and tumor eradication. The model exhibits damped, as well as stable oscillations in a range of parameter values. These oscillatory states are organized by a Hopf bifurcation.","Recent research has indicated that viruses specifically infecting tumor cells could be used as an alternative therapeutic approach in cancer patients. A particular example is the adenovirus ONYX-015, which has entered clinical trials in the context of head and neck cancer. Successful therapy crucially requires an understanding about how viral and host parameters influence tumor load. The interactions between the growing tumor, the replicating virus, and possible immune responses are multifactorial and nonlinear. Hence, a complete understanding of how virus and host characteristics influence the outcome of therapy requires mathematical models. In this study, such mathematical models are presented and analyzed. The study investigates three possible scenarios that could be relevant for therapy: (a) viral cytotoxicity alone kills tumor cells; (b) a virus-specific lytic CTL response contributes to killing of infected tumor cells; (c) the virus elicits immunostimulatory signals within the tumor that promote the development of tumor-specific CTL. The models precisely define conditions required for successful therapy. They identify the parameters that need to be measured and modulated to evaluate and refine the existing therapy regimes."],"pubmed_title":["Modeling of cancer virotherapy with recombinant measles viruses.","Viruses as antitumor weapons: defining conditions for tumor remission."],"pubmed_authors":["Wodarz D D","Bajzer Zeljko Z, Carr Thomas T, Josić Kresimir K, Russell Stephen J SJ, Dingli David D"],"additional_accession":[]},"is_claimable":false,"name":"Bajzer2008 - Modeling of cancer virotherapy with recombinant measles viruses","description":"\n      \n        This model describes the interactions between tumor cells and virus particles, with particular reference to virus-induced syncytium formation and ultimately death of tumor cells. Dynamics of infected cells, and production of new virus particules by infected cells, is also included.\n      \n    ","dates":{"last_modification":"2024-08-22","publication":"2024-09-02","submission":"2019-07-31"},"accession":"BIOMD0000000771","cross_references":{"sbo":["SBO:0000179"],"pubmed":["18316099","11309314"],"ncit":["C94498","C62713","C717","C18081","C3439","C16401"],"biomodels__db":["BIOMD0000000771","MODEL1907310005"],"go":["GO:0008219","GO:0019076"],"cl":["CL:0001063"],"bto":["BTO:0000152"]}}