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Replication linkage study for prostate cancer susceptibility genes.

B K Suarez1, J Lin, J S Witte

  • 1Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri, USA.

The Prostate
|October 12, 2000
PubMed
Summary

This study found no evidence for prostate cancer (CaP) susceptibility loci HPC1 or PCaP on chromosome 1. However, strong evidence for a CaP locus on chromosome 16p was observed, while evidence for 16q was weakened.

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Area of Science:

  • Genetics
  • Oncology
  • Human Genetics

Background:

  • Over a dozen linkage studies for prostate cancer (CaP) susceptibility loci have been published.
  • Previous research identified potential loci HPC1 (1q24-25) and PCaP (1q42.2-43) on chromosome 1, and loci on chromosome 16.

Purpose of the Study:

  • To perform a replication linkage study for prostate cancer susceptibility loci on chromosomes 1 and 16.
  • To validate findings from previous genome screens in new and expanded multiplex CaP families.

Main Methods:

  • Utilized linkage analysis in 45 new and 4 expanded multiplex prostate cancer families.
  • Analyzed 30 short-sequence tandem repeat markers on chromosome 1 and 22 markers on chromosome 16.
  • Calculated multipoint Z-scores to assess linkage evidence.

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Main Results:

  • No evidence for a prostate cancer susceptibility locus was found in the 1q24-25 region (HPC1).
  • Equivocal evidence for a locus at 1q42.2-43 (PCaP) was observed.
  • Strong evidence for a susceptibility locus on chromosome 16p was detected, with weakened evidence for 16q.

Conclusions:

  • The replication study does not support the existence of the HPC1 locus.
  • Evidence for the PCaP locus on chromosome 1 remains equivocal.
  • A prostate cancer susceptibility locus on 16p is strongly supported, but evidence for 16q is diminished.