How should we manage the (personal) data we collect and process as researchers? Research Data Management & Ethics workshop

Over the last three decades, the development of information and communication technologies has increased the number of ways in which (personal) data can be collected, stored, processed and shared. In this context, various regulations - including the famous European GDPR - have emerged to regulate the processing of personal data. Scientific research is no exception, and new rules are now being imposed. While the initial determination to ensure that researchers comply with these new standards was relatively timid, a new impetus is now emerging, particularly through the main funding bodies - Belgian and European - which are now imposing increasingly strict rules on ethics and data protection. When is data considered "personal"? What is the difference between pseudonymised, anonymous and encrypted data? What can easily be put in place at the different stages of research to limit ethical and data protection issues? How to navigate these sometimes confusing and/or technical legal obligations? Certain practices put in place at the earliest stages of research often make it possible to limit the constraints (and unpleasant surprises) later on. During this workshop we will explore these issues together and try to identify the main challenges we face in the course of our research. So don't hesitate to come with your own questions. Together we will try to get a clearer picture so that these 'new' obligations are not just seen as an additional constraint, but also as an opportunity to strengthen the quality of our research and the bond of trust that binds us to our fieldwork and, more broadly, to society

Decreased PCSK9 expression in human hepatocellular carcinoma

BACKGROUND: The management of hepatocellular carcinoma (HCC) is limited by the lack of adequate screening biomarkers and chemotherapy. In response, there has been much interest in tumor metabolism as a therapeutic target. PCSK9 stimulates internalization of the LDL-receptor, decreases cholesterol uptake into hepatocytes and affects liver regeneration. Thus, we investigated whether PCSK9 expression is altered in HCC, influencing its ability to harness cholesterol metabolism. METHODS: Thirty-nine patients undergoing partial hepatectomy or liver transplantation for HCC were consented for use of HCC tissue to construct a tissue microarray (TMA). The TMA was immunostained for PCSK9. Imagescope software was used to objectively determine staining, and assess for pathological and clinical correlations. PCSK9 and LDL receptor mRNA levels in flash-frozen HCC and adjacent liver tissue were determined by quantitative RT-PCR. Serum PCSK9 levels were determined by ELISA. RESULTS: By immunohistochemistry, there was significantly lower expression of PCSK9 in HCC as compared to adjacent cirrhosis (p-value < 0.0001, wilcoxon signed-rank test). Significantly greater staining of PCSK9 was present in cirrhosis compared to HCC (p value <0.0001), and positivity (percentage of positive cells) was significantly greater in cirrhosis compared to HCC (p-value < 0.0001). Conversely, significantly higher expression of LDL-R was present in HCC as compared to the adjacent cirrhosis (p-value < 0.0001). There was no significant correlation of PCSK9 staining with grade of tumor, but there were significant correlations between PCSK9 staining and stage of fibrosis, according to spearman correlation test. PCSK9 mRNA levels were relatively less abundant within HCC compared to adjacent liver tissue (p-value =0.08) and normal control tissue (p-value =0.02). In contrast, serum PCSK9 levels were significantly increased among patients with HCC compared to those with chronic liver disease without HCC (p-value =0.029). LDL receptor mRNA was consistantly greater in HCC when compared to normal control tissue (p-value = 0.06) and, in general, was significantly greater in HCC when compared to adjacent liver (p-value = 0.04). CONCLUSIONS: The decreased expression of PCSK9 and conversely increased LDL-R expression in HCC suggests that HCC modulates its local microenvironment to enable a constant energy supply. Larger-scale studies should be conducted to determine whether PCSK9 could be a therapeutic target for HCC