Loss of heterozygosity on the long arm of human chromosome 7 in sporadic renal cell carcinomas

Viji Shridhar, Qi C. Sun, Orlando J. Miller, Gregory P. Kalemkerian, John Petros, David I. Smith

Research output: Contribution to journalArticlepeer-review

64 Scopus citations


Cytogenetic and molecular analysis of DNA sequences with highly polymorphic microsatellite markers have implicated allele loss in several chromosomal regions including 3p, 6p, 6q, 8p, 9p, 9q, 11p and 14q in the pathogenesis of sporadic renal cell carcinomas (RCCs). Deletions involving the long arm of chromosome 7 have not been described in RCCs although they have been seen in several other tumor types. However, there have been no detailed analysis of loss of heterozygosity (LOH) of 7q sequences in sporadic RCCs. We therefore studied LOH for DNA sequences on 7q with 10 highly polymorphic markers in 92 matched normal/tumor samples representing sporadic RCCs including papillary, nonpapillary, and oncocytomas in order to determine whether allelic loss could be detected in a tumor type with no visible 7q rearrangements at the cytogenetic level. We found chromosome 7q allele loss in 59 of 92 cases (64%) involving one, two, or more microsatellite markers. The most common allele loss included loci D7S522 (24%) and D7S649 (30%) at 7q31.1-31.2, a region that contains one of the common fragile sites, FRA7G. By comparative multiplex PCR analysis, we detected a homozygous deletion of one marker in the 7q31.1-31.2 region in one tumor, RC21. These results support the idea that a tumor suppressor gene in 7q31 is involved in the pathogenesis of sporadic renal cell carcinomas.

Original languageEnglish (US)
Pages (from-to)2727-2733
Number of pages7
Issue number22
StatePublished - 1997


  • 7q31.2 loss
  • Fragile sites
  • Renal cell carcinoma

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research


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