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

Am J Pathol. 1999 Oct;155(4):1039-45. doi: 10.1016/S0002-9440(10)65205-4.


Genetic changes underlying the tumorigenesis of sporadic adrenocortical tumors are poorly characterized. To search for characteristic genomic imbalances involved in adrenocortical tumors, we examined 41 adrenocortical lesions (12 carcinomas, 23 adenomas, and 6 hyperplasias) by comparative genomic hybridization. Our results show that genetic alterations are more frequent in malignant than in benign lesions and that they rarely occur in hyperplastic lesions. The most frequent DNA copy number changes in adrenocortical carcinomas included losses of 1p21-31, 2q, 3p, 3q, 6q, 9p, and 11q14-qter, as well as gains and amplifications of 5q12, 9q32-qter, 12q, and 20q. The genomic aberrations prevalently occurring in adrenocortical adenomas were gains of 17q, 17p, and 9q32-qter. Gains found in 2 of 6 adrenocortical hyperplastic lesions involved chromosome 17 or 17q only. These data indicate that oncogenes determining the early tumorigenesis of adrenocortical tumors may exist on chromosome 17 and that the number of genomic alterations is closely associated with tumor behavior in adrenocortical tumors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adrenal Cortex Neoplasms / genetics*
  • Adrenal Glands / pathology
  • Adrenocortical Adenoma / genetics*
  • Adrenocortical Carcinoma / genetics*
  • Adult
  • Aged
  • Aged, 80 and over
  • Cell Transformation, Neoplastic / genetics
  • Child
  • Chromosome Aberrations
  • Chromosomes, Human, Pair 17 / genetics*
  • Female
  • Gene Dosage
  • Humans
  • Hyperplasia / genetics
  • In Situ Hybridization, Fluorescence
  • Infant
  • Male
  • Middle Aged
  • Nucleic Acid Hybridization
  • Regression Analysis
  • Trisomy