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Career Development
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Role of Bile Acids in the Activation of the Antiapoptotic IL-6/Stat3 Pathway in Barrett's Esophagus
Specific Aims
To evaluate the effect of bile acids on the secretion and expression of the antiapoptotic interleukin (IL), IL-6, in human squamous esophageal epithelium and Barrett's esophagus (BE) tissue ex vivo and in a normal squamous esophageal cell line (Het-1A) in vitro.
To test effect of bile acids on Stat3 activation in human esophageal epithelium and BE and normal squamous cell line.
To evaluate whether bile acids treatment upregulates expression of antiapoptotic Bcl-2 family proteins (e.g. Bcl-xL, Bcl-2) in human esophageal mucosa and BE and in a normal esophageal squamous cell line through an IL-6 modulated signalling pathway.
Identification and Frequency of VDR and RXR Polymorphisms
Specific Aims
To conduct a pilot study with DNA samples from healthy controls in order to:
Describe the frequency of polymorphic alleles in the Cdx binding site of the Vitamin D Receptor gene
Identify and determine the frequency of polymorphic variation in the Retinoid X Receptor gene
Determine the haplotype structure of the Retinoid X Receptor gene
Regulation of Cadherin Function by Wnt signaling in Morphogenesis and Neoplasia
Hypothesis: Dysregulation of E-cadherin and Cadherin-6 by mutations in components of the Wnt signaling pathway, such as -catenin, can result in neoplasia rather than normal morphogenesis.
Specific Aims:
To determine if there is differential localization and regulation of E-cadherin and Cadherin 6 levels during epithelial tubule morphogenesis.
To test if -catenin/Lef/TCF signaling is necessary for epithelial morphogenesis.
To test whether altered E-cadherin, Cadherin 6 and -catenin localization and regulation cause the formation of polyps rather than tubules.
Neurological Effects of Chemotherapy and Radiation Treatment: Colon Cancer
Specific Aims
Cancer therapies that impact the central nervous system (CNS), including those used to treat colon cancer, are often successful at eradicating neoplastic cells and preventing relapse. However, these treatments can have long-term neurological effects. The precise nature and long-term ramifications of such CNS injury are currently under investigation. With a career development award from the Arizona Cancer Center SPORE in GI Cancer, I propose to address the following hypotheses:
Structural MRI of the brains of individuals treated with chemotherapy will show evidence of volume changes in several CNS structures. Specifically, it is predicted that there would be a reduction in white matter volume, corpus callosum volume, and hippocampal volume.
Diffusion-weighted imaging (DWI) and magnetic resonance spectroscopy (MRS) will show evidence of a breakdown in neuronal integrity in the white matter of individuals treated with chemotherapy.
In cancer survivors, MRI data will show a positive relationship to neuropsychological performance. Specifically, it is predicted that there would be a relationship between hippocampal volume and memory performance, a relationship between the white matter volume and psychomotor speed, and a relationship between DWI/MRS measures and attention and higher order function.
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