Frequent Loss of Chromosome Arms 8p and 13q in Collecting Duct Carcinoma (CDC) of the Kidney

Authors

  • Mark Schoenberg,

    Corresponding author
    1. Departments of Urology, The Johns Hopkins University School of Medicine, Baltimore, Maryland
    • The James Buchanan Brady Urological Institute and The Department of Urology, Johns Hopkins University School of Medicine, Marburg 143, 600 North Wolfe Street, Baltimore, MD 21287–2101, U.S.A.
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  • James D. Brooks,

    1. Departments of Urology, The Johns Hopkins University School of Medicine, Baltimore, Maryland
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  • Fray F. Marshall,

    1. Departments of Urology, The Johns Hopkins University School of Medicine, Baltimore, Maryland
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  • Jonathan I. Epstein,

    1. Departments of Urology, The Johns Hopkins University School of Medicine, Baltimore, Maryland
    2. Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland
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  • William B. Isaacs,

    1. Departments of Urology, The Johns Hopkins University School of Medicine, Baltimore, Maryland
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  • Paul Cairns,

    1. Otorhinolaryngology and the Head and Neck Cancer Research Laboratory, The Johns Hopkins University School of Medicine, Baltimore, Maryland
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  • David Sidransky

    1. Otorhinolaryngology and the Head and Neck Cancer Research Laboratory, The Johns Hopkins University School of Medicine, Baltimore, Maryland
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Abstract

Collecting duct carcinoma (CDC) is a malignant renal neoplasm that is believed to arise from the epithelium of the ducts of Bellini in the distal nephron. These tumors are clinically aggressive and more often occur in a younger population than is typical of the more common clear cell renal carcinoma (RCC). Using highly informative polymorphic microsatellite markers on chromosome arms 3p, 5q, 6q, 8p, 9p, 9q, 11p, 13q, 17p, and 18q, we analyzed DNA from nonmalignant and tumor tissue in 6 cases of CDC. We found no evidence of 3p loss of heterozygosity (LOH) in these renal tumors by using multiple markers, a finding that distinguishes CDC from RCC in which 3p LOH has frequently been observed. We found LOH of 8p in 50% of the tumors examined; in addition, we observed LOH of 13q in 50% of the tumors studied. Interestingly, 8p LOH may be associated with high stage and poor clinical prognosis. These data suggest that the molecular events responsible for the development of CDC differ from those associated with the origin of RCC, and that tumor suppressor genes on 8p and 13q may be involved in the pathogenesis of CDC.

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