Familial and sporadic renal oncocytomas--a comparative molecular-genetic analysis.
OBJECTIVE
Genetic causes of sporadic and familial renal oncocytomas are not known. We analyzed these tumors genetically in order to detect tumor-specific chromosome alterations.


METHODS
DNA from 26 sporadic and 31 familial renal oncocytomas were screened by comparative genomic hybridization according to standard protocols including degenerate oligonucleotide-primed PCR.


RESULTS
Chromosome alterations were detected in 19/26 sporadic (73%) and in 4/31 familial renal oncocytomas (13%). Partial or complete losses of chromosome 1 were most frequently found in both sporadic (15/26) and familial tumors (2/4). Less frequently, loss of chromosome 14 (3/26) was detected in sporadic renal oncocytomas as well as losses of 2p, 2q, 4q, 10 and 18 and gains of 1q and 17q in individual sporadic tumors. Inter-tumor variation of chromosome aberrations was prominent in 1 patient, where 1 tumor showed gains of chromosomes 5, 6q, 7, 10p, 12 and 13q, whereas the second tumor exhibited gains of chromosomes 5 and 7 and loss of 10q. In contrast to sporadic renal oncocytomas, most familial tumors (87%) were devoid of chromosome instabilities.


CONCLUSIONS
Our results demonstrate that partial or complete loss of chromosome 1 is the most common alteration in renal oncocytomas, sporadic and familial. However, chromosome changes are much rarer in familial than in sporadic renal oncocytomas.
Junker
K
K
Department of Urology, Jena, Germany. kerstin.junker@med.uni-jena.de
Weirich
G
G
Moravek
P
P
Podhola
M
M
Ilse
B
B
Hartmann
A
A
Schubert
J
J
D018249:Adenoma, Oxyphilic / Q000235:genetics*; D000368:Aged; D002869:Chromosome Aberrations; D006801:Humans; D007680:Kidney Neoplasms / Q000235:genetics*; D008875:Middle Aged; D009693:Nucleic Acid Hybridization