Endoscopic ultrasound for structured surveillance after curative treatment of esophageal cancer.

BACKGROUND: Structured surveillance after treatment of esophageal cancer is not established. Due to a paucity of data, no agreement exists on how surveillance should be performed. The main argument against intensive follow-up in esophageal cancer is that it may not lead to true survival advantage. METHODS: Structured surveillance was performed in 42 patients after multimodal therapy with peri-operative chemotherapy (29) or definitive chemoradiotherapy (13) of esophageal cancer. The surveillance protocol included gastroscopy, endoscopic ultrasound, chest X-ray, abdominal ultrasound, and CEA measurement at regular intervals of up to five years. We analyzed relapse rate, time to relapse, localization of recurrence, diagnosis within or without structured surveillance, diagnostic method providing the first evidence of a relapse, treatment of recurrence, and outcome. RESULTS: Median follow-up was 48 months; 18/42 patients suffered from tumor relapse, with 16 asymptomatic patients diagnosed within structured surveillance. Median time to recurrence was 9 months. Isolated local or locoregional recurrence occurred in 6, and isolated distant relapse in 9 patients. All patients with isolated locoregional recurrence were exclusively diagnosed with endoscopic ultrasound. Six patients received curatively intended therapy with surgery or chemoradiation, leading to long-lasting survival. CONCLUSION: Structured surveillance offers the chance to identify limited and asymptomatic tumor relapse. Especially in cases of locoregional recurrence, long-lasting survival or even a cure can be achieved. Endoscopic ultrasound is the best method for the detection of locoregional tumor recurrence and should be an integral part of structured surveillance after curative treatment of esophageal cancer.

Involvement of Neuropeptide Galanin Receptors 2 and 3 in Learning, Memory and Anxiety in Aging Mice.

The neuropeptide galanin (GAL), which is expressed in limbic brain structures, has a strong impact on the regulation of mood and behavior. GAL exerts its effects via three G protein-coupled receptors (GAL1-3-R). Little is known about the effects of aging and loss of GAL-Rs on hippocampal-mediated processes connected to neurogenesis, such as learning, memory recall and anxiety, and cell proliferation and survival in the dorsal dentate gyrus (dDG) in mice. Our results demonstrate that loss of GAL3-R, but not GAL2-R, slowed learning and induced anxiety in older (12-14-month-old) mice. Lack of GAL2-R increased cell survival (BrdU incorporation) in the dDG of young mice. However, normal neurogenesis was observed in vitro using neural stem and precursor cells obtained from GAL2-R and GAL3-R knockouts upon GAL treatment. Interestingly, we found sub-strain differences between C57BL/6J and C57BL/6N mice, the latter showing faster learning, less anxiety and lower cell survival in the dDG. We conclude that GAL-R signaling is involved in cognitive functions and can modulate the survival of cells in the neurogenic niche, which might lead to new therapeutic applications. Furthermore, we observed that the mouse sub-strain had a profound impact on the behavioral parameters analyzed and should therefore be carefully considered in future studies.