Variation in gene expression patterns in effusions and primary tumors from serous ovarian cancer patients

We observed multidimensional variation in expression patterns among the cancers. Coordinate variation in expression of genes from two chromosomal regions, 8q and 19q, was seen in subsets of the cancers indicating possible amplifications in these regions. A set of 112 unique genes of known function was differentially expressed between primary tumors and effusions using supervised analysis. Relatively few differences were seen between effusions isolated from the pleural and peritoneal cavities or between effusions from patients diagnosed with stage III and stage IV cancers. A set of 84 unique genes was identified that distinguished high from lower grade ovarian cancers. The results were corroborated using immunocytochemistry, mRNA in situ hybridization, and immunoblotting.The extensive variation in expression patterns observed underscores the molecular heterogeneity of ovarian cancer, but suggests a similar molecular profile for ovarian carcinoma cells in serosal cavities.Epithelial ovarian carcinoma claims more lives than any other gynecologic malignancy, largely because it frequently escapes detection after it has metastasized [1]. Ovarian carcinoma initially metastasizes primarily to the serosal surface of the peritoneal cavity and abdominal organs. The pleural space is often involved as well, either at diagnosis or, more commonly, at later stages of clinical progression. Pleural effusion is the most common presentation of stage IV disease [2]. A number of metastasis-associated molecules have been reported to be differentially expressed between primary ovarian tumors and tumor cells in effusions [3-12], but little is known regarding the mechanism of metastases.Molecular characterization of ovarian carcinoma using DNA microarrays has so far focused on primary tumors [13-22]. The paucity of data regarding the biological characteristics of ovarian carcinoma cells in effusions at both the phenotypic and genotypic level limits our understanding of tumor progression in t