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Objectives. Our aim is evaluating the need for repeating tests for syphilis on pregnant women in the third trimester. Study design. A single-center retrospective cohort study was performed on all women delivering7/03–6/04. Results. During the study interval, 2244 women delivered at our hospital. Of those women having available records and attending at least one prenatal visit, 1940(98.9%)were screened for syphilis at the first prenatal visit. Of the 1627 women beginning prenatal care prior to 27 weeks and delivering after 32 weeks, 1377(84.6%)were rescreened in the third trimester. No cases of syphilis were identified with either the initial (upper limit of 95% CI0.24%) or repeat (upper limit of 95% CI0.34%) screening. Conclusions. In our obstetric population, syphilis is so uncommon that mandated prenatal screening on more than one occasion seems unjustified and laws requiring repeated screening should be reevaluated.

Objectives: Readmission after epithelial ovarian cancer (EOC) surgery consumes valuable healthcare resources and entails high physical and emotional demands. To facilitate early recognition of patients at risk for postoperative morbidities, we evaluated factors associated with 30-day readmission after EOC surgery. Methods: Patients who underwent primary debulking for EOC between 1/2/2003 and 12/29/2008 were evaluated. Follow-up duration was calculated from the date of dismissal after primary surgery to the date of first readmissionwithin 30 days. Cox regressionmodels were fit to take into account the timing of readmissions and those with b30 days of clinical follow-up. Demographic and perioperative clinical factors (preoperative, intraoperative and postoperative variables) were first assessed univariately for an association with 30-day readmission. A parsimonious multivariable model was identified using backwards and stepwise variable selection. Results: Of 538 eligible patients, 107 (19.9%) were readmitted within 30 days. In total, 324 (60.2%) were stage III and 91 (16.9%) were stage IV. Optimal debulking (≤1 cm residual disease) was achieved in 467 (86.8%) patients. The most common indications for readmission were dehydration/nausea and vomiting, surgical site infection, bowel complications, urinary tract infection, pleural effusion and thromboembolic events. Nine (8.4%) of readmitted patients required reoperation at the time of readmission. ASA score ≥3 was the only preoperative factor associated with 30-day readmission on univariate analysis, while intraoperative factors predictive of readmission included ascites, residual disease, estimated blood loss, and small bowel serosal involvement. Time to first postoperative flatus, postoperative complications, and length of initial hospital stay were suggestive of higher readmission rates on univariate analysis. Multivariate analysis identified ASA score ≥3 (HR 1.67 (95% CI 1.13–2.45), small bowel serosal involvement (1.51 (1.02–2.24)), and ascites (1.58 (1.04–2.41)) (p= 0.009, 0.04 and 0.03, respectively) to be independently associated with 30-day readmission (c-index= 0.617). Conclusions: Patients with severe underlying comorbidities (based on ASA score) are at risk for readmission and should be closely assessed prior to dismissal. Due to lack of clinical significance, all other perioperative factors are relatively poor predictors of the need for readmission after EOC surgery. Thus, 30-day readmissions after EOC surgery may be unavoidable.

Objective: Mullerian inhibiting substance type II receptor (MISRII) is a tissue-specific target for therapy in gynecologic cancers. MISRII plays a specialized role in regression of the mullerian tracts embryologically. Analogous to other TGF-β family members, ligand (MIS) binding to the type II receptor leads to a heteromeric complex with type I receptors, downstream Smad signaling, cell cycle arrest and regression. We previously published that the majority of epithelial ovarian cancers (EOC) and endometrial cancers (EC) express MISRII in a tissue specific manner. The purpose of these studies was to investigate the biologic significance of MISRII expression in EOC. Methods: For in vitro studies, we developed both chimeric and endogenous cell models to study MISRII. Chimeric MIS type I and II receptors were created by fusing the ligand binding domain of GM-CSF (α or β subunit) to the transmembrane and cytoplasmic domains of the type I/II receptor; these receptors were stably transfected into Ovcar8 cells. The chimera system allows specific signaling of the receptor complex and the ability to separately analyze candidate type I receptors. The endogenous cell model was created in SKOV3 (MISRII- EOC cell line) by stably expressing full-length MISRII. Growth inhibition was assessed by colony formation in soft agar in response to receptor activation and cisplatin. A BRE-luciferase reporter construct was used to measure Smad 1/5 activation after exposure to MIS. FACS analysis was used to assess cell cycle progression. Results: In the chimeric model, receptor activation resulted in up to 60% inhibition of colony formation (dependent on which candidate type I receptor was targeted). Additionally, receptor activation sensitized cells to the effects of cisplatin (1μM) with nearly 4-fold inhibition of colony formation. In the endogenous MISRII expressing EOC cell model, functional signaling was first confirmed using a BRE-luciferase reporter assay to document induction of Smad activation after exposure to rhMIS (3.2 relative light units increase after 20nM MIS). This model was then assessed for cell cycle progression in the presence of MIS. We observed a strong G1 arrest (62% vs. 43% untreated) after 15h exposure to 25nM MIS in cells expressing the receptor with no change in the MIS- parental cell line. These in vitro data are consistent with our survival results in EOC demonstrating a significantly improved overall survival (p=0.04) in MISRII expressing cancers. Conclusions: The majority of gynecologic cancers express MISRII. Our in vitro studies demonstrate that receptor activation results in cell cycle arrest, reduced colony formation, and sensitization to cisplatin. Confirming this in vitro data is the observation that EOC expressing MISRII have improved response to therapy and longer survival. Together, these results support further targeting of the MISRII pathway as an anticancer strategy in gynecologic malignancy. 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 1586.