The diagnosis of prostate cancer (adenocarcinoma) relies on screening for elevated prostate-specific antigen (PSA) in blood samples and on digital rectal examination (DRE). With high PSA levels and/or abnormal DRE, physicians recommend a biopsy, which often misses the location of the adenocarcinoma and results in false negatives. Previous studies have shown expression of the key transcription factor early growth response 1 (EGR-1), the pro-survival factor macrophage inhibitor cytokine 1 (MIC-1), and the growth stimulatory platelet derived growth factor A (PDGF-A) to be up-regulated in histologically normal tissues 1 centimeter adjacent to prostate adenocarcinomas. We hypothesize that tumors emerge from “field cancerized” tissues, and while such tissues appear normal under gross histological examination, further analysis reveals a molecular history that adds insight into development of oncogenesis. We aim to explore EGR-1, MIC-1, and PDGF-A as essential markers of field cancerization and prostate oncogenesis that may also provide an early detection of premalignant cells by biochemical and molecular biological methods. We present here data from our ongoing investigations into the effect of tissue microenvironmental factors involved in tumorigenesis, for example oxidative stress and telomere-mediated genomic instability in human prostate cancer cell models. We also present data on the regulation of expression of MIC-1 and PDGF-A by EGR-1 using human prostate cancer cell models
