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Genetic Changes in Inherited and Sporadic Ovarian Carcinomas by Comparative Genomic Hybridization: Extensive Similarity Except for a Difference at Chromosome 2q24–q32¹

Departments of Obstetrics and Gynecology [J. T., L. S., P. V., H. N., M. S., R. B.], Oncology [S. H.], and Pathology [R. B.], Helsinki University Central Hospital, 00290 Helsinki, and Department of Medical Genetics, Haartman Institute and Helsinki University Central Hospital, University of Helsinki, 00014, Helsinki [S. K.], Finland

Germ-line mutations in the BRCA1 and BRCA2 genes confer a predisposition to breast as well as ovarian carcinoma. Except for loss of the respective wild-type allele, somatic genetic changes needed for the progression of inherited ovarian tumors are unknown. A genome-wide search for such alterations was performed by comparative genomic hybridization analysis on BRCA1 and BRCA2 mutation-positive (n = 20) ovarian carcinoma specimens. Comparison with sporadic ovarian carcinomas (n = 20) revealed extensive genetic similarity between the inherited and sporadic carcinomas with the sole exception of a frequent gain of 2q24–q32 in the inherited group, suggesting the presence of an oncogene at 2q24–q32 operating in the absence of BRCA1 function. The overall similarity of gains and losses by comparative genomic hybridization suggests a common main pathway in tumor progression of both inherited and sporadic ovarian carcinomas.

¹ Supported by grants from the Helsinki University Central Hospital Research Fund and the Helsingin Sanomat Fund.

² To whom requests for reprints should be addressed, at Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Haartmaninkatu 2, 00290 Helsinki, Finland. Phone: 358-09-4714912; Fax: 358-09-4714801; E-mail: ralf.butzow@huch.fi.

Received 3/ 3/98. Accepted 5/15/98.

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