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Annals of Surgical Oncology 10:136-143 (2003)
© 2003 Society of Surgical Oncology

ORIGINAL ARTICLES

Fine Mapping of Wilms’ Tumors With 16q Loss of Heterozygosity Localizes the Putative Tumor Suppressor Gene to a Region of 6.7 Megabases

Shawn D. Safford, MD, Dominique Goyeau, MS, Alex J. Freemerman, PhD, Rex Bentley, MD, Mary Lou Everett, MS, Paul E. Grundy, MD and Michael A. Skinner, MD

From the Department of Surgery (SDS, DG, AJF, MLE, MAS), Division of Pediatric Surgery, and Department of Pathology (RB), Duke University Medical Center, Durham, North Carolina; and Department of Pediatric Oncology (PEG), Cross Cancer Institute, Alberta, Canada.

Correspondence: Address correspondence and reprint requests to: Michael A. Skinner, MD, PO Box 3815, Duke University Medical Center, Durham, NC 27710; Fax: 919-681-8353; E-mail: skinn009{at}mc.duke.edu

Background: The aim of this study was to more precisely map the region of 16q loss of heterozygosity (LOH) in Wilms’ tumors and to examine the expression of putative tumor suppressor.

Methods: We performed polymerase chain reaction–based LOH analysis on the 185 sample pairs from 21 to 80 megabases (Mb) on chromosome 16q. Expression of two candidate tumor suppressor genes located within the identified consensus region of 16q LOH was examined by immunohistochemistry.

Results: We identified 16q LOH in 7 (4%) of 185 Wilms’ tumors not previously thought to demonstrate such genetic loss. The smallest common region of genetic loss was located between 67.3 and 74.0 Mb on chromosome 16. Within this 6.7-Mb region, there reside only three recognized tumor suppressor genes: E-cadherin, P-cadherin, and E2F4. E-cadherin demonstrates statistically significantly reduced expression in Wilms’ tumors with 16q LOH.

Conclusions: We have localized the consensus region of 16q LOH in Wilms’ tumor to a 6.7-Mb locus and have identified three candidate Wilms’ tumor suppressor genes within this narrowed region. Our data support E-cadherin as a candidate tumor suppressor gene in Wilms’ tumor; however, further studies are needed to definitively prove its role as the tumor suppressor gene associated with 16q LOH.

Key Words: Wilms’ tumor • Loss of heterozygosity • Chromosome 16 • Neoplasia • Tumor suppressor






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