Abstract
Abstract The molecular basis for gynecologic tumor dissemination into the peritoneum is not well understood, however it is the primary mechanism of death in advanced stage ovarian cancers. Although serous borderline and serous invasive ovarian cancers are similar, they differ in their ability to implant and invade peritoneal structures. Vascular cell adhesion molecule-1 (VCAM-1), a cell surface receptor expressed on activated endothelial and mesothelial cells, regulates leukocyte attachment and extravasation at sites of inflammation. Recent studies by our group demonstrated the ability of ovarian carcinoma to induce the expression of VCAM-1 on mesothelial cells, and correlated the presence of VCAM-1 with peritoneal dissemination of the tumor. We undertook the current study to determine whether VCAM-1 is expressed on the mesothelium of patients with borderline ovarian tumors. After IRB approval was obtained, cell blocks containing peritoneum and omentum from 10 patients with borderline tumors were processed and stained using antibodies to VCAM-1. Mesothelial expression of VCAM-1 was determined by a single pathologist blinded to tumor type and stage. Samples were determined to be positive if mesothelial cells demonstrated membrane staining. Cytoplasmic staining for VCAM-1 was not considered positive, nor was staining of non-mesothelial cells. Of the 10 patients, four were stage 1a and six were stage 1c serous borderline tumors. Nine of 10 had peritoneal or omental biopsies that did not stain for VCAM-1. The one sample which did stain positively was micropapillary type, which is an invasive sub-type of borderline ovarian cancers. Together, these observations support the hypothesis that VCAM-1 expression correlates with ovarian cancer peritoneal invasion and offers a possible explanation for the inability of borderline tumors to invade peritoneal structures. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 845.
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