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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.

Patients diagnosed with molar pregnancy are treated by either suction curettage or hysterectomy, depending on their desire to preserve fertility. We use single-agent chemotherapy, preferably methotrexate, to treat low- or moderate-risk persistent trophoblastic tumors. High-risk patients who have metastatic disease are treated primarily with combination chemotherapy and, as indicated, adjuvant radiotherapy or surgery. We perform a hysterectomy in all cases of placental-site trophoblastic tumors; combination chemotherapy is used if there is evidence of metastatic disease. [ABSTRACT FROM AUTHOR]

Using RNA fingerprinting (RAP) strategy and Northern blot analysis, we identified a differentially expressed sequence DOC-2 which is detectable in all normal human ovarian surface epithelial (HOSE) cell cultures but not in ovarian cancer cell lines and tissues. Subsequent cloning of DOC-2 from a cDNA library generated from the HOSE cells was carried out using the 3′ and 5′ RACE approach. A 3268 base pair full length cDNA of DOC-2 was isolated and sequenced. The predicted protein has a length of 770 amino acids. Homology search of all NCBI sequences indicated that the amino acid sequence of DOC-2 shares 93% homology with the mouse p96/mDab2 phosphoprotein and has a phosphotyrosine interacting domain (PID) and multiple SH3 binding motifs. Chromosomal localization by FISH showed that the DOC-2 gene is located on 5p13. Western blot analysis showed that the 105 kDa DOC-2 protein was down-regulated in all the carcinoma cell lines. In-situ immunohistochemistry performed on normal ovaries, and benign, borderline and invasive ovarian tumor tissues showed down regulation of DOC-2 protein particularly in serous ovarian tumor tissues. When DOC-2 was transfected into the ovarian carcinoma cell line SKOV3, the stable transfectants showed significantly reduced growth rate and ability to form tumors in nude mice. These data suggest that down-regulation of DOC-2 may play an important role in ovarian carcinogenesis. [ABSTRACT FROM AUTHOR]

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]

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]