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Prostate cancer is the most common cancer in males and, despite its high incidence, only limited data are available on which genes or chromosome regions are specifically involved in its initiation and progression. We studied 72 prostate tumor samples by array-CGH, using a platform containing 60.000 oligonucleotides spread over the whole genome (60K Agilent Technologies). No chromosome alterations (CNA) were detected in 13 samples. The array-CGH profiles of the remaining samples showed losses at 8p and gains on 8q, often with narrow peaks of amplification, in ∼50% of the tumors. Additionally, losses at 6q, 13q and 16q were observed in ∼25% of the samples. Although these results are in general agreement with the location of alterations described earlier, the altered chromosome segments are often several megabases long. Mapping of minimum regions altered in several tumors, or pronounced copy number changes in smaller segments, permits a more precise definition of the relevant chromosome regions that are relevant for tumor development and progression. Current prognostic variables include prostatic specific antigen (PSA), the pathologically defined Gleason score (GS) and T-category (of the TNM staging). There is a great heterogeneity within the intermediate risk group and further genetic markers are needed to refine disease diagnosis and prognosis. So, we analyzed the copy number alteration signatures for the intermediate risk group, Gleason 7. In the comparison between samples related as GS 6 versus GS 7, we found that losses on 5q21.1 and gains on 7q11.21 are more frequent in GS 7. In other hand, losses on 22q13.33 are more frequent in GS 7 than in GS 8 and 9, while losses on 6q21 and 18q21 are correlated with GS 8 and 9. Additionally, we have medical follow-up of only 46 of the 72 samples. Fifteen of these patients had present recurrence after treatment. We analyzed this group versus the group with no recurrence. Losses at 2p21, 6q12, 7q36.3 and 16q13 are more frequent in the group of patients in which there is recurrence of the tumor. This suggests that these alterations could also be hallmarks for recurrence. Further studies with array-CGH of prostate tumors samples will ultimately lead to defining much smaller regions of overlap than at present, which in turn will indicate which specific individual genes and/or combinations of genes are the real “drivers” in prostate cancer or could act as hallmarks for prognosis and recurrence. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1168. doi:1538-7445.AM2012-1168