 centered on and covering the entire *LSAMP* gene (Supplementary Fig. 6c). A probe derived from chromosome 3-specific alpha satellite centromeric DNA, labeled with CytoGreen fluorescent dye was used as a control. Before use on tissue samples, locus-specific and control probes were mapped to normal human peripheral blood lymphocyte metaphases to confirm location and performance in interphase nuclei. Tumor cells with at least two centromeres were counted. Numbers of centromeres and *LSAMP*/*PTEN* signals were compared to determine whether cells were homozygous or heterozygous for this locus. Deletions were called when more than 75% of evaluable tumor cells showed loss of allele. Focal deletions were called when more than 25% of evaluable tumor cells showed loss of allele or when more than 50% evaluable tumor cells in each gland of a cluster of two or three tumor glands showed loss of allele. Benign prostatic glands and stroma served as built in control.

3. Results {#s0055}
==========

3.1. Tumor and whole genome sequencing data of African American and Caucasian American prostate cancer patients {#s0060}
---------------------------------------------------------------------------------------------------------------

We focused this study on early stage CaP (Gleason score 6 or 7 with primary pattern, 3) because it represents the majority of newly diagnosed prostate cancers in the United States ([@bb0240]). We evaluated histologically defined manually dissected tumor specimens (80--95% tumor purity, primary Gleason pattern 3) and matched normal prostate tissue or peripheral blood lymphocytes from seven AA and seven CA patients, yielding a total of 28 whole genome sequences ([Table 1a](#t0005){ref-type="table"}). The overall landscape of primary CaP genomic alterations (single nucleotide variations \[SNVs\], structural variation \[SVs\], and indels) from this study revealed similarities, as well as differences compared to previous reports ([@bb0010], [@bb0020], [@bb0090]) ([Table 1b](#t0010){ref-type="table"}; [Fig. 1]