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Objective To evaluate calcifications ⩾ 5 mm in length in ovaries that are otherwise normal on ultrasound, and to determine whether such large ovarian calcifications are an indicator of ovarian neoplasm. Methods This was a retrospective study reviewing pelvic ultrasound results at our unit between October 1994 and April 2002 to identify patients with ovarian calcifications that were ⩾ 5 mm in maximum length in otherwise normal ovaries, and who also had follow-up imaging studies. Patient medical histories were reviewed, calcification characteristics, including number, size, shape and laterality of calcifications, were recorded and follow-up imaging studies were reviewed to assess change in size of the calcification and to see if a neoplasm had developed. Results The study group consisted of 28 patients. The mean length of imaging follow-up was 35.2 ± 30.7 months. The mean size of the calcifications was 7.4 ± 2.3 (range, 5-13) mm. The calcification remained stable in all 28 patients and no ovarian neoplasms developed in any of the patients. Histological confirmation was available in one patient and this revealed dystrophic calcification in a corpus albicans. Conclusion Calcifications ranging from 5 to 13 mm in length in otherwise normal ovaries remain stable on follow-up imaging and are not an indicator of current or future ovarian neoplasm. [ABSTRACT FROM AUTHOR]

Ovarian cancer survival rates have stagnated in the last 20 years despite the development of novel chemotherapeutic agents. Modulators of gene expression, such as histone deacetylase (HDAC) inhibitors, are among the new agents being used in clinical trials. Predictors of sensitivity to chemotherapy have remained elusive. In this study, we show that the expression of the transcriptional corepressor C-terminal binding protein-2 (CtBP2) is elevated in human ovarian tumors. Downregulation of CtBP2 expression in ovarian cancer cell lines using short-hairpin RNA strategy suppressed the growth rate and migration of the resultant cancer cells. The knockdown cell lines also showed upregulation of HDAC activity and increased sensitivity to selected HDAC inhibitors. Conversely, forced expression of wild-type CtBP2 in the knockdown cell lines reversed HDAC activity and partially rescued cellular sensitivity to the HDAC inhibitors. We propose that CtBP2 is an ovarian cancer oncogene that regulates gene expression program by modulating HDAC activity. CtBP2 expression may be a surrogate indicator of cellular sensitivity to HDAC inhibitors. [ABSTRACT FROM AUTHOR]

The article comments on a study which screened the entire transcriptome of mucinous ovarian tumors and compared them to other ovarian cancers in order to discover genes and metabolic pathways responsible for the clinical characteristics of the disease conducted by F. W. Wamunyokoli et al. It cites that ovarian cancer is considered as one of the neoplasms with the worst prognosis due to delayed diagnosis. It notes that tumors in ovaries can show up as borderline disease with metastatic potential.

We have used polymerase chain reaction (PCR) amplification of tandem repeats to study the pattern of allelic loss on chromosome X11.2-q12 in borderline and invasive epithelial ovarian tumors. Using eight microsatellite markers spanning Xq11.2-q12, 41 borderline and 65 invasive ovarian tumors, together with their corresponding normal tissues, were analysed. The highest percentage of loss of heterozygosity (LOH) was observed at the DXS1194 locus in borderline tumors (four of 16 informative cases, 25%) and at the androgen receptor (AR) locus in invasive epithelial ovarian tumors (18 of 47 informative cases, 38%). X chromosome activation studies performed in cases with LOH at the AR locus showed that the allelic loss at the AR locus is not confined to the inactive allele. A one centimorgan region including the AR locus and flanked by the primers DXS1161 and PGK1P1 was identified as the smallest common loss region in both borderline and invasive epithelial ovarian tumors. [ABSTRACT FROM AUTHOR]

We have used polymerase chain reaction (PCR) amplification of tandem repeats to study the pattern of allelic loss on chromosome 7q31 in invasive epithelial ovarian carcinomas and borderline ovarian tumors. Using 13 primer sets spanning loci from 7q31 to 7q32, 16 borderline and 54 invasive ovarian tumor tissue, together with their corresponding normal tissue, were analysed. Invasive epithelial ovarian tumors demonstrated loss of heterozygosity (LOH) at one or more loci on 7q in 32 of 54 cases (59%). The invasive epithelial ovarian tumors demonstrated the highest percentage of LOH at the loci D7S643 (20 of 40 informative cases, 50%) and GATA44F09 (18 of 42 informative cases, 43%). In contrary, only one borderline ovarian tumor showed LOH at one locus (GATA44F09, one of 14 informative cases, 7%). Our results display a sharp contrast in the pattern of LOH between invasive and borderline ovarian tumors suggesting that allelic loss at chromosome 7q31.3 may be involved in the development and progression of invasive epithelial ovarian tumors but not borderline ovarian tumors. Further analysis of the deletion map for the invasive epithelial ovarian tumors showed two regions likely to harbor ovarian tumor suppressor genes including a novel 1300 kilobase common loss region flanked by GATA44F09 and D7S643. [ABSTRACT FROM AUTHOR]

In a case-control study, consumption of dairy foods by 235 white women with epithelial ovarian cancer and by 239 control women, and activity of red blood cell galactose-1-phosphate uridyl transferase (transferase) in a subset of 145 cases and 127 controls were determined. Yogurt was consumed at least monthly by 49% of cases and 36% of controls. The mean transferase activity of cases was significantly lower than that of controls. When a ratio of lactose consumption to transferase (L/T) was calculated, cases had a mean L/T of 1.17 compared with 0.98 for controls; there was a highly significant trend for increasing ovarian cancer risk with increasing L/T ratio. Lactose consumption may be a dietary risk factor and transferase a genetic risk factor for ovarian cancer. [ABSTRACT FROM AUTHOR]

Background: Papillary serous carcinoma of the peritoneum (PSCP) diffusely involves peritoneal surfaces, while it spares or only superficially involves the ovaries. PSCP is histologically indistinguishable from serous epithelial ovarian carcinoma, and it may develop years after oophorectomy. The molecular pathogenesis of PSCP remains unresolved, although preliminary data suggest a multifocal origin in some cases. Patients with germline BRCA1 mutations may develop PSCP in addition to breast and ovarian carcinomas. The purpose of this study was to utilize the androgen receptor (AR) gene locus to test the hypothesis that some cases of PSCP have a multifocal origin and to determine if patients with germline BRCA1 mutations develop multifocal PSCP.Methods: Specimens of normal and tumor tissues from 22 women with PSCP were obtained, and DNA was extracted. The AR gene locus was evaluated for patterns of loss of heterozygosity (LOH) and X-chromosome inactivation. The methylation-sensitive Hpa II restriction enzyme was used to differentiate the active and inactive X chromosomes. Germline BRCA1 mutation status of the patients was determined previously.Results: Genetic analysis of tumor specimens indicated that five (23%) of 22 case subjects had patterns of selective LOH at the AR locus, consistent with multifocal, polyclonal disease origin. Two patients with selective LOH also had alternating X-chromosome inactivation patterns. Patients with germline BRCA1 mutations were more likely to have evidence of multifocal disease (two-sided Fisher's exact test, P = .01).Conclusions: Our results show that PSCP has a multifocal origin in at least some cases. Furthermore, patients with germline BRCA1 mutations are more likely to develop multifocal PSCP than are patients without BRCA1 mutations. [ABSTRACT FROM AUTHOR]