Studies have demonstrated a similar biodistribution pattern for 131I and 188Re in mice, with the exception of the thyroid gland, in which only 131I is retained by organification. In fact, the absence of organification of 188Re by the thyroid gland may also be considered an advantage for therapy of nonthyroidal hNIS-bearing tissues, in that the thyroid will not serve as a sink for radiopharmaceuticals and will sustain less radiation damage, and more 188Re can be uptaken by U87-hNIS cells due to 188Re recirculation. Considering that in our current study a stably hNIS transfected cell line was used with maximum hNIS expression SF 11 levels, which is not directly applicable for clinical use in humans, the efficacy of 188Re needs to be evaluated further in future studies after systemic in vivo hNIS gene transfer with the typical limited transduction efficiency and a more heterogeneous hNIS expression pattern. Provided that these studies confirm our findings, 188Re may serve as an attractive alternative to 131I, particular in tumors with short iodide retention time. Due to aggressive growth and a high metastatic rate during the early stage, pancreatic cancer remains a highly lethal malignant Sivelestat sodium salt disease, and only approximately 10�C20% of pancreatic cancer is resectable at the time of diagnosis. Gemcitabine has been the standard treatment for advanced pancreatic cancer; however, the median survival is 5�C6 months, with the frequent development of chemo-resistance during the treatment. Thus, pancreatic cancer remains a dreadful disease, and there is an urgent need of further studies to reveal the molecular mechanisms of tumor invasion and metastasis to develop an effective therapeutic approach to prevent and/or treat of pancreatic cancer. Cancer associated fibroblasts, predominant components of the tumor stroma, have been extracted from several invasive human carcinomas, including pancreatic cancer. Pancreatic ductal adenocarcinoma is characterized by an extensive stromal response called desmoplasia. Within the tumor stroma, CAFs are the primary cell type, which play an important role in tumor progression. CAFs secrete multiple factors, including CXC, CC chemokines, and other inflammatory mediators, that promote the proliferation, invasion, and metastasis of cancer cells. Moreover, accumulating evidence has demonstrated that CAFs play a key role in the acquisition of drug resistance in tumor therapy, which negatively impacts clinical outcomes.