Extending chemotherapy with capecitabine following CAPOX chemotherapy improves survival of Stage 3 gastric carcinoma after radical surgery: a 5-year analysis.

OBJECTIVE: To assess the effectiveness and safety of treatment consisting of extending chemotherapy (ECT) with capecitabine following capecitabine plus oxaliplatin (CAPOX) chemotherapy for stage 3 gastric carcinoma (GC) after D2 gastrectomy. PATIENTS AND METHODS: In this retrospective study, we included 214 patients with stage 3 GC who underwent D2 gastrectomy between January 2012 and April 2014. The CAPOX regimen chemotherapy was administrated to all of the patients as adjuvant therapy. The CAPOX regimen consisted of capecitabine (1000 mg/m2, in 2 divided doses for 14 d) and oxaliplatin (130 mg/m2 given on Day 1), repeated every 21 d for 8 cycles. Following CAPOX chemotherapy, 102 of these patients received extending chemotherapy (the ECT group) with capecitabine, whereas 112 patients (the control group) received no ECT. The ECT consisted of capecitabine (1000 mg/m2, in 2 divided doses for 14 d), repeated every 21 d for 8 cycles at most. The chemotherapy was discontinued if unacceptable toxicity or disease progression occurred or upon the request of the patient. All cases were followed up, and overall survival (OS), recurrence-free survival (RFS), and toxicities were compared. RESULTS: The ECT group exhibited a distinctly higher 5-year OS (p=0.0468) and RFS (p=0.0483) than those of the control group. The incidence of hand-foot syndrome was markedly greater in the ECT group (p=0.0043). No toxicity-related death occurred. CONCLUSIONS: Extending chemotherapy with capecitabine following the CAPOX regimen chemotherapy provides significant survival benefit for stage 3 GC after D2 gastrectomy.

Effects of microinjection of melatonin and its receptor antagonists into anterior hypothalamic area on blood pressure and heart rate in rats.

AIM: To examine the effects of microinjection of melatonin and its receptor antagonists into the anterior hypothalamic area (AHA) on blood pressure (BP) and heart rate (HR) in normotensive and stress-induced hypertensive rats. METHODS: Melatonin and its receptor antagonists were microinjected into the AHA, then BP, mean arterial pressure (MAP), and HR were synchronously recorded. RESULTS: Microinjection of melatonin produced a fall in MAP. Prazosin, an antagonist of melatonin ML2 receptor, could not antagonize the depressive response induced by melatonin. While luzindole, a competitive antagonist of melatonin ML1 receptor, was able to almost completely prevented the depressive response induced by injection of melatonin. CONCLUSION: Melatonin acts as a hypotensive factor and the effects are mainly due to activation of ML1 receptors in rat brain, and the AHA may be one of the important central areas where melatonin can exert modulatory effects on BP and HR.