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dc.contributor.supervisor Mai, Sabine (Physiology) en
dc.contributor.author Hagerty, Marlon
dc.date.accessioned 2008-04-14T17:32:20Z
dc.date.available 2008-04-14T17:32:20Z
dc.date.issued 2008-04-14T17:32:20Z
dc.identifier.uri http://hdl.handle.net/1993/3028
dc.description.abstract Murine plasmacytoma is induced by plastic implants, injection of paraffin oil or pristane, or through viral infection, and Myc is invariably overexpressed in the tumour cells. Although translocation and juxtaposition of the Myc locus to an immunoglobulin locus is the prominent nonrandom cytogenetic aberration observed, the significance of other karyotypic instabilities in murine plasmacytoma is not clear, including the previously observed occurrence of trisomy 11. As well as identifying new cytogenetic mutations in murine plasmacytomagenesis, this study provides evidence for their combined and sequential accumulation that may offer new parallels to human B-cell malignancies. Plasmacytomas were induced in Balb/c Rb6.15 mice by intraperitoneal (i.p.) pristane injection prior to infection with the ABL-MYC retrovirus, and confirmed by histological examination. Spectral karyotype analysis of tumour samples identified frequent aneuploidy, tetraploidy, and amplification of chromosomes 11, 12 and 16. In contrast, control mice treated by i.p. pristane injection did not develop plasmacytoma, and lipopolysaccharide-stimulated splenocytes from control mice had mainly normal diploid karyotypes. However, karyotypic instability in a minority of splenocytes indicated that control mice showing no signs of plasmacytoma development nevertheless are prone to numerical and structural cytogenetic mutations that may possibly result in plasmacytoma initiation and progression under favourable conditions, such as infection with ABL-MYC virus with the resulting high expression of v-abl and Myc in target cells. These results indicate the possible existence of proto-oncogenes present on murine chromosomes 11, 12, and 16 that are important for plasmacytoma initiation and/or progression. There are also indications that T(1;6) and monosomy of the X chromosome may also play roles in plasmacytomagenesis, and that trisomy 12 may only occur in cells with pre-existing nonrandom mutations, thereby acting as a late mutation event. As other experimental models of murine plasmacytoma have not shown a similar karyotypic etiology, there appears to be several possible redundant cytogenetic mutation events that lead to plasmacytoma. Also, as tumours in this study present various combinations of the aforementioned amplified chromosomes, their combined amplification may serve redundant purposes as well. en
dc.format.extent 5162427 bytes
dc.format.mimetype application/pdf
dc.language.iso en_US
dc.rights info:eu-repo/semantics/openAccess
dc.subject plasmacytoma en
dc.subject cytogenetics en
dc.subject myc en
dc.subject abl en
dc.subject trisomy en
dc.title Trisomy 11, 12, and 16 in v-abl/myc-induced murine plasmacytomagenesis en
dc.type info:eu-repo/semantics/masterThesis
dc.type master thesis en_US
dc.degree.discipline Physiology en
dc.contributor.examiningcommittee Dawson, Angelika (Biochemistry and Medical Genetics) Duckworth, Mary Lynn (Physiology) Shiu, Robert (Physiology) en
dc.degree.level Master of Science (M.Sc.) en
dc.description.note May 2008 en


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