Abstract 4843: Genomic analysis of prostate cancer
Authors: Reams Romonia R. 
Published: June 2012

Abstract
Introduction: The most common male malignancy in the United States is prostate cancer; however its rate of occurrence varies significantly among ethnic groups. African American (AA) males have a 1.6 higher incidence rate for prostate cancer (CaP) and a 2.5 higher death rate as compared to Caucasian American (CA) Males in the USA. To date, no clear explanation is known for this glaring difference in CaP health disparity. A number of factors have been offered including genetic susceptibility, gene-environment interactions, presentation with late stage prostate cancer at diagnosis or presentation with more aggressive tumors, despite the stage and grade. We favor the hypothesis that altered gene expression plays a major role in the disparity observed in CaP incidence and mortality between AA/CA. Methods: We posed the question, what would be the result of Cap Tumor gene expression profiling if bioinformatics analysis of our existing cDNA microarray datasets did not focus on or stratify tumors based on race populations. Using data from our previously conducted micro array pilot project study which used AA and CA CaP tumors with a Gleason score of six and their matched controls;. We compared gene expression profiling in all non-tumor CaP tissue to all CaP tumors using the following filter conditions: minimal fold change of 2.0; t-test and Benjamin Hochberg. Results We identified thirty-one differentially expressed genes in tumors relative to non-tumor controls. Cystatin SN gene was down-regulated 13.19 fold in CaP tumors. Z-score analysis implicated the importance of multiple pathways: Toll-like receptor signaling, Colorectal cancer, MAPK signaling and Pathways in cancer. Genes common to some of the pathways included v-foes FBJ marine osteosarcoma viral oncogene, a key component of the activator protein-1 (AP-1) transcription factor or FOS; MAPK 13 and one DNA excision repair enzyme. MAPK13 (also known as p38δ) is a member of the p38 subfamily of Mitogen-activated protein kinase (MAPK). p38 MAPKs regulate diverse cellular responses including proliferation, differentiation, transformation, and programmed cell death. V-fos FBJ murine osteosarcoma viral oncogene homology (FOS) oncogene is a key component of the activator protein-1 (AP-1) transcription factor. Work is currently underway to determine if expression of either of the above genes is same for AA and CA males. To address this question we will use RT-PCR to determine expression in a panel of novel AA and CA prostate cancer cell lines. Conclusions: Results showed that the decision to not stratify tumors based on self-identified race when studying the genomics of prostate cancer revealed distinctly different genomic profile than those obtained when CaP tumors are stratified according to race. While a wealth of genetic information was uncovered in this study; the definitive next step will be to validate expression levels in AA and CA cell lines or tumor tissues.
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 4843. doi:10.1158/1538-7445.AM2011-4843