Jc. Presti et al., INITIATING GENETIC EVENTS IN SMALL RENAL NEOPLASMS DETECTED BY COMPARATIVE GENOMIC HYBRIDIZATION, The Journal of urology, 160(4), 1998, pp. 1557-1561
Purpose: To identify the genetic alterations associated with renal ade
nomas. Materials and Methods: We analyzed 37 renal adenomas obtained a
t autopsy (23 papillary and 14 non-papillary) by comparative genomic h
ybridization. Results: In papillary tumors, the median number of gains
and losses of genetic material per tumor was 2.0 and 1.0, respectivel
y. Papillary tumors were characterized predominantly by gains of genet
ic material on chromosomes 7 (57%), 17 (35%), 16 (26%), 12 (26%), 3 (2
2%), 20 (22%) and loss of a sex chromosome (83%). In 6 papillary tumor
s less than or equal to 5 mm. in diameter, gain of chromosome 7 occurr
ed in 4 specimens. Initiating events for papillary renal adenomas incl
ude gain of chromosome 7 and loss of a sex chromosome. In non-papillar
y tumors, the median number of gains and losses of genetic material pe
r tumor was 1.0 and 1.0, respectively. Nonpapillary tumors were charac
terized by loss of genetic material on chromosome 3p (50%), loss of a
sex chromosome (36%) and a gain of chromosome 5 (43%). The initiating
event for non-papillary renal adenomas is the loss of chromosome 3p. C
onclusions: Renal adenomas demonstrate similar genetic alterations as
clinically detected renal, cell carcinomas. Their clinically indolent
course may, in part, be a result of the lower number of genetic altera
tions per tumor than their clinically detected counterparts. Renal ade
nomas are thus small carcinomas which have not yet acquired the necess
ary genetic alterations leading to tumor progression.