Induction of the somatostatin receptor on colon carcinoma cells as a target for radiolabeled or cytotoxic somatostatin analogs

__Abstract__ In 1973 Brazeau et al. isolated and identified a 14-amino acid peptide, named somatotropin-release inhibiting factor (SRIF), later changed to somatostatin (SS)(1). Subsequently, research showed that somatostatin had two forms of bioactive peptides, somatostatin 14 and somatostatin 28, and that SS was widely distributed throughout the body with a wide variety of effects on endocrine, gastrointestinal and central nervous systems. The diversity of effects mediated by SS led to the suggestion that the hormone could have a therapeutical purpose in a great number of indications. However, due to the short half-life of SS (approximately 2 minutes) there were some restrictions in the use of natural SS as a drug. Therefore, researchers began to synthesize more stable peptide analogs with a longer duration of action, such as octreotide (SMS 201-995), lanreotide (BIM 23014) and vapreotide(2). These analogs not only proved to be more stable, but had also different affinity for the five

Hypothermic perfusion with retrograde outflow during right hepatectomy is safe and feasible

Background: In situ hypothermic perfusion during liver resection performed under vascular inflow occlusion decreases hepatic ischemia-reperfusion injury, but technical limitations have restricted its widespread use. In situ hypothermic perfusion with retrograde outflow circumvents these impediments and thus could extend the applicability of in situ hypothermic perfusion. The safety and feasibility of in situ hypothermic perfusion with retrograde outflow were analyzed in selected patients undergoing right (extended) hepatectomy and compared to intermittent vascular inflow occlusion, the gold standard method, in this randomized pilot study. Methods: Patients were first screened for parenchymal liver disease (exclusion criteria: steatosis ≥30%, cirrhosis, or cholestasis). Study participants were randomized intraoperatively to undergo in situ hypothermic perfusion with retrograde outflow (n = 9) or intermittent vascular inflow occlusion (n = 9). The target liver core temperature during in situ hypothermic perfusion with retrograde outflow was 28°C. The primary end point was ischemia-reperfusion injury (expressed by peak postoperative transaminase levels). Secondary outcomes included functional liver regeneration (assessed by hepatobiliary scintigraphy) and clinical outcomes. Results: Peak transaminase levels, total bilirubin, and the international normalized ratio were similar between both groups, although a trend toward more rapid normalization of bilirubin levels was noted for the in situ hypothermic perfusion with retrograde outflow group. Functional liver regeneration as evaluated by hepatobiliary scintigraphy was improved on postoperative day 3 following in situ hypothermic perfusion with retrograde outflow but not after intermittent vascular inflow occlusion. Furthermore, in situ hypothermic perfusion with retrograde outflow (requiring continuous ischemia) was comparable to intermittent vascular inflow occlusion for all clinical outcomes, including postoperative complications and hospital stay. Conclusion: The use of in situ hypothermic perfusion with retrograde outflow appears to be safe and feasible in selected patients with healthy liver parenchyma and may benefit early functional liver regeneration. Future applications of in situ hypothermic perfusion with retrograde outflow include patients with damaged liver parenchyma who would require major hepatic resection with a prolonged vascular inflow occlusion duration.</p