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dc.contributor.authorFeller, J. Kyleen_US
dc.date.accessioned2015-08-04T20:19:21Z
dc.date.available2015-08-04T20:19:21Z
dc.date.issued2012
dc.date.submitted2012
dc.identifier.other(ALMA)contemp
dc.identifier.urihttps://hdl.handle.net/2144/12373
dc.descriptionThesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.en_US
dc.description.abstractThe c-myc proto-oncogene is involved in various cellular processes including cell growth, proliferation, and apoptosis. Overexpression and deregulated expression of the gene have been previously linked to several lineage-unrelated, aggressive, poorly differentiated tumors. Oncogenic expression of c-myc has also been implicated in several vascular neoplasms as having a crucial role in angiogenesis. This gives c-myc a dual oncogenic function in that tumor growth requires both cell proliferation and angiogenesis to ensure survival and confer an effective malignancy. In vitro studies have shown that the c-Myc protein is an important regulatory molecule of spindle cell proliferation and migration in Kaposi's sarcoma (KS), an angioproliferative tumor that is commonly associated with HIV. In light of the above and recent findings demonstrating amplification of c-myc in select angiosarcomas secondary to irradiation or chronic lymphedema, our primary aim was to ascertain the same in KS. We also attempted to determine what correlation existed, if any, between the immunohistochemical (IHC) expression of the c-Myc protein and c-myc gene copy amplification using fluorescent in situ hybridization (FISH). Samples analyzed during this study included archival tissue samples of KS (N=24 ). For FISH analyses, a dual-labeled technique was employed and probes against the c-myc gene and chromosome 8 (CEP-8) were used. For IHC, the monoclonal anti-c-myc antibody, 9E10, was used and tissue from hemangiomas (N=11) and non-radiation induced angiosarcomas (N=6) served as the controls. PCR for detection of KS-associated herpesvirus (KSHV) DNA was performed on all KS cases. While FISH analyses revealed no amplification of c-myc in any of the cases of KS, IHC analyses revealed positive staining for c-Myc in 13/24 cases (54%) with stain localization throughout the cell. As such, no correlation could be found between gene amplification and protein expression. KSHV-PCR analyses revealed that 19/24 cases (79%) were positive for KSHV-DNA. Ten of 24 cases (42%) were positive for c-Myc IHC and KSHV-PCR, while one case (4%) was negative for both indicating a lack of correlation (using McNemar's test for statistical analysis) between c-Myc IHC protein levels and presence of KSHVDNA. Our findings indicate that c-myc gene amplification is not normally found in KS and cannot be correlated with the expression of the c-Myc protein. Thus, unlike other tumors we have discussed where gene amplification was a common occurrence; it seems to have little clinical significance in KS. The absence of c-myc amplification raises the question of why 54% of the samples in this study still exhibited protein expression as determined by IHC. To grasp a further understanding of what is truly going on in these cases, it would be necessary to use techniques such as RT-PCR or in situ hybridization to study c-myc at the RNA level.en_US
dc.language.isoen_US
dc.publisherBoston Universityen_US
dc.titleCorrelation of amplification and expression of the c-myc oncogene in Kaposi's sarcomaen_US
dc.typeThesis/Dissertationen_US
etd.degree.nameMaster of Artsen_US
etd.degree.levelmastersen_US
etd.degree.disciplineMedical Sciencesen_US
etd.degree.grantorBoston Universityen_US


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