The autophagic tumor stroma model of cancer metabolism suggests that the loss of stromal Cav-1 as a key regulator is a potential therapy target, further suggesting that stromal Cav-1 expression in stromal cells can be of prognostic EHT 1864 significance. Moreover, a loss of stromal Cav-1 has been reported to be a predictor of early tumor recurrence, lymph node metastasis, tamoxifen resistance, and poor clinical outcome in human breast cancer patients. We investigated stromal Cav-1 expression in pancreatic cancer to evaluate a potential role for stromal Cav-1 as a prognostic marker. Stromal Cav-1 was downregulated in pancreatic cancer compared with paraneoplastic and normal tissue. Loss of stromal Cav-1 is closely correlated with advanced TNM stage, lymph node metastasis, distant metastasis, and poor prognosis. The loss of stromal Cav-1 was correlated with the amplification of classic markers for tumor progression. More importantly, the loss of stromal Cav-1 was associated with metastasis because circulating tumor cells were found in patient blood. These findings extend our understanding of the function of stromal Cav-1 as a diagnostic marker. Most importantly, to our knowledge, this study is the first to show that loss of stromal Cav-1 in pancreatic cancer is a negative prognostic indicator. However, the work of Witkiewicz et al. revealed that the co-expression of FASN and Cav-1 may be an informative clinical marker. Witkiewicz et al. found that Cav-1 and FASN had higher expressions in PDAs than in PanIN. In addition to staining neoplastic epithelial cells, Cav-1 was also present in fibroblasts of the desmoplastic cancer stroma. Stromal cells in normal pancreas or chronic pancreatitis tissue adjacent to tumor cells were negative, which is in contrast to our findings. This difference may be attributed to the possibility that the study by Witkiewicz et al. occurred during the immunolocalization of the two molecules, and the results may be attributed to mutual interference. Moreover, the used Cav-1 Ab had a different specificity. The method used by Witkiewicz et al. is different from that used in this study, in which PCR was employed with respect to quantification. Finally, sample heterogeneity may have also affected the results. Although the findings of Witkiewicz et al. are consistent with those of our study, further study should be Eact conducted on this topic. CTCs are tumor cells shed from the primary tumor into blood circulation. The presence of CTCs in the peripheral blood of patients has long been associated with metastasis and poor survival and is now considered an acceptable cancer marker. However, current techniques are limited. The only commercially available CTC test has a detection rate of 50% in late-stage patients. In this study, we detect circulating tumor cells harboring negative enrichment by using the immunomagnetic bead method, followed by identification with cytology analysis, immunofluorescence, and imFISH.