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Open Access Research article

Genomic profile of ovarian carcinomas

Francesca Micci12*, Lisbeth Haugom12, Vera M Abeler3, Ben Davidson34, Claes G Tropé5 and Sverre Heim124

Author Affiliations

1 Section for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, The Norwegian Radium Hospital, Oslo University Hospital, 0310 Oslo, Norway

2 Centre for Cancer Biomedicine, University of Oslo, Oslo, Norway

3 Department of Pathology, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway

4 Faculty of Medicine, University of Oslo, Oslo, Norway

5 Department of Gynecology, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway

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BMC Cancer 2014, 14:315  doi:10.1186/1471-2407-14-315

Published: 5 May 2014

Abstract

Background

It is known that all tumors studied in sufficient number to draw conclusions show characteristic/specific chromosomal rearrangements, and the identification of these chromosomes and the genes rearranged behind the aberrations may ultimately lead to a tailor-made therapy for each cancer patient. Knowledge about the acquired genomic aberrations of ovarian carcinomas is still unsatisfactory.

Methods

We cytogenetically analyzed 110 new cases of ovarian carcinoma of different histological subtypes using karyotyping of G-banded chromosomes and high-resolution comparative genomic hybridization. We first compared the aberration patterns identified by the two genomic screening techniques using the so-called “classical” pathological classification in which the carcinomas are grouped as tumors of types I and II. We also broke down our findings according to the more “modern” classification which groups the carcinomas in five different categories.

Results

The chromosomal breakpoints identified by karyotyping tended to cluster to 19p/q and to 11q, but no unquestionably recurrent rearrangement could be seen. Common imbalances were scored as gains from 1q, 3q, 7q, and 8q and losses from 17p, 19q, and 22q. Gain of material from 8q23 and losses from 19q and 22q have previously been described at high frequencies in bilateral and borderline ovarian carcinomas. The fact that they were present both in “precursor” lesions, i.e., borderline tumors, as well as in tumors of more advanced stages, i.e., carcinomas, highlights the possibility of an adenoma-carcinoma sequence in ovarian carcinogenesis.

Conclusion

Based on the relatively simple genomic changes we identified in the low-grade serous carcinomas examined (n = 7) and which largely corresponded to the aberration pattern formerly identified in borderline tumors, one can interpret the cytogenetic data as supporting the view that the low-grade carcinomas represent a phenotypically more advanced stage of borderline tumors. Whether transition from low-grade to high-grade carcinoma also occurs, is a question about which the genomic data is still inconclusive.

Keywords:
Ovarian carcinoma; Karyotyping; HR-CGH