Chapman access only poster or presentation
Detection of prostate cancer, while still confined to the prostate, has a good chance for successful treatment. High levels of prostate specific antigen and/or abnormal digital rectal antigen cause physicians to recommend a biopsy, which often misses the location of the adenocarcinoma and results in false negatives. Field cancerization denotes the occurrence of molecular alterations in structurally intact cells in histologically normal tissues surrounding tumors. Our research features complementary approaches towards revealing the importance of potential mediators of prostate field cancerization, such as early growth response 1 (EGR-1), fatty acid synthase (FAS), macrophage inhibitory cytokine 1 (MIC-1), and platelet derived growth factor A (PDGF-A). We explored the potential regulatory function of the transcription factor EGR-1 for FAS, MIC-1, and PDGF-A towards the identification of functional pathways of prostate field cancerization. This hypothesis was tested by over-expressing and down-regulating EGR-1 using recombinant DNA technology and determining the effect on FAS, MIC-1, and PDGF-A protein expression in human prostate cell models. A better understanding of such pathways will ultimately lead to an enhanced indication of cancer presence regardless of whether the biopsy cores contain cancerous tissue.
Frisch, Emily; Gabriel, Kristin; and Bisoffi, Marco, "Molecular Insights into Prostate Cancerization: Telomere Length, EGR-1 Expression, and Regulation of MIC‐1, PDGF-A, and FAS" (2015). Student Scholar Symposium Abstracts and Posters. 90.