Allelic loss of chromosomes 16q and 10q in human prostate cancer

Bob S. Carter, Charles M. Ewing, W. Steven Ward, Brent F. Treiger, Tilly W. Aalders, Jack A. Schalken, Jonathan I. Epstein, William B. Isaacs

Research output: Contribution to journalArticlepeer-review

455 Scopus citations


Recent advances in understanding the molecular genetics of common adult tumors have indicated that multiple genetic alterations including the activation of oncogenes and the inactivation of tumor suppressor genes are important in the pathogenesis of these tumors. Loss of heterozygosity is a hallmark of tumor suppressor gene inactivation and has been used to identify chromosomal regions that contain these genes. We have examined allelic loss in the most common tumor in men, prostate cancer. Twenty-eight prostate cancer specimens have been examined for loss of heterozygosity at 11 different chromosomal arms including 3p, 7q, 9q, 10p, 10q, 11p 13q, 16p, 16q, 17p, and 18q. Fifty-four percent (13/24) of clinically localized tumors and 4 of 4 metastatic tumors showed loss of heterozygosity on at least one chromosome. Chromosomes 16q and 10q exhibited the highest frequency of loss of heterozygosity with 30% of tumors showing loss at these chromosomes. These data demonstrate that allelic loss is a common event in prostate cancer and suggest that chromosomes 16q and 10q may contain the sites of tumor suppressor genes important in the pathogenesis of human prostate cancer.

Original languageEnglish (US)
Pages (from-to)8751-8755
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number22
StatePublished - Nov 1990


  • DNA polymorphism
  • Loss of heterozygosity
  • Tumor suppressor genes

ASJC Scopus subject areas

  • General


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