Clinical Report

Prostate cancer is part of the hereditary non-polyposis colorectal cancer (HNPCC) tumor spectrum

  1. Claudio Soravia1,*,
  2. Heleen van der Klift2,
  3. Marie-Anne Bründler3,
  4. Jean-Louis Blouin4,
  5. Juul Wijnen2,
  6. Pierre Hutter5,
  7. Riccardo Fodde2,
  8. Célia Delozier-Blanchet4

Article first published online: 26 MAR 2003

DOI: 10.1002/ajmg.a.20106

Issue

American Journal of Medical Genetics Part A

American Journal of Medical Genetics Part A

Volume 121A, Issue 2, pages 159–162, 30 August 2003

Additional Information

How to Cite

Soravia, C., van der Klift, H., Bründler, M.-A., Blouin, J.-L., Wijnen, J., Hutter, P., Fodde, R. and Delozier-Blanchet, C. (2003), Prostate cancer is part of the hereditary non-polyposis colorectal cancer (HNPCC) tumor spectrum. Am. J. Med. Genet., 121A: 159–162. doi: 10.1002/ajmg.a.20106

Author Information

  1. 1

    Clinic of Digestive Surgery, Geneva University Hospital, Geneva, Switzerland

  2. 2

    Department of Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands

  3. 3

    Division of Clinical Pathology, Geneva University Hospital, Geneva, Switzerland

  4. 4

    Division of Medical Genetics, Geneva University Hospital, Geneva, Switzerland

  5. 5

    Unit of Genetics, Institut Central des Hôpitaux Valaisans, Sion, Switzerland

*Route de Chêne 11, 1207 Geneva, Switzerland.

Publication History

  1. Issue published online: 1 AUG 2003
  2. Article first published online: 26 MAR 2003
  3. Manuscript Accepted: 17 FEB 2003
  4. Manuscript Received: 19 AUG 2002

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Keywords:

  • HNPCC;
  • prostate cancer;
  • mismatch repair genes

Abstract

The recognized urologic tumor spectrum in hereditary non-polyposis colon cancer includes ureteral and renal pelvis malignancies. Here, we report a family in which the proband, who had three metachronous adenocarcinomas of the colon and rectum (at ages 54, 57, and 60), presented with an adenocarcinoma of the prostate at age 61. Immunohistochemical (IHC) staining of colonic, rectal, and prostatic tumor tissues demonstrated lack of expression of both MSH2 and MSH6. Accordingly, microsatellite instability (MSI) was found in the rectal, colonic, and prostatic tumors. The kindred complies with the Amsterdam criteria for HNPCC, as five members over three generations had colorectal cancer. Molecular investigations were initiated when the proband's son presented with an adenocarcinoma of the colon at age 35. Southern blotting analysis of genomic DNA led to identification of a novel genomic deletion encompassing exon 5 of the MSH2 gene. Although prostate cancer has occasionally been described in HNPCC families, to the best of our knowledge, this is the first report where the MSI and IHC analysis of the prostatic adenomcarcinoma clearly link its aetiology to the germline mismatch repair mutation. Hence, prostate cancer should be included in the HNPCC tumor spectrum. © 2003 Wiley-Liss, Inc.

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