F. Fogt et al., UTILIZATION OF MOLECULAR-GENETICS IN THE DIFFERENTIATION BETWEEN ADRENAL-CORTICAL ADENOMAS AND CARCINOMAS, Human pathology, 29(5), 1998, pp. 518-521
Distinction between benign adrenal cortical proliferative lesions and
adrenal cortical carcinoma has been approached by a combination of his
tological, immunohistochemical, and macroscopical parameters. Modern i
maging studies allow detection of small adrenal cortical lesions that
may be incorrectly diagnosed. Differentiation between benign and malig
nant tumors of the adrenal cortex nas attempted by microdissection of
nine cases of adrenal cortical hyperplasia, 10 cortical adenomas, and
18 adrenalcortical carcinomas with subsequent polymerase chain reactio
n (PCR) amplification for loss of heterozygosity (LOH) of five microsa
tellites of putative tumor suppressor gene loci: p53 gene (17p), the n
euroblastoma candidate gene (Ip), the p16 gene (9p), the von Hippel Li
ndau gene (3p), and the retinoblastoma gene (13q). None of the hyperpl
astic lesions or cortical adenomas showed LOH of any of the gene marke
rs used. Conversely, genetic changes were observed in 61% (11 of 18) o
f the cases of carcinoma. Forty-four percent of the lesions showed LO
for p53 (7 of 16). LOH of Ip, 3p, and 9p ic ere seen in 22%, 22%, and
26%, respectively LOH of the retinoblastoma gene was seen in 80% or fo
ur of five of the informative cases studied. We conclude that LOH stud
ies may be used to distinguish malignant from nonmalignant adrenal cor
tical proliferations. Relative infrequency of LOH in 3p may furthermor
e help to differentiate adrenal lesions from clear cell carcinomas of
the kidney. Copyright (C) 1998 by W.B. Saunders Company.