Context.-Lysophosphatidic acid (LPA) has been shown to stimulate proliferation of ovarian cancer cells and is present in the ascitic fluid of patients with ovarian cancer.Objectives.-To determine whether elevated levels of LPA are present in plasma from patients with ovarian cancer and other gynecologic malignancies compared with healthy controls and to evaluate whether an elevated LPA plasma level may be a biomarker for these diseases.Design.-A research assay was used to measure total LPA levels in plasma from healthy women and women with different diseases. All LPA assays and comparison of LPA levels and CA125 (an ovarian cancer biomarker) levels were performed by observers blinded to patient status or group.Setting.-The Cleveland Clinic Foundation.Participants.-A convenience sample of 48 healthy control women, 48 women with ovarian cancer, 36 women with other gynecologic cancers, 17 women with benign gynecologic diseases, 11 women with breast cancer, and 5 women with leukemias.Main Outcome Measures.-Total LPA levels in plasma samples from patients and controls.Results.-Patients in the ovarian cancer group had significantly higher plasma LPA levels (mean, 8.6 µmol/L; range, 1.0-43.1 µmol/L) compared with the healthy control group (mean, 0.6 µmol/L; range, Ͻ0.1-6.3 µmol/L) (PϽ.001). Elevated plasma LPA levels were detected in 9 of 10 patients with stage I ovarian cancer, 24 of 24 patients with stage II, III, and IV ovarian cancer, and 14 of 14 patients with recurrent ovarian cancer. Of 36 patients with other gynecologic cancers, 33 also showed higher LPA levels (mean, 14.9 µmol/L; range, Ͻ0.1-63.2 µmol/L), compared with healthy controls (PϽ.001). Elevated plasma LPA levels were detected in 5 of 48 controls and 4 of 17 patients with benign gynecologic diseases and in no women with breast cancer or leukemia. In comparison, among a subset of patients with ovarian cancer, 28 of 47 had elevated CA125 levels, including 2 of 9 patients with stage I disease.Conclusions.-Plasma LPA levels may represent a potential biomarker for ovarian cancer and other gynecologic cancers. However, these findings are preliminary and require confirmation in larger studies.

PURPOSE: Despite decades of effort, burnout among physicians remains elevated compared with that of other working populations, and it yields catastrophic consequences, including medical errors and physician suicide. Burnout leaves oncologists feeling like they are alone, but this is not the case—it affects everyone. To effectively address burnout, it is not enough to look only at oncologists; instead, we must include all those involved in the delivery of cancer care. With this aim, we present an overview of the organizational science strategies and initial evidence for the value of a comprehensive, team-focused approach to addressing oncology provider burnout. METHODS: We describe the development of a team-focused burnout intervention approach, implemented for oncology providers, which focuses on the importance of encouraging communication and psychological safety to reduce feelings of isolation and fragmentation. We discuss the initial findings from 1 such team-based initiative currently underway within an academic medical center, presenting data from 409 cancer care providers embedded in 30 oncology units participating in this intervention approach. RESULTS: Preliminary results demonstrate that units that integrated a team-focused intervention for burnout reported significantly higher levels of teamwork and lower levels of burnout. We also describe lessons learned and recommendations for implementing this type of intervention on the basis of best practices from organizational science. CONCLUSION: This approach can positively affect the delivery of cancer care, interprofessional relationships among oncology staff, and the well-being of both patients and providers. Treating physician burnout alone will treat 1 symptom of the overall issue of burnout in oncology. As burnout pulls oncology clinicians apart, our solution must be to bring them together.

To assess the efficacy of low dose praziquantel regimens in comparison with standard 40 mg/kg dosing in the treatment of urinary schistosomiasis, a random allocation dose-finding trial was performed in children and adults from a Schistosoma haematobium endemic region in Coast Province, Kenya. Following an initial screening, 280 individuals with greater than or equal to 50 eggs/10 ml urine were randomly assigned to receive either 10, 20, 30, or 40 mg/kg of the drug in a single oral dose. Two to three months later, cure rates of 26%, 68%, 78%, and 84% were found for the 10, 20, 30, and 40 mg/kg doses, respectively. The results of 10 mg/kg oral dosing were significantly worse than for all other doses in terms of cure rate and of post-treatment prevalence of morbidity. The 40 mg/kg dosing resulted in a significantly higher cure rate than the 20 mg/kg doses; nevertheless, there was no significant difference between 20 mg/kg and 40 mg/kg doses in terms of mean post-treatment intensity of infection or post-treatment prevalence of hematuria or proteinuria. For large-scale control programs, oral 20 mg/kg praziquantel therapy for urinary schistosomiasis may prove as effective as the standard oral 40 mg/kg dosing for control of infection-associated morbidity and reduction of parasite transmission.

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Proliferation of acute myeloblastic leukemia (AML) cells in vitro is limited in most cases to a small subset of blasts that have several properties of stem cells. These leukemic colony-forming cells (AML-CFU) generally require addition of exogenous growth factors for proliferation in agar or methylcellulose. These factors can be supplied by media conditioned by phytohemagglutinin-stimulated normal leukocytes or by CSF-secreting tumor cell lines. However, the exact factor or factors required for stimulation of AML-CFU growth have not been defined. We compared the AML-CFU stimulatory activity of a human recombinant GM-CSF with that of GCT-CM, Mo-CM, and the PHA-leukocyte feeder system in 15 cases of AML. In each of the 12 cases that required exogenous growth factors for maximum AML-CFU growth, recombinant GM-CSF could replace either GM-CSF or Mo-CM, and could partially replace the PHA-leukocyte feeder system. These results indicate that this GM-CSF is a growth promoter of AML-CFU in these culture systems.