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• W1989032020 abstract "Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FLProstate cancer (PC) is the most common form of cancer in all men and also the second leading cause of cancer related deaths. On average, African American (AA) males are twice as likely to develop prostate cancer and three times more likely to die from it compared with Caucasian men. Previously we combined nonsense-mediated RNA decay microarrays and array-based comparative genomic hybridization for the genome-wide identification of genes with biallelic inactivation involving nonsense mutations and loss of the wild-type allele (Huusko et al, Nature Genetics 2004). This approach enabled us to identify previously unknown mutations in the receptor tyrosine kinase gene EphB2 in ∼7% of prostate tumors. EPHB2 is a member of the tyrosine kinase receptor family of proteins and regulates intracellular signaling pathways involved in cell growth, migration, adhesion, and polarity. Furthermore, there is also strong evidence for EphB2 as a tumor suppressor in colorectal cancer. There are two main isoforms (1 and 2) of the EphB2 gene, which is the result of alternative splicing. Previous studies from our lab also shows that a germline 3055A>T nonsense variant (K1019X) in the EphB2 gene differs in frequency between AA and Caucasian males, is associated with increased risk for PC in AA men with a positive family history, and may be an important genetic risk factor for prostate cancer in AA. The DU145 prostate cancer cell line, originating from a brain metastasis, carries a truncating mutation of isoform 1 of EphB2 and a deletion of the remaining allele. Transfection of DU145 cells, which lack functional EPHB2, with wild-type EPHB2 suppresses clonogenic growth. The goal of this project is to determine the effect of the K1019X mutation on the growth of DU145 cells. Introduction of wild-type and 3055A>T EphB2 into DU145 cells using a lentiviral-based vector led to successful expression as seen by RT-PCR and western blot analysis. We also demonstrated using RT-PCR and western blot analysis that while DU145 cells lack functional expression of the isoform 1, there is expression of the second isoform, implying that the tumor suppressing function of EPHB2 may be unique to isoform 1. Using a sulforhodamine B assay we demonstrated that the K1019X mutation inhibits growth suppression of DU145 cells as compared with wild-type EPHB2. These initial findings suggest that the K1019X is a true functional variant and support the role of the K1019X in increasing prostate cancer risk in AA.Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2102. doi:10.1158/1538-7445.AM2011-2102" @default.
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• W1989032020 title "Abstract 2102: The germline nonsense variant K1019X results in loss of tumor suppressing function of EphB2 in prostate cancer cells" @default.
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