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Abstract

Abstract 

  1. Prostate cancer is the most commonly diagnosed cancer in men. The incidence of this disease shows strong age, race, and geographic dependence, with African Americans and Asians being examples of high- and low-risk populations, respectively.

  2. Although no hereditary prostate cancer genes have been cloned, familial clustering data and segregation analyses are consistent with the existence of dominant high-risk alleles for prostate cancer. Genome-wide scans for linkage in prostate cancer families have implicated loci on 1q and Xq as harboring prostate cancer-susceptibility genes.

  3. Deletion of sequences from the short arm of chromosome 8 is perhaps the most frequent chromosomal alteration in prostate cancer, occurring at high frequency even in precursor lesions. Gain of sequences on chromosome 8q and loss of sequences on 13q are only slightly less common than 8p loss of heterozygosity (LOH). Gain and deletion of chromosome 7 sequences, along with deletions of chromosomes 5q, 6q, 10q, and 16q, are also frequent events in the prostate cancer cell genome. The genes driving the apparent selection of these abnormalities are largely unknown.

  4. Methylation of a CpG island in the promoter of the GSTP1 gene is the most common genomic alteration yet identified in prostate cancer, occurring in virtually every case. The common inactivation of this carcinogen-defense pathway suggests a potentially important role of environmental carcinogens during prostatic carcinogenesis.

  5. Although mutations of p53, PTEN, Rb, ras, CDKN2, and other tumor-suppressors and oncogenes have been detected at varying frequencies in prostate cancer, no single gene has been identified as being mutated in the majority of prostate cancers.

  6. The androgen receptor gene, when either mutated or amplified, may play a critical role in prostate tumorigenesis both at the early stages and during progression to androgen-insensitive disease. Polymorphic variants of the androgen receptor and other genes involved in androgen metabolism that differ in their biologic activity may modulate risk for prostate cancer or for the tendency to develop more aggressive forms of this disease.

  7. Prostate cancers vary tremendously in their biologic aggressiveness. The ability of various genetic alterations to serve as much-needed molecular diagnostic and prognostic indicators is being evaluated.

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