Dimova Ivanka, Zaharieva Boriana, Raicheva Sashka, Milev Ivan, Dimitrov Rumen, Doganov Nicolai, Aleksandrov Marin, Todorov Todor, Toncheva Draga
Department of Medical Genetics, Faculty of Medicine, Medical University of Sofia, Bulgaria.
Acta Oncol. 2004;43(7):675-9. doi: 10.1080/02841860410018548.
Literature data on the occurrence of CCND1 alterations in ovarian tumors are insufficient. The objective of this study was to assess the incidence of CCND1 copy number changes in a large number of ovarian tumors and its relation to the tumor phenotype: degree of malignancy, histological type, tumor stage, and grade. Fluorescence in situ hybridization (FISH) for analysis of CCND1 copy number changes was applied on a collection of 1 006 ovarian tumors--468 malignant, 48 with low malignant potency, and 490 benign tumors--arranged in tissue microarray. CCND1 amplification was found in 8.46% of the malignant cases and in 8.11% of those with low malignant potency. It was not found in benign ovarian tumors. CCND1 amplification was associated with the mucinous type of ovarian cancer (p<0.0001). CCND1 genetic gain was revealed in 9.06% of the malignant tumors, in 2.70% of the tumors with low malignant potency, and in 4.87% of the benign ovarian tumors. CCND1 gains and amplifications were not associated with the tumor grade and stage. Our results suggest that CCND1 gains are early events in ovarian tumorogenesis.
