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Blood Biomarker Levels to Aid Discovery of Cancer-Related Single-Nucleotide Polymorphisms: Kallikreins and Prostate Cancer.

In English

Författare

  • Robert J Klein
  • Christer Halldén
  • Angel M Cronin
  • Alexander Ploner
  • Fredrik Wiklund
  • Anders Bjartell
  • Pär Stattin
  • Jianfeng Xu
  • Peter T Scardino
  • Kenneth Offit
  • Andrew J Vickers
  • Henrik Grönberg
  • Hans Lilja
Visa allt

Summary, in English

Polymorphisms associated with prostate cancer include those in three genes encoding major secretory products of the prostate: KLK2 (encoding kallikrein-related peptidase 2; hK2), KLK3 (encoding prostate-specific antigen; PSA), and MSMB (encoding beta-microseminoprotein). PSA and hK2, members of the kallikrein family, are elevated in sera of men with prostate cancer. In a comprehensive analysis that included sequencing of all coding, flanking, and 2 kb of putative promoter regions of all 15 kallikrein (KLK) genes spanning approximately 280 kb on chromosome 19q, we identified novel single-nucleotide polymorphisms (SNP) and genotyped 104 SNPs in 1,419 cancer cases and 736 controls in Cancer Prostate in Sweden 1, with independent replication in 1,267 cases and 901 controls in Cancer Prostate in Sweden 2. This verified prior associations of SNPs in KLK2 and in MSMB (but not in KLK3) with prostate cancer. Twelve SNPs in KLK2 and KLK3 were associated with levels of PSA forms or hK2 in plasma of control subjects. Based on our comprehensive approach, this is likely to represent all common KLK variants associated with these phenotypes. A T allele at rs198977 in KLK2 was associated with increased cancer risk and a striking decrease of hK2 levels in blood. We also found a strong interaction between rs198977 genotype and hK2 levels in blood in predicting cancer risk. Based on this strong association, we developed a model for predicting prostate cancer risk from standard biomarkers, rs198977 genotype, and rs198977 x hK2 interaction; this model had greater accuracy than did biomarkers alone (area under the receiver operating characteristic curve, 0.874 versus 0.866), providing proof in principle to clinical application for our findings. Cancer Prev Res; 3(5); 611-9. (c)2010 AACR.

Avdelning/ar

Publiceringsår

2010

Språk

Engelska

Sidor

611-619

Publikation/Tidskrift/Serie

Cancer Prevention Research

Volym

May 4

Dokumenttyp

Artikel i tidskrift

Förlag

American Association for Cancer Research

Ämne

  • Cancer and Oncology

Status

Published

Forskningsgrupp

  • Clinical Chemistry, Malmö
  • Urological cancer, Malmö

ISBN/ISSN/Övrigt

  • ISSN: 1940-6207