CLINICAL FOLLOW-UP IN 24 NONFAMILIAL RENAL TUMORS CYTOGENETICALLY CHARACTERIZED IN TISSUE-CULTURE

Citation
M. Golimbu et al., CLINICAL FOLLOW-UP IN 24 NONFAMILIAL RENAL TUMORS CYTOGENETICALLY CHARACTERIZED IN TISSUE-CULTURE, Urology, 43(1), 1994, pp. 26-30
Citations number
29
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00904295
Volume
43
Issue
1
Year of publication
1994
Pages
26 - 30
Database
ISI
SICI code
0090-4295(1994)43:1<26:CFI2NR>2.0.ZU;2-5
Abstract
Objective. This study investigates the relationship between clonal chr omosomal abnormalities detected in nonfamilial renal cell carcinoma an d the clinical outcome, specifically, whether or not patients whose tu mors had karyotypic changes have a different prognosis than those whos e tumors did not. Method. Fresh tumor tissue obtained from 32 cases wa s grown in tissue culture. Twenty four grew successfully and were harv ested and multiple cells of each karyotyped. Clinical follow-up was ob tained for at least five years or until the time of death. Results. Fo urteen of 24 cases demonstrated karyotypic abnormalities including los s of Y chromosome (64%), trisomy 7 (50%), trisomy 12 (14%), trisomy 9, 10, 14, 15, 16, and 17, monosomy 9 and 20, and long-arm deletion of c hromosome 16 (1 case each). Tumors were well-differentiated in 16 case s, moderately differentiated in 5 cases, and poorly differentiated in 1 case; 13 cases were pathologic Stage 1, 5 Stage II, and 6 Stage III. Thirty-three percent of the patients demonstrated clinical progressio n. Conclusions. No significant difference in prognosis could be found between patients with and without karyotypic abnormalities. The only c linical or pathologic difference which could be established was sex di stribution. Significantly greater numbers of males had karyotypic abno rmalities than females, but this could be explained by the high number of Y chromosome deletions that were detected. The lack of correlation between karyotypic abnormalities and clinical outcome may reflect a c onfounding factor in genetic evolution such that clinically determinin g chromosomal changes present early in a tumor's growth in vivo may no longer be present when the tumor is diagnosed, treated, or after it i s grown in culture. This may make demonstration of such clinically sig nificant chromosomal changes very difficult.