A similar pattern of chromosomal alterations in prostate cancers from African-Americans and Caucasian Americans

Department of Urology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
Clinical Cancer Research (Impact Factor: 8.72). 06/1998; 4(5):1273-8.
Source: PubMed


A combination of genetic and epigenetic factors may explain the disproportionate incidence and mortality of prostate cancer among African-American males (AAMs) as compared with Caucasian American males (CAMs). We wished to determine whether primary prostate cancers from AAMs and CAMs harbor different patterns or frequencies of chromosomal alterations. Comparative genomic hybridization (CGH) was performed on clinically localized, untreated primary prostate cancers from 16 AAMs and 16 CAMs. Detailed statistical analysis was used to delineate gains and deletions with high sensitivity and specificity and to compare the frequency and pattern of alterations between the two groups of tumors. The two groups of patients had indistinguishable preoperative serum prostate-specific antigen levels, and the two groups of tumors had similar pathological stages and grades. Chromosomal gains and deletions occurred in regions known to be frequently altered in prostate cancer. Specifically, the most frequent alterations were deletions of regions on chromosomes 13q, 5q, 16q, and 8p and gains of regions on 8q and 5q. When tumors from AAMs and CAMs were compared, the frequencies of alteration (deletion, gain, or no alteration) were similar across 98.9% of the length of the genome. The patterns of alterations of the most frequently altered chromosomes were also similar between tumors from AAMs and CAMs. We concluded that primary prostate cancers from AAMs and CAMs harbor a similar pattern and frequency of chromosomal alterations. These data support the notion that sporadic prostate cancers from AAMs and CAMs develop by similar chromosomal mechanisms. Biological differences, if present, do not occur on the chromosomal level.

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    • "Very few studies have been carried out to determine whether there are areas of allelic loss or gain in prostate cancers from AA men that are overrepresented in or specific to this group. Cher et al. [12] compared primary prostate cancers from 16 AA and 16 white Americans using cytogenetic CGH. They did not observe any significant differences in overall loss or gain of chromosomal regions between these two groups, although they did observe increased rates of loss at 12q21, 15q21, and 17p12-13 in AA men. "
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    ABSTRACT: African American (AA) men have a higher incidence and significantly higher mortality rates from prostate cancer than white men, but the biological basis for these differences are poorly understood. Few studies have been carried out to determine whether there are areas of allelic loss or gain in prostate cancers from AA men that are overrepresented in or specific to this group. To better understand the molecular mechanisms of prostate cancer in AA men, we have analyzed 20 prostate cancers from AA men with high-density single-nucleotide polymorphism arrays to detect genomic copy number alterations. We identified 17 regions showing significant loss and 4 regions with significant gains. Most of these regions had been linked to prostate cancer by previous studies of copy number alterations of predominantly white patients.We identified a novel region of loss at 4p16.3, which has been shown to be lost in breast, colon, and bladder cancers. Comparison of our primary tumors with tumors from white patients from a previously published cohort with similar pathological characteristics showed higher frequency of loss of at numerous loci including 6q13-22, 8p21, 13q13-14, and 16q11-24 and gains of 7p21 and 8q24, all of which had higher frequencies in metastatic lesions in this previously published cohort. Thus, the clinically localized cancers from AA men more closely resembled metastatic cancers from white men. This difference may in part explain the more aggressive clinical behavior of prostate cancer in AA men.
    Neoplasia (New York, N.Y.) 04/2009; 11(3):305-12. DOI:10.1593/neo.81530 · 4.25 Impact Factor
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    • "Accumulating evidence suggests that both lifestyle and genetic factors affect these geographic differences [2] [3]. Few studies, however, have reported geographic differences in the genetic changes that occur during prostate cancer [4] [5]. "
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    ABSTRACT: Incidence of prostate cancer in Japan and resultant mortality rates are lower than in Western countries. To elucidate the reasons behind this, the genetic characteristics of prostate cancer in Japanese patients were investigated. Comparative genomic hybridization was applied in 27 cases of prostate cancers in Japanese patients. Frequent gains were found at Xq, 8q, Xp, and 7q and frequent losses at 8p, 6q, 2q, 16q, and 17p (in decreasing order of frequency). Loss of 6q was frequently detected in both early and advanced tumors. Gains of 7q and 8q and loss of 8p were more frequent in advanced than early tumors. The frequency of 13q loss in primary tumors was significantly lower in patients in Japan than in European countries. These data suggest that a loss of 6q is associated with the development of prostate cancer, and that gains of 7q and 8q and a loss of 8p are linked with cancer progression. The frequency of 13q loss may imply differences in biological behavior of prostate cancer between Japan and Western countries.
    Cancer Genetics and Cytogenetics 08/2004; 152(2):119-23. DOI:10.1016/j.cancergencyto.2003.11.017 · 1.93 Impact Factor
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    ABSTRACT: A flow-cytometric (FCM) and fluorescence in situ hybridization (FISH) study was performed in 153 patients with clinically localised prostate cancer (PC) to evaluate retrospectively the prognostic significance of DNA ploidy, S-phase fraction (SPF) and chromosome 7 copy number. Deletions in 7q31.1 were analysed in a subset of 26 tumours. The mean follow-up time was 6 years (range 4-16 years). Twelve cases of benign prostatic hyperplasia (BPH) were studied as a control. Chromosome 7 enumeration and deletion studies were conducted using the alpha-satellite D7Z1 probe and a cosmid probe specific for the marker D7S522 on 7q31.1. Higher SPF was associated with shorter overall survival and shorter time to local progression and metastasis. Near diploid (DNA index 1.05-1.20) cases had a lower frequency of metastases and lower Gleason scores than aneuploid cases. Increased absolute chromosome 7 copy number (centromere count) was associated with higher Gleason score, higher SPF and shorter local progression-free and prostate cancer survival. Absolute chromosome 7 copy number was concordant with FCM DNA ploidy in the majority (75%) of cases. Relative gain or loss of chromosome 7 (centromere counts compared to ploidy) was infrequent, and no correlation was found with clinical parameters. Deletions in 7q31.1 were infrequent. Our results indicate that in localised PC (i) SPF is a prognostic factor, (ii) absolute chromosome 7 copy number is concordant with the ploidy status of the tumour (relative gain or loss of chromosome 7 is infrequent and has no independent prognostic value) and (iii) the frequency of deletions in 7q31.1 is low and not correlated with clinical outcome.
    International Journal of Cancer 01/1999; 79(6):553-9. DOI:10.1002/(SICI)1097-0215(19981218)79:63.3.CO;2-J · 5.09 Impact Factor
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