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dc.contributor.supervisor Mowat, Michael (Biochemistry and Medical Genetics) en_US
dc.contributor.author Buse, Cordula
dc.date.accessioned 2012-10-25T13:12:07Z
dc.date.available 2012-10-25T13:12:07Z
dc.date.issued 2012-10-25
dc.identifier.uri http://hdl.handle.net/1993/9675
dc.description.abstract This thesis investigated the cooperation of the Kras2 oncogene with the tumor suppressor gene Dlc1 in lung tumor development. Dlc1 is a negative regulator of RhoGTPase proteins, which are mainly involved in the regulation of the actin cytoskeleton and cell migration. We hypothesized that loss of Dlc1 expression leads to more aggressive tumors, which should also result in increased incidence of metastasis. All experiments were performed in mice containing a heterozygous oncogenic Kras allele and a heterozygous gene trapped Dlc1 allele (KD) and in mice only carrying the oncogenic Kras allele (K+). Throughout all experiments we have consistently found no significant differences between the two groups in terms of tumor burden (tumor numbers, sizes and areas), metastases or methylation patterns. These results suggest that heterozygous downregulation of Dlc1 is not enough to increase tumor formation and metastasis development in the Kras lung tumors. en_US
dc.rights info:eu-repo/semantics/openAccess
dc.subject lung cancer en_US
dc.subject mouse model en_US
dc.subject Kras en_US
dc.subject Dlc1 en_US
dc.subject oncogene en_US
dc.subject tumor suppressor en_US
dc.title The cooperation of the tumor suppressor gene Dlc1 and the oncogene Kras in tumorigenesis en_US
dc.type info:eu-repo/semantics/masterThesis
dc.degree.discipline Biochemistry and Medical Genetics en_US
dc.contributor.examiningcommittee Mai, Sabine (Biochemistry and Medical Genetics) Merz, David (Biochemistry and Medical Genetics) Halayko, Andrew (Physiology) en_US
dc.degree.level Master of Science (M.Sc.) en_US
dc.description.note February 2013 en_US


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