Clonal chromosome abnormalities in tumor cells from patients with sporadic renal cell carcinomas.

TLDR

The karyotype of 75 sporadic, nonpapillary renal cell carcinomas was analyzed using chromosome banding techniques. Among these tumors, most were near‑diploid, yet frequent chromosome 3 abnormalities (monosomy, deletions, translocations) and recurrent trisomies of chromosomes 5 and 7, along with losses of 14q, 8, and 9, were observed, indicating that multiple specific chromosomal sites contribute to renal cell carcinoma development.

Abstract

The karyotype of 75 sporadic, nonpapillary renal cell carcinomas was analyzed using chromosome banding techniques. Sixty-five tumors had near-diploid stemlines, and ten had near-triploid or near-tetraploid stemlines. Aberration of chromosome 3 was detected in 71 cases. The nonrandom changes on chromosome 3 were monosomy 3, terminal deletions, or unbalanced translocations; the 3p13-pter segment was identified as the minimal common deletion. The rearrangement of chromosome 3p was the only karyotype change in 13 tumors. Abnormalities of chromosome 5 resulting in trisomy for the 5q22-qter region were found in 36 cases, while the loss of 14q22-qter segment was observed in 34 tumors. Trisomy for chromosome 7 was detected in 17 cases, and monosomy 8 and 9 occurred 14 times each. Our data show that more than one specific chromosomal site may be involved in the development of human renal cell carcinomas.