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Replication linkage study for prostate cancer susceptibility genes
Author(s) -
Suarez Brian K.,
Lin Jennifer,
Witte John S.,
Conti David V.,
Resnick Martin I.,
Klein Eric A.,
Burmester James K.,
Vaske David A.,
Banerjee Tarit K.,
Catalona William J.
Publication year - 2000
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/1097-0045(20001001)45:2<106::aid-pros4>3.0.co;2-h
Subject(s) - locus (genetics) , genetics , biology , genetic linkage , microsatellite , prostate cancer , chromosome , gene , cancer , allele
BACKGROUND Since the publication of the first genome screen for prostate cancer (CaP) 5 years ago, over a dozen linkage studies have appeared. Most attention has been directed to chromosome 1, where two separate regions have been identified as harboring a prostate cancer susceptibility locus: HPC1 in the 1q24–25 interval and PCaP in the 1q42.2–43 interval. Linkage analysis of chromosome 16 has also provided evidence of harboring two loci predisposing to CaP. METHODS We report on a replication linkage study of chromosomes 1 and 16 in 45 new and 4 expanded multiplex CaP families. Multipoint Z‐scores were obtained for 30 highly polymorphic short‐sequence tandem repeat markers spanning chromosome 1, and 22 markers spanning chromosome 16. RESULTS The replication sample gave no evidence for a CaP susceptibility locus in the 1q24–25 interval and equivocal evidence for such a locus at 1q42.2–43. With respect to chromosome 16, positive Z‐scores were obtained over a contiguous interval covering the entire p arm and the proximal half of the q arm. CONCLUSIONS The linkage analysis of our replication sample does not support the existence of HPC1, and the evidence for the existence of PCaP remains equivocal. Evidence of a susceptibility locus on 16p remains strong, but the evidence for a susceptibility locus on 16q is weakened. Prostate 45:106–114, 2000. © 2000 Wiley‐Liss, Inc.