Based on these findings, the FISH assays were highly accurate, with immunohistochemical assays performed with R60 and 10H8 nearly as accurate. The DAKO HercepTest and the Ventana CB11 immunohistochemical assay were statistically significantly different from the Vysis FISH assay in evaluating these previously molecularly characterized breast cancer specimens.

BackgroundDespite universal population coverage and equity being a stated policy goal of its NHIS, over a decade since passage of the first law in 2003, Ghana continues to struggle with how to attain it. The predominantly (about 70 %) tax funded NHIS currently has active enrolment hovering around 40 % of the population. This study explored in-depth enablers and barriers to enrolment in the NHIS to provide lessons and insights for Ghana and other low and middle income countries (LMIC) into attaining the goal of universality in Universal Health Coverage (UHC).MethodsWe conducted a cross sectional mixed methods study of an urban and a rural district in one region of Southern Ghana. Data came from document review, analysis of routine data on enrolment, key informant in-depth interviews with local government, regional and district insurance scheme and provider staff and community member in-depth interviews and focus group discussions.ResultsPopulation coverage in the NHIS in the study districts was not growing towards near universal because of failure of many of those who had ever enrolled to regularly renew annually as required by the NHIS policy. Factors facilitating and enabling enrolment were driven by the design details of the scheme that emanate from national level policy and program formulation, frontline purchaser and provider staff implementation arrangements and contextual factors. The factors inter-related and worked together to affect client experience of the scheme, which were not always the same as the declared policy intent. This then also affected the decision to enrol and stay enrolled.ConclusionsUHC policy and program design needs to be such that enrolment is effectively compulsory in practice. It also requires careful attention and responsiveness to actual and potential subscriber, purchaser and provider (stakeholder) incentives and related behaviour generated at implementation levels.Electronic supplementary materialThe online version of this article (doi:10.1186/s12913-016-1758-y) contains supplementary material, which is available to authorized users.

Our data demonstrate that hypertension is by far the most important contributor to stroke mortality in Shanghai and that among dietary factors, only alcohol consumption shows any evidence whatsoever of being a risk factor.

BackgroundPancreatic cancer (PC) hijacks innate cellular processes to promote cancer growth. We hypothesized that PC exploits PD-1/PD-L1 not only to avoid immune responses, but to directly enhance growth. We also hypothesized that immune checkpoint inhibitors (ICIs) have direct cytotoxicity in PC. We sought to elucidate therapeutic targeting of PD-1/PD-L1.MethodsPD-1 was assessed in PC cells, patient-derived organoids (PDOs), and clinical tissues. Then, PC cells were exposed to PD-L1 to evaluate proliferation. To test PD-1/PD-L1 signaling, cells were exposed to PD-L1 and MAPK was examined. Radio-immunoconjugates with anti-PD-1 drugs were developed to test uptake in patient-derived tumor xenografts (PDTXs). Next, PD-1 function was assessed by xenografting PD-1-knockdown cells. Finally, PC models were exposed to ICIs.ResultsPD-1 expression was demonstrated in PCs. PD-L1 exposure increased proliferation and activated MAPK. Imaging PDTXs revealed uptake of radio-immunoconjugates. PD-1 knockdown in vivo revealed 67% smaller volumes than controls. Finally, ICI treatment of both PDOs/PDTXs demonstrated cytotoxicity and anti-MEK1/2 combined with anti-PD-1 drugs produced highest cytotoxicity in PDOs/PDTXs.ConclusionsOur data reveal PCs innately express PD-1 and activate druggable oncogenic pathways supporting PDAC growth. Strategies directly targeting PC with novel ICI regimens may work with adaptive immune responses for optimal cytotoxicity.