| Abstract: |
We used cytogenetic and restriction fragment length polymorphism(RFI.P) analysis methods to define genetic alterations and also correlatethe changes with histopathology in renal cortical tumors. The study seriesis comprised of 50 renal tumors in 4 histolã3gica!categories: (a) clearcell, nonpapillary, renal cell carcinoma (RCC) in = 32); (b) nonclear cell,nonpapillary RCC (n = 10); (c) papillary RCC'(n = 3); and oncocytictumors (n = 5).Successful karyotypes »ereobtained from 28 tumors (56%), of which17 (61%) were abnormal. Abnormalities of chromosome 3p were seen in9 tumors, which included unbalanced translocations and terminal orinterstitial deletions. Abnormalities of chromosome 5 were identified in11 tumors, 8 of which were due to unbalanced translocations between 3pand 5q, resulting in an extra copy for the region 5q22â€′′»teInr. addition,trisomy or tetrasomy of chromosome 17 was seen in 6 (5 with normalchromosome 3 and one with 3p deletion), trisomy or more copies ofchromosome 7 in8 (4 with 3p deletion, 2 with trisomy or tetrasomy 17,and 2 with trisomy alone), and trisomy 12 in 3 (all with trisomy 17)tumors. Furthermore, relative deficiency of chromosome 17p was seen in3 (all with deletion 3p) and chromosome 18 in 4 (all with deletion 3p)tumors. RFI.P analysis with four chromosome 3 specific probes detected3p deletions in 19 tumors with the most common breakpoint locatedbetween 3p 14-21. The 19 3p deletions detected by RFI.P included tumorsthat also showed rearrangement of 3p by cytogenetics (n = 4) and thosethat showed normal karyotypes (n = 3) in addition to cytogenetic failures(n = 12). Deletions of 17p were seen in5 of 31 informative cases. Thus,deletions of 3p were seen in a total of 24 tumors by cytogenetic and/orRFI.P analysis, 21 of which were clear cell, nonpapillary RCC, whereas3 had a minor clear-cell component. Oncocytic and nonclear, nonpapillarytumors, on the other hand, did not demonstrate 3p deletions by eithertechnique, whereas trisomy 17 was seen in 3 of the 3 papillary tumors.The loss of allelesfromchromosome I7p and 18 and an increased dosageof gene or genes on chromosomes 5q and 7 as seen in high-stage tumorsof various histolã3gica!subtypes may be associated with progression ofdisease. © 1991, American Association for Cancer Research. All rights reserved. |
| Keywords: |
adult; clinical article; controlled study; human tissue; aged; histopathology; cytogenetics; kidney neoplasms; kidney tumor; carcinoma, renal cell; chromosome aberrations; chromosome deletion; chromosome 18; chromosome 17; chromosome 3p; chromosomes, human, pair 3; kidney cortex; chromosomes, human, pair 17; middle age; chromosome 5; restriction fragment length polymorphism; polymorphism, restriction fragment length; chromosomes, human, pair 18; human; male; female; priority journal; article; support, u.s. gov't, p.h.s.; endogenous compound
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