Abstract Purpose The totally implanted venous access port (TIVAP) is widely applied to chemotherapy. The traditional approach is to implant the port by directly cutting skin at the chest wall, but surgical scarring on the chest wall may bring permanent psychological trauma to patients and affect the port once the incision is infected. In this study, the effect and safety of an improved port implantation (noninvasive chest wall implantation) via the axillary approach on breast cancer patients were evaluated. Methods This study discusses the surgical steps of the improved port implantation. The incidences of complication, comfort, convenience, aesthetics, and privacy from the improved operation were analyzed and compared with the traditional operation. Results All patients successfully presented improved infusion port implantation through the axillary access (noninvasive chest wall implantation). Two cases had a hemorrhage during the operation. One case had a postoperative subcutaneous hemorrhage, and one case had a folded catheter. Nevertheless, the patients did not need a secondary operation for adjustment. The average operation time of the improved infusion port implantation was 51.85 min (range: 37–69 min). The improved operation was significantly better than the traditional operation in terms of aesthetics and privacy. In terms of comfort and convenience, the difference between the two operations was not significant. Conclusions This study described the specific steps and particular aspects of the improved operation. The effectiveness and safety of the improved operation were reported for the first time. The improved operation has been proven safe and reliable, and it entails only a few intraoperative and postoperative complications.

OBJECTIVES:Several prospective trials had been reported on chemotherapy with or without antiangiogenic agents in patients with advanced malignant pleural mesothelioma (MPM), with diverse results. We performed this systematic review and meta-analysis to evaluate the efficacy and safety of the combination regimen.METHODS:We systematically identified trials in several databases, including MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, ASCO Abstracts and ESMO Abstracts. All the randomized controlled trials (RCTs) about chemotherapy combined with antiangiogenic agents in advanced MPM were identified. Overall survival (OS) was the primary outcome, while progression-free survival (PFS), overall response rate (ORR) and serious toxicities were the secondary outcomes. Review Manager 5.3 was used to perform the statistical analyses. Stata 12.0 was used to assess the publication bias of egger's test.RESULTS:5 randomized controlled trials containing 1250 patients were finally included in this analysis. Statistical analyses showed that the addition of antiangiogenic agents to chemotherapy could prolong OS [HR 0.79 (0.71-0.89), p<0.0001] and PFS [HR 0.75 (0.68-0.84), p<0.00001] in advanced MPM, especially in the epithelioid subgroup, with a tolerable toxicity profile. No significant difference was found in the analysis of ORR [HR 1.13 (0.95-1.35), p = 0.18]. Heterogeneity was found in the analyses of PFS and ORR, which might be caused by the limitation in uniform evaluation of tumor response.CONCLUSIONS:The combination of antiangiogenic agents with chemotherapy showed superior over chemotherapy alone in patients with advanced MPM. More prospective trials should be warranted to identify patients who would most likely benefit from the combination regimen.

ANGPTL4, a member of the angiopoietin-like protein family, is reported to be involved in angiogenesis regulation, lipid metabolism, glucose metabolism and redox reactions, among others. Our previous study showed that the plasma ANGPTL4 level was lower in coronary atherosclerotic heart disease (CAHD) and could be a useful predictor of coronary atherosclerosis. However, the molecular mechanism underlying the function of ANGPTL4 in atherosclerosis is poorly understood. In this study, we found that overexpression of ANGPTL4 in HUVECs enhanced cell proliferation and clone-forming ability in vitro, whereas knockdown of ANGPTL4 resulted in the opposite. The expression of ANGPTL4 was upregulated in palmitic acid (PA)-treated HUVECs. Overexpression of ANGPTL4 protected against PA-induced endothelial injury. Knockdown of ANGPTL4 exacerbated the effects of PA on HUVECs. Mechanistically, we demonstrated that ANGPTL4 promoted endothelial cell proliferation through the regulation of autophagy. Knockdown of ATG7 or 3-MA (an autophagy inhibitor) attenuated the effects of ANGPTL4 on endothelial cells. The serum level of ANGPTL4 was downregulated in atherosclerosis mice. Furthermore, the expression of ANGPTL4 was correlated with autophagy-related proteins in aortic tissues of atherosclerotic mice. ANGPTL4 promotes endothelial cell proliferation and suppresses PA-induced endothelial cell injury by increasing autophagy, which may protect against the development of atherosclerosis.

Soy consumption has received considerable attention for its potential role in reducing cancer incidence and mortality. However, its effects on gastrointestinal (GI) cancer are controversial. Therefore, we performed a meta-analysis to evaluate the association between soy consumption and gastrointestinal cancer risk by searching for prospective studies in PubMed, Web of Science, EMBASE and the reference lists of the included articles. The study-specific odds ratio (OR), relative risk (RR) or hazard ratio (HR) estimates and 95% confidence intervals (CIs) were pooled using either a fixed-effect or random-effect model. Twenty-two independent prospective studies were eligible for our meta-analysis, including 21 cohort studies and one nested case-control study. Soy product consumption was inversely associated with the incidence of overall GI cancer (0.857; 95% CI: 0.766, 0.959) and the gastric cancer subgroup (0.847; 95% CI: 0.722, 0.994) but not the colorectal cancer subgroup. After stratifying the results according to gender, an inverse association was observed between soy product intake and the incidence of GI cancer for females (0.711; 95% CI: 0.506, 0.999) but not for males.

