A potential 157716-52-4 confounder in our study is that the patient group was not perfectly age-matched with the control group. Inflammation and metabolic changes could possibly be influenced by age. However, when analysing the microarray and qPCR data on agematched subgroups we found the same patterns of differential gene regulation. Another limitation of the study is that circulating inflammatory markers or biochemical parameters indicating insulin resistance were not available. This could have given additional information concerning the changes observed in this study. It CYT 11387 should also be noted that the control group consisted of patients operated for benign thyroid diseases. For ethical reasons these patients were the healthiest group possible to obtain as controls for our study. Our findings highlight potentially important non-skeletal effects of elevated PTH levels in patients with PHPT. In recent years the importance of increased cardiovascular risk factors in these patients has been discussed. Our study shows highly significant alterations in gene expression in adipose tissue of PHPT patients compared to controls in regards to inflammatory and metabolic processes. The data suggest an increase in monocyte/macrophage activation in the adipose tissue. Elevated PTH and calcium may directly mediate the alterations in adipose tissue gene expression, which may in turn promote the release of pathogenic factors. Our data shed new light on inflammatory and metabolic alterations in adipose tissue in patients with PHPT that are independent of BMI, and which may confer increased risk of CVD. Pancreatic adenocarcinoma is the fourth leading cause of cancer mortality in the United States and is characterized by early metastasis and resistance to conventional therapies . Overall prognosis for pancreatic cancer patients remains poor due largely to late diagnosis and our limited understanding of genetic and epigenetic factors contributing to disease progression and therapy resistance. In recent years, cancer stem cells , also referred to as tumor-initiating cells , have been implicated in tumor formation, progression, and therapy-resistance in multiple solidorgan cancers, including pancreatic adenocarcinoma . As such, identifying the molecular markers that best discern pancreatic TIC populations may provide opportunities to characterize critical molecular pathways involved in tumorigenesis for targeted therapies .