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dc.contributor.authorLadd, Ericeng
dc.contributor.authorZhuang, Yieng
dc.contributor.authorBurks, Amoseng
dc.contributor.authorSlusarz, Annaeng
dc.contributor.authorLubahn, Dennis B. (Dennis Bryant), 1954-eng
dc.contributor.corporatenameUniversity of Missouri-Columbia. Office of Undergraduate Researcheng
dc.contributor.meetingnameSummer Undergraduate Research and Creative Achievements Forum (2005 : University of Missouri--Columbia)eng
dc.date2005eng
dc.date.issued2005eng
dc.descriptionAbstract only availableeng
dc.description.abstractProstate cancer is one of the most common forms of cancer in men. Our lab is currently investigating changes in DNA methylation that occur during cancer progression, and in response to the soy phytoestrogen genistein treatment. We analyze genome-wide methylation differences by using the mouse DMH (mouse-Differential Methylation Hybridization) assay, a form of microarray. We are specifically looking at broad sets of CpG islands, areas rich in cytosine-guanine dinucleotides, that are subject to epigenetic modifications. The hypermethylation of CpG islands is correlated with the silencing of a gene while hypomethylation is correlated with a gene being actively transcribed. We were looking for potential new oncogenes or tumor suppressors. To study these genes we have a mouse model called TRAMP (TRansgenic Adenocarcinoma of the Mouse Prostate), which is a good model to study the progression of prostate cancer and metastasis because it is similar to human prostate cancer. We are using double transgenic mice that are WT or KO for the transcription factor estrogen receptor alpha, on a TRAMP background. The removal of ERα has been correlated with DNA methylation changes. These methylation changes showed up in our microarray screen that led us to find a set of genes that were differentially methylated across cancer progression. We selected one gene: Kinesin superfamily protein 9 (K3_E17) which has been shown on our microarrays to be methylated in well differentiated carcinoma and unmethylated in hyperplasia and poorly differentiated carcinoma. To confirm the methylation status we performed pyrosequencing, a new method to specifically study short sequences of DNA for methylation at specific CG sites. Our hypothesis is that in well differentiated carcinoma Kinesin 9 is hypermethylated, which will correlate with this gene being turned off. This would mean that Kinesin 9 might be acting as a tumor suppressor.eng
dc.description.sponsorshipLife Sciences Undergraduate Research Opportunity Programeng
dc.identifier.urihttp://hdl.handle.net/10355/2153eng
dc.languageen_USeng
dc.publisherUniversity of Missouri--Columbia. Office of Undergraduate Researcheng
dc.relation.ispartof2005 Summer Undergraduate Research and Creative Achievements Forum (MU)eng
dc.relation.ispartofcommunityUniversity of Missouri-Columbia. Office of Undergraduate Research. Undergraduate Research and Creative Achievements Forumeng
dc.source.urihttp://undergradresearch.missouri.edu/forums-conferences/abstracts/abstract-detail.php?abstractid=eng
dc.subjectprostate cancereng
dc.subjectpyrosequencingeng
dc.subjectDNA methylationeng
dc.subjectsoy phytoestrogen genistein treatmenteng
dc.subjectdifferential methylation hybridization (DMH)eng
dc.subjectCpG islandseng
dc.subjectTRansgenic Adenocarcinoma of the Mouse Prostate (TRAMP)eng
dc.subjectKinesin 9eng
dc.titleStudying DNA methylation changes of CpG islands in different stages of prostate cancer by pyrosequencingeng
dc.typePresentationeng


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