PurposeTo evaluate the association between cigarette smoking and glaucoma in the United States population.Patients and methodsUS civilian, non-institutionalized population from 2005 to 2008 administrations of the National Health and Nutrition Examination Survey that were ≥40 years of age with visual fields and optic disc photographs were included. Diagnosis of glaucoma was based on the Rotterdam criteria. Logistic regression modeling was performed to assess the association between glaucoma and smoking history, while controlling for age, gender, ethnicity, household income, alcohol consumption, diabetes, and hypertension.ResultsIn 3864 participants, 212 (5.5%) had glaucoma (corresponds to a population weighted glaucoma prevalence of 3.7% in a total of 83 570 127 subjects). Population weighted proportion of current smokers was 20.6% and ex-smokers was 28.3%. Participants with glaucoma were older (63.0±11.6 vs 56.1±11.2, P=0.002), likely to be male (57.1% vs 49.2%, P=0.03), to be Black (36.3% vs 20.7%, P<0.001), and to have diabetes (18.9% vs 12.4%, P=0.006) and hypertension (50.5% vs 39.7%, P=0.003). Current smokers had a lower odds of glaucoma compared to non-smokers (OR=0.61, 95% CI=0.41-0.88, P=0.009), and ex-smokers (OR=0.46, 95% CI=0.28-0.76, P=0.002). The effect estimates were similar in adjusted models, but not statistically significant. Among smokers, greater pack/day of smoking history was associated with statistically significantly higher odds of glaucoma (OR=1.70, 95% CI=1.08-2.67, P=0.02).ConclusionsAmong cigarette smokers, heavy smoking defined by greater number of pack of cigarettes smoked per day is associated with higher odds of glaucoma. Health care providers should include this association when counseling patients on their smoking habit.

Little is known about the role of epithelial membrane protein-2 (EMP2) in breast cancer development or progression. In this study, we tested the hypothesis that EMP2 may regulate the formation or self-renewal of breast cancer stem cells (BCSC) in the tumor microenvironment. In silico analysis of gene expression data demonstrated a correlation of EMP2 expression with known metastasis related genes and markers of cancer stem cells (CSC) including aldehyde dehydrogenase (ALDH). In breast cancer cell lines, EMP2 overexpression increased and EMP2 knockdown decreased the proportion of stem-like cells as assessed by the expression of the CSC *

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PurposePathologic corneal neovascularization is a major cause of blindness worldwide, and treatment options are currently limited. VEGF is one of the critical mediators of corneal neovascularization but current anti-VEGF therapies have produced limited results in the cornea. Thus, additional therapeutic agents are needed to enhance the antiangiogenic arsenal. Our group previously demonstrated epithelial membrane protein-2 (EMP2) involvement in pathologic angiogenesis in multiple cancer models including breast cancer and glioblastoma. In this paper, we investigate the efficacy of anti-EMP2 immunotherapy in the prevention of corneal neovascularization.MethodsAn in vivo murine cornea alkali burn model was used to study pathologic neovascularization. A unilateral corneal burn was induced using NaOH, and subconjunctival injection of either anti-EMP2 antibody, control antibody, or sterile saline was performed after corneal burn. Neovascularization was clinically scored at 7 days postalkali burn, and eyes were enucleated for histologic analysis and immunostaining including VEGF, CD31, and CD34 expression.ResultsAnti-EMP2 antibody, compared to control antibody or vehicle, significantly reduced neovascularization as measured by clinical score and central cornea thickness, as well as by histologic reduction of neovascularization, decreased CD34 staining, and decreased CD31 staining. Incubation of corneal limbal cells in vitro with anti-EMP2 blocking antibody significantly decreased EMP2 expression, VEGF expression and secretion, and cell migration.ConclusionsThis work demonstrates the effectiveness of EMP2 as a novel target in pathologic corneal neovascularization in an animal model and supports additional investigation into EMP2 antibody blockade as a potential new therapeutic option.