Analysis of genomic alterations in sporadic adrenocortical lesions - Gain of chromosome 17 is an early event in adrenocortical tumorigenesis

Genetic changes underlying the tumorigenesis of sporadic adrenocortical tum ors are poorly characterized. To search for characteristic genomic imbalanc es involved in adrenocortical tumors, we examined 41 adrenocortical lesions (12 carcinomas, 23 adenomas, and 6 hyperplasias) by comparative genomic hy bridization, Our results show that genetic alterations are more frequent in malignant than in benign lesions and that they rarely occur in hyperplasti c lesions. The most frequent DNA copy number changes in adrenocortical carc inomas included losses of 1p21-31, 2q, 3p, 3q, 6q, 9p, and 11q14-qter, as w ell as gains and. amplifications of 5q12, 9q32-qter, 12q, and 20q. The geno mic aberrations prevalently occurring in adrenocortical adenomas were gains of 17q, 17p, and 9q32-qter. Gains found in 2 of 6 adrenocortical hyperplas tic lesions involved chromosome 17 or 17q only. These data indicate that on cogenes determining the early tumorigenesis of adrenocortical tumors may ex ist on chromosome 17 and that the number of genomic alterations is closely associated with tumor behavior in adrenocortical tumors.