However, the prognostic value of ERG rearrangements in prostate Everolimus cancer is still controversial . Some genes showed an expression pattern suggestive of a mutually exclusive association with the TMPRSS2-ERG fusion gene. Interestingly, SPINK1 has recently been shown to be upregulated, in a mutually exclusive pattern, in a small percentage of TMPRSS2-ERG-negative carcinomas . In the same study, the outlier profile of ORM1 was also noteworthy and concordant with our current data . Other genes were significantly overexpressed in carcinomas as compared to non-malignant tissue, but with no association to the TMPRSS2-ERG status. These genes likely play a role in prostate carcinogenesis independent of ERG rearrangement, and noteworthy hits based on fold-change and function are AK5, RELN and HPN. Finally, a list of genes showed overexpression in TMPRSS2- ERG-negative carcinomas but an even more significant foldincrease in TMPRSS2-ERG-positive tumors, suggesting a role in malignant transformation in the prostate that is potentiated by ERG expression. Noteworthy hits in this subset include several previously described prostate cancer markers such as AMACR and PCA3 . Interestingly, most of the genes in this list are known to be under androgen-regulation, which may explain the increased levels also in malignant samples with no ERG fusion. RBMS2 displayed a massive fold-change reduction in the array data in TMPRSS2-ERG-positive tumors, but this inverse correlation could not be confirmed in the larger validation series. It is thus likely that RBMS2 reduction may play a role in malignant transformation but independently of ERG rearrangement. In conclusion, we show that the TMPRSS2-ERG fusion gene is associated with up-regulation of several metabolic enzymes, as well as extracellular/transmembrane proteins involved in cell adhesion, matrix remodeling and signal transduction pathways. We observed a massive fold-increase of CRISP3 in fusion-positive carcinomas as compared to non-malignant tissue or fusion-negative carcinomas and found that ERG genomic rearrangement and ERG and CRISP3 mRNA overexpression are associated with pT3 locally advanced tumors. We further show that CRISP3 is a direct target of overexpressed ERG, suggesting that CRISP3 may be a mediator of tumor progression driven by the TMPRSS2-ERG rearrangement. Calcium signaling is an important regulator in all eukaryotic cells for a wide variety of physiological processes. The cells have evolved mechanisms to regulate cytoplasmic Ca2+ homeostasis in response to external or internal stress. Small changes in cytoplasmic Ca2+ levels can activate various Ca2+ -sensing proteins, such as calmodulin and calcineurin, which then lead to the induction of various downstream signal transduction pathways. In response to external or internal stress the cells have evolved mechanisms to regulate cytoplasmic Ca2+ homeostasis. In mammalian cells, various channels including the voltage-gated calcium channels and the transient receptor potential channels play important roles in regulating cytoplasmic Ca2+ . In budding yeast Saccharomyces cerevisiae, vacuolar TRP channel Yvc1p mediates the NVP-BKM120 abmole release of Ca2+ from the vacuole in response to hyperosmotic shock , and Cch1p and Mid1p form a mechano-sensitive channel complex for Ca2+ influx at the plasma membrane . In fission yeast Schizosaccharomyces pombe, the TRP channel Pkd2 plays important roles in cell wall synthesis and membrane trafficking , and Yam8/Ehs1 is involved in maintaining cell wall integrity and in calcium uptake . In our previous study, we monitored the cytoplasmic Ca2+ levels for 10 min using aequorin in living fission yeast cells transformed with pREP1-AEQ . However, it was necessary to concentrate the cells to improve the sensitivity of the measurement, and the increased cell concentration makes it unsuitable for monitoring the Ca2+ levels over a long period of time.