Abstract
BackgroundAccording to the scientific literature, less than 30 borderline ovarian tumors have been karyotyped and less than 100 analyzed for genomic imbalances by CGH.MethodsWe report a series of borderline ovarian tumors (n = 23) analyzed by G-banding and karyotyping as well as high resolution CGH; in addition, the tumors were analyzed for microsatellite stability status and by FISH for possible 6q deletion.ResultsAll informative tumors were microsatellite stable and none had a deletion in 6q27. All cases with an abnormal karyotype had simple chromosomal aberrations with +7 and +12 as the most common. In three tumors with single structural rearrangements, a common breakpoint in 3q13 was detected. The major copy number changes detected in the borderline tumors were gains from chromosome arms 2q, 6q, 8q, 9p, and 13q and losses from 1p, 12q, 14q, 15q, 16p, 17p, 17q, 19p, 19q, and 22q. The series included five pairs of bilateral tumors and, in two of these pairs, informative data were obtained as to their clonal relationship. In both pairs, similarities were found between the tumors from the right and left side, strongly indicating that bilaterality had occurred via a metastatic process. The bilateral tumors as a group showed more aberrations than did the unilateral ones, consistent with the view that bilaterality is a sign of more advanced disease.ConclusionBecause some of the imbalances found in borderline ovarian tumors seem to be similar to imbalances already known from the more extensively studied overt ovarian carcinomas, we speculate that the subset of borderline tumors with detectable imbalances or karyotypic aberrations may contain a smaller subset of tumors with a tendency to develop a more malignant phenotype. The group of borderline tumors with no imbalances would, in this line of thinking, have less or no propensity for clonal evolution and development to full-blown carcinomas.
Highlights
Borderline ovarian tumors are of low malignant potential
A comparison of the cytogenetic abnormalities occurring in ovarian carcinomas and tumors of borderline malignancy could provide insights into their pathogenetic relationship, little information is available on the karyotypic patterns of the latter tumors
The major copy number changes detected in the borderline tumors were gains from chromosome arms 2q, 6q, 8q, 9p, and 13q and losses from 1p, 12q, 14q, 15q, 16p, 17p, 17q, 19p, 19q, and 22q (Fig. 2)
Summary
Borderline ovarian tumors are of low malignant potential. They exhibit more atypical epithelial proliferation than is seen in adenomas, their benign counterpart, but are without the destructive stromal invasion characteristic of overt adenocarcinomas [1]. A comparison of the cytogenetic abnormalities occurring in ovarian carcinomas and tumors of borderline malignancy could provide insights into their pathogenetic relationship, little information is available on the karyotypic patterns of the latter tumors. Whereas chromosomal abnormalities have been reported in over 400 ovarian carcinomas [3], the corresponding cytogenetic information on borderline tumors is limited to only 27 cases [4,5,6,7,8,9,10,11]. According to the scientific literature, less than 30 borderline ovarian tumors have been karyotyped and less than 100 analyzed for genomic imbalances by CGH
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