BACKGROUND: Fatigue is the most common symptom associated with cancer and its treatment, and profoundly affects all aspects of quality of life for cancer patients. It is very important to measure and manage cancer-related fatigue. Usually, the cancer-related fatigue scores, which estimate the degre e of fatigue, are self-reported by cancer patients using standardized assessment tools. But most of the classical methods used for measurement of fatigue are subjective and inconvenient. OBJECTIVE: In this study, we try to establish a new method to assess cancer-related fatigue objectively and accurately by using smart bracelet. METHODS: All patients with metastatic pancreatic cancer wore smart bracelet for recording the physical activity including step count and sleep time before and after chemotherapy. Meantime, their psychological state was assessed by completing questionnaire tables as cancer-related fatigue scores. RESULTS: Step count record by smart bracelet reflecting the physical performance dramatically decreased in the initial days of chemotherapy and recovered in the next few days. Statistical analysis showed a strong and significant correlation between self-reported cancer-related fatigue and physical performance (P= 0.000, r=-0.929). Sleep time was also significantly correlated with fatigue (P= 0.000, r= 0.723). Multiple regression analysis showed that physical performance and sleep time are significant predictors of fatigue. CONCLUSIONS: Measuring activity using smart bracelets may be an appropriate method for quantitative and objective measurement of cancer-related fatigue by using smart bracelet devices.

Abstract Background:Arsenic compound has shown excellent activity in APL. Its anticancer activity in solid tumors is still being explored. We have tested realgar, arsenic sulfide (As4A4), in gastric cancer cells to understand its anticancer activity and mechanism. Methods: The effects of the realgar on cell proliferation and apoptosis of AGS and MGC803 cell lines were determined using methyl thiazolyl tetrazolium (MTT) assay and Annexin V assay. Western blot analysis was used to detect the related pathways by measuring the expression levels of apoptotic proteins such as Bax, Bcl-2, c-myc, p53 and mdm2. Real-time PCR analysis was used to measure the mRNA levels of the related genes. Results: Realgar significantly inhibited proliferation and induced apoptosis in gastric cancer cell lines AGS and MGC803 in a dose- and time-dependent manner, particularly in AGS cells. Realgar up-regulated the expression of p53 and p53 target genes MDM2 and Bax, down-regulated the expression of Bcl-2 and c-Myc in AGS cell lines, indicating that realgar could induce apoptosis via p53-bax pathway in AGS cell lines. However, similar dose of realgar up-regulated the expression of Bax, down-regulated the expression of Bcl-2 and c-Myc in MGC803 cell lines, with much less effect on the expression of p53. Conclusion: Realgar has significant anti-cancer effect on gastric cancer cell lines through inhibiting cell proliferation and inducing apoptosis. Our findings suggest a potential therapeutic effect of realgar in gastric cancer and further study in this area is needed. Citation Format: Siyu Chen, Wei Tian, Wenping Ding, Leizhen Zheng, Xiaoping Li, Li Zhang, Jianchun Gu, shuangfen Tao, Sungkyoung Kim, Wenhua Gu. Realgar exerts cytotoxic killing of gastric cancer cells through Bax apoptotic pathway. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2110. doi:10.1158/1538-7445.AM2013-2110

Objectives: Several clinical trials have been published on gemcitabine-based chemotherapy with or without addition of agents against epidermal growth factor receptor (EGFR) or vascular endothelium growth factor receptor (VEGFR) in patients with advanced pancreatic cancer, however, with diverse results. The objective of this study was to perform a meta-analysis of the published trials.Methods: The database of CENTRAL, MEDLINE and EMBASE were searched. Eligible studies were randomized clinical trials (RCTs) that evaluated the efficacy and safety profile of adding targeted agents against EGFR or VEGFR to gemcitabine-based chemotherapy in patients with advanced pancreatic cancer. The primary outcome was overall survival (OS) while secondary outcomes included progression free survival (PFS) and overall response rate (ORR). Toxicity profiles were also assessed. Review Manager 5.1 was used to perform the analysis.Results: Results reported from 6 RCTs involving 2733 patients were included in the analysis. Compared to gemcitabine-based chemotherapy alone, addition of an agent against EGFR resulted in significant longer OS [Hazard ratios (HR) 0.89 (0.79-0.99), p = 0.04] and longer PFS [HR 0.87 (0.79-0.97), p = 0.01], but no significant difference in ORR [RR 1.18 (0.82-1.70), p = 036]. The addition of an agent against VEGFR resulted in higher ORR [RR 1.54 (1.03-2.30), p = 0.04], but no advantage in OS [HR 0.95 (0.83-1.09), p = 0.47] or PFS [HR 0.97 (0.77-1.23), p = 0.82].Conclusions: Addition of an agent against EGFR to gemcitabine-based chemotherapy improved OS compared to gemcitabine-based chemotherapy alone in patients with advanced pancreatic cancer, while addition of an agent against VEGFR showed a modest improvement in ORR but not PFS and OS. Copyright (C) 2013, IAP and EPC. Published by Elsevier India, a division of Reed Elsevier India Pvt. Ltd. All rights reserved.

Objective To evaluate the efficacy and safety profile of combining vandetanib with chemotherapy in patients with advanced non-small cell lung cancer (NSCLC). Methods MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials (CENTRAL), ASCO Abstracts, ESMO Abstracts, Wanfang Database, CNKI were searched. Eligible studies were the randomized clinical trials (RCTs) that compared the efficacy and safety profile of adding vandetanib to chemotherapy with single chemotherapy in patients with advanced NSCLC. The outcomes included overall survival (OS), progression-free survival (PFS), overall response rate (ORR) and toxicities. All meta-analysis were performed using Review Manager 5.1. The fixed-effect model weighted by the Mantