An ideal tumor marker should be capable of being detected at any stage of the disease. However, gastric cancer patients do not always have elevated serum carcinoembryonic antigen (CEA) levels, even in advanced cases. Recently, several studies have investigated the associations between preoperative PNI and postoperative long-term outcomes. In this study, we focused on the significance of the prognostic nutritional index (PNI) as a potential predictor of survival in resectable gastric cancer patients with normal preoperative serum CEA levels. We retrospectively conducted cohort study to evaluate the PNI as a predictor of survival in 368 resectable gastric cancer patients who underwent potentially curative gastrectomy at our institute between January 2010 and December 2016. We selected 218 patients by propensity score matching to reduce biases due to the different distributions of co-variables among the comparable groups. In the multivariate analysis, pStage (hazard ratio [HR]: 14.003, 95% confidence interval [CI]: 5.033–44.487; p < 0.001), PNI (HR: 2.794, 95% CI: 1.352–6.039; p < 0.001) were identified as independent prognostic factors of CSS in 218 propensity matched gastric cancer patients. The Kaplan-Meier analysis demonstrated that low PNI patients had a significantly poorer cancer specific survival (CSS) than high PNI patients (p = 0.008). Among 166 propensity matched gastric cancer patients with normal preoperative serum CEA levels, multivariate analysis demonstrated that pStage (HR: 7.803, 95% CI: 3.015–24.041; p < 0.001) and PNI (HR: 3.078, 95% CI: 1.232–8.707; p = 0.016) were identified as independent prognostic factors of CSS. And Kaplan-Meier analysis demonstrated that low PNI had a significantly poorer CSS than high PNI value (p = 0.011). This study demonstrates that a low preoperative PNI value is a potential independent risk factor for poorer CSS in patients with gastric cancer, even in those with normal serum CEA levels.

Introduction: Although acute liver failure (ALF) is a rare disease, it continues to have high mortality and morbidity rates due to its many causes. High mobility group box 1 (HMGB1), originally reported as a ubiquitous non-histone chromosomal protein, is a multi-functional protein with varying functions depending on its location, such as in the nucleus, cytoplasm and extracellular space. The role of extracellular HMGB1 as an inflammatory mediator has been well studied, and the elevation of serum HMGB1 has been reported in several diseases that are closely associated with ALF. Areas covered: In this review, we focus on the relationship between causes of acute liver failure, such as viral infection, drug-induced liver injury, ischemia/reperfusion injury, and acute-on-chronic liver failure, and the role of HMGB1. Furthermore, we also consolidate and summarize the current reports of HMGB1-targeting therapies in hepatic injury models. Expert commentary: HMGB1 could be a novel therapeutic candidate for ALF, and the clinical testing of HMGB1-targeting therapies for ALF patients is expected.

Objective: High-mobility group box 1, a ubiquitous nonhistone chromosomal protein, is passively released from necrotic cells and actively secreted by inflammatory cells. Extracellular high-mobility group box 1 has recently been recognized to be a mediator of hepatic ischemia–reperfusion injury; however, the kinetics of high-mobility group box 1 during hepatic ischemia–reperfusion and the role of high-mobility group box 1 in ischemia–reperfusion injury still remain poorly understood. This study was designed to assess the localization and the kinetics of high-mobility group box 1 during hepatic ischemia–reperfusion injury and the effects of high-mobility group box 1 adsorption column in hepatic ischemia-reperfusion injury. Design: A prospective, randomized animal study. Setting: University medical center research laboratory. Subjects: Male Sprague-Dawley rats. Investigation: The animals underwent 70% partial hepatic ischemia for 60 or 90 mins and were then reperfused. To investigate the high-mobility group box 1 levels in the serum and in the liver, the animals were killed at predetermined periods. As a lethal model, global hepatic ischemia–reperfusion was induced by portal triad cross-clamping for 30 mins. Hemoperfusion therapy using a cellulofine sulfate bead column (high-mobility group box 1 adsorption column) was performed during global hepatic ischemia. Measurements and Main Results: During 60 mins of 70% hepatic ischemia, nuclear high-mobility group box 1 was translocated to the cytoplasm in hepatocytes; however, serum high-mobility group box 1was not increased. Immediately after reperfusion, the serum high-mobility group box 1 was significantly increased (p < .05). High-mobility group box 1 mediated ischemia–reperfusion injury in not only liver but also the remote organ, lung. Removal of excess high-mobility group box 1 in blood using an adsorption column significantly improved animal survival (p < .03) and liver and lung injuries. Conclusions: High-mobility group box 1 plays an important role in the systemic as well as local pathogenesis of hepatic ischemia–reperfusion injury. The removal of excessive high-mobility group box 1 with adsorption column was beneficial and promising option in ischemia-related liver injuries.

Gastrointestinal perforation is known as a serious adverse event, but, for breast cancer, there are very few reports of gastrointestinal perforation. This report highlights gastrointestinal perforation caused by bevacizumab for breast cancer, which is of special interest because gastrointestinal perforations caused by bevacizumab are very rare in breast cancer. We describe the case of 54-year-old Japanese woman. She was diagnosed as having inoperable breast cancer T2 N1 M1 (pleura, peritoneum), Stage IV, and received chemotherapy by paclitaxel. There was reduction in the primary tumor and disappearance of the pleural effusion; however, the ascites did not change. We performed diagnostic laparoscopy which revealed that her whole peritoneum was thickened, and her small intestine, colon, and her omentum were grouped and formed an omental cake. We submitted a part of her peritoneum to pathological examination and diagnosed the peritoneum dissemination of breast cancer. On the basis of these results, paclitaxel and bevacizumab combination chemotherapy was started, and a decrease in ascites was seen. However, a gastrointestinal perforation occurred on 26th day of second cycle of bevacizumab + paclitaxel, and we performed an emergency operation. In the operation, the omental cake was resolved, and we could search the full length of the gastrointestinal tract. Two small perforations of her small intestine were seen. We performed simple closures for perforations, and peritoneal lavage and drainage. She was in a state of septic shock, but it improved. It was thought that the small intestinal perforations were caused by the bevacizumab-additional chemotherapy which was very effective. We report a very rare and valuable case. This case suggests that the risk of gastrointestinal perforation must be considered in a case of bevacizumab administration, and it is necessary to determine carefully the patient administered bevacizumab, regardless of the type of cancer.