1. ¹Departments of Pathology and Medical Genetics, Haartman Institute and Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland
2. ²Department of Pathology, Haartman Institute, University of Helsinki, Helsinki, Finland
3. ³Department of Epidemiology and Biostatistics, Finnish Institute of Occupational Health, Helsinki, Finland
4. ⁴Department of Internal Medicine, Division of Pulmonary Medicine, Helsinki University Central Hospital, Helsinki, Finland

Correspondence: Sakari Knuutila, Ph.D., Department of Medical Genetics, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland. fax: 358-9-19126788; e-mail: sakari.knuutila@helsinki.fi.

Accepted 20 December 2001.

Abstract

We performed a comparative genomic hybridization study on 25 lung adenocarcinoma samples from younger patients (<41 y of age) and compared the results with a previous comparative genomic hybridization analysis of lung adenocarcinoma samples from older patients (50–81 y of age). Twenty of the 25 tumor samples from younger patients had DNA copy number changes. Gains, losses, and high-level amplifications were seen more frequently in the specimens from the younger group. The most striking difference between the two groups was the high frequency of gains and/or high-level amplifications in the long arm of chromosome 20 in the samples from the younger patients (14/25, 56%) compared with that in the samples from the older patients (2/24, 8%, P < .001). Gains in the long arm of chromosome 22 and of the chromosomal band 11q13 were also detected significantly more often in the younger group. No correlation was found between DNA copy number changes and clinical parameters. Our results suggest that amplification of genes in the long arm of chromosome 20 may be important in the tumorigenesis of lung adenocarcinoma in young adults. Several candidate genes have already been described in the long arm of chromosome 20, particularly in breast cancer.