Molecular Medicine II: Hormone Dependent Cancers
Annual rept. 1 Apr 2004-31 Mar 2005
NOTRE DAME UNIV IN
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Metastatic cancers arise in a variety of epithelial tissues but acquire characteristics of motile cells to invade other tissues. The genetic basis of these transitions is not known, but genetic propensities have been identified for several organ-specific cancers. Mutations in the APC gene adenomatous polyposis coli predispose individuals to colon cancer, although the exact mechanisms of colon cancer induction are not clear. One proposed mechanism involves defects in the B-catenin signaling pathways which are activated in patients with a defective APC gene. In this project we are testing the hypothesis that abnormal regulation of the search-capture process is the basis of colon cancer initiation. Task 1 is to compare the distributions of proteins involved in search capture in normal and colon cancer cell lines. Progress On Task 1 includes mapping of dynactin and EBl distributions in several cell lines. Task 2 is to test the impact of APC mutations on microtubule plus-end tracking. Progress on Task 2 includes live-cell imaging of motors and search-capture proteins in normal and colon cancer lines. Task 3 is to determine if APC and dynactin share common regulatory mechanisms. Progress on Task 3 includes identification of dynactin kinases and analysis of kinases inhibitors on other search-capture proteins.
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