Evaluating the impact of social deprivation on Press Ganey® Outpatient Medical Practice Survey Scores.

BACKGROUND: Social deprivation has been shown to affect access to health care services, and influences outcomes for a variety of physical and psychological conditions. However, the impact on patient satisfaction remains less clear. The objective of this study was to determine if social deprivation is an independent predictor of patient satisfaction, as measured by the Press Ganey® Outpatient Medical Practice Survey (PGOMPS). METHODS: We retrospectively reviewed unique new adult patient (≥ 18 years of age) seen at a tertiary academic hospital and rural/urban outreach hospitals/clinics between January 2014 and December 2017. Satisfaction was defined a priori as achieving a score above the 33rd percentile. The 2015 Area Deprivation Index (ADI) was used to determine social deprivation (lower score signifies less social deprivation). Univariate and multivariable binary logistic regression were used to determine the impact of ADI on PGOMPS total and provider sub-scores while controlling for variables previously shown to impact scores (wait time, patient age, sex, race, specialty type, provider type, and insurance status). RESULTS: Univariate analysis of PGOMPS total scores revealed a 4% decrease in odds of patient satisfaction per decile increase in ADI (p < 0.001). Patients within the most deprived quartile were significantly less likely to report satisfaction compared to the least deprived quartile (OR 0.79, p < 0.001). Multivariable analysis revealed that the odds of achieving satisfaction decreased 2% for each decile increase in ADI on the Total Score (p < 0.001), independent of other variables previously shown to impact scores. For PGOMPS Provider Sub-Score, univariate analysis showed that patients in the lowest ADI quartile were significantly less likely be satisfied, as compared to the least deprived quartile (OR 0.77; 95% CI 0.70-0.86; p < 0.001). A 5% decrease in a patient being satisfied was observed for each decile increase in ADI (OR 0.95; 95% CI 0.94-0.96; p < 0.001). CONCLUSIONS: Social deprivation was an independent predictor of outpatient visit dissatisfaction, as measured by the Press Ganey® Outpatient Medical Practice Survey. These results necessitate consideration when developing health care delivery policies that serve to minimize inequalities between patients of differing socioeconomic groups.

Sarcoma-The standard-bearer in cancer discovery.

Sarcoma is a rare tumor type that occurs most frequently in connective tissue. Despite its uncommon occurrence, sarcoma research has provided the means for groundbreaking research that has advanced our understanding of general cancer mechanisms. It is through sarcoma research that the pioneering efforts of cancer immunotherapy were explored, that we understand the inherent genetic nature of cancer mutations, and that we appreciate the subclassification of general cancer types to make more accurate prognoses. This review explores the brief history of sarcoma research and what sarcomas can still teach us about the future of cancer research, especially in regard to novel immunotherapy targets, the role of epigenetics in disease progression and chemoresistance, and the benefits of more focused clinical trials.

Modeling synovial sarcoma metastasis in the mouse: PI3'-lipid signaling and inflammation.

Solid tumor metastasis is a complex biology, impinged upon by a variety of dysregulated signaling pathways. PI3'-lipid signaling has been associated with metastasis and inflammation in many cancers, but the relationship between tumor cell-intrinsic PI3'-lipid signaling and inflammatory cell recruitment has remained enigmatic. Elevated PI3'-lipid signaling associates with progression of synovial sarcoma, a deadly soft tissue malignancy initiated by a t(X;18) chromosomal translocation that generates an SS18-SSX fusion oncoprotein. Here, we show in genetically engineered mouse models of locally induced expression of SS18-SSX1 or SS18-SSX2 that Pten silencing dramatically accelerated and enhanced sarcomagenesis without compromising synovial sarcoma characteristics. PTEN deficiency increased tumor angiogenesis, promoted inflammatory gene expression, and enabled highly penetrant spontaneous pulmonary metastasis. PTEN-deficient sarcomas revealed infiltrating myeloid-derived hematopoietic cells, particularly macrophages and neutrophils, recruited via PI3'-lipid-induced CSF1 expression in tumor cells. Moreover, in a large panel of human synovial sarcomas, enhanced PI3'-lipid signaling also correlated with increased inflammatory cell recruitment and CSF1R signal transduction in both macrophages and endothelial cells. Thus, both in the mouse model and in human synovial sarcomas, PI3'-lipid signaling drives CSF1 expression and associates with increased infiltration of the monocyte/macrophage lineage as well as neutrophils.