Heat induced epitope retrieval (HIER) was performed by immersing the tissue sections at 98C for 20 minutes in 10 mM citrate buffer (pH 6

Heat induced epitope retrieval (HIER) was performed by immersing the tissue sections at 98C for 20 minutes in 10 mM citrate buffer (pH 6.0) with 0.05% Tween. (OR=1.9, 95% confidence interval 0.88C4.0, p value =0.10). Conclusions Our results demonstrate that ERG protein expression is readily quantifiable with an existing commercial antibody. Evaluating ERG protein expression may improve our ability to identify the subset of more aggressive, invasive prostate cancers. L 006235 Introduction Prostate cancer remains a significant medical problem, and over 32,000 U.S. men are expected to die from the disease this year. 1 There is a paucity of data to distinguish between L 006235 aggressive and indolent prostate cancer, although a number of molecular markers have been studied. is a member of the ETS family of transcription factors.2,3 In 2005, Tomlins, et al reported that fusions between and gene fusion.9C11 However, these techniques are not readily performed in many clinical laboratories. For QPCR, high tumor content in a specimen or frozen samples is also often necessary. For these reasons, several groups have used immunohistochemistry (IHC) to quantify ERG protein expression.12C16 However, the association between ERG expression and important clinico-pathological features of this disease remains unclear. Additionally, none of the prior reports included sufficient numbers of patients with prostate cancer-specific mortality to determine this association. In this study, we sought to examine how ERG protein expression by IHC is associated with clinico-pathological and mortality outcomes. Materials and Methods Case-Control Study Description The Molecular Epidemiology of Fatal Prostate Cancer (MEFPC) study is a population-based case-control study conducted in three Kaiser Permanente regions. This analysis focused on the subjects from the Kaiser Permanente Northwest (KPNW) and Kaiser Permanente Northern California (KPNC) regions. Men who had prostatectomy as part of prostate cancer treatment and who died from 1971C2001 at KPNW (546) and from 1980C2001 at KPNC (1,026) were selected from the L 006235 KPNW electronic cancer registry files and National Cancer Institute (NCI) Surveillance, Epidemiology, and End Results (SEER) program files (for KPNC). We then restricted the group to men coded as dying from prostate cancer or from a list of immediate causes for which prostate cancer might be the underlying cause (eg. unknown cause, pneumonia, renal failure) (1,006). From the subset with formalin fixed paraffin-embedded tumor tissue in health plan archives, the medical records of men who were diagnosed with prostate cancer before age Plxna1 81 years; were Caucasian, African-American, or Hispanic race; and were members of the health plan when diagnosed and for at least 12 months following their diagnoses or until death, if death occurred within 12 months, were evaluated using a cause-of-death algorithm developed for this study to select men whose deaths were due to prostate cancer (192). Of these 192 cases, tumor tissue for 99 cases was available for this secondary analysis. Controls (n=109 for this analysis) were originally matched to study cases on health plan, race, tumor SEER stage at diagnosis as recorded in the health plan tumor registries, age at diagnosis, year of diagnosis, and duration of health plan membership and had to be alive at the time of their matched cases death. We abstracted medical records for prostate cancer tumor characteristics, treatment outcome, co-morbidities, clinical characteristics, and demographics. We collected other pertinent information from automated laboratory, cancer registry, and health plan membership files. Not all subjects in this secondary.