Aneusomy of chromosome 7 and loss at 7q (especially 7q31.1) have been reported in prostate cancer. To further investigate abnormalities of 7q and the relationship with whole chromosome 7 changes, we have conducted a dual-color fluorescence in situ hybridization (FISH) analysis on isolated nuclei from 28 primary prostate cancers. A pericentromeric probe for chromosome 7, five newly isolated sequence-specific bacterial artificial chromosome (BAC) probes from 7q31.1, and one BAC for the epidermal growth factor receptor (EGFR) gene at 7p12 were used in dual color hybridizations. Pericentromeric probes for chromosomes X and 4 were also used as controls. Sixteen (57.1%) of the 28 tumors showed clonal aberrations. Nine of them were trisomy 7 and four were hypertetrasomy for chromosome 7. Deletions at 7q31.1 were found in two of the high grade tumors. With the exception of these two cases, all other cases showed concordant results using all probes. These findings confirm previous studies that aneusomy of 7 is associated with prostate cancer progression, and there may be a tumor suppressor gene (TSG) at 7q31.1 which is associated with tumor progression. In addition, our study indicates: (1) the deletion pattern of individual nuclei infers that deletions at 7q31.1 precede reduplications of chromosome 7; and (2) the amplification of EGFR was not detected at the DNA level, suggesting that activation of this oncogene may play a minor role in prostate cancer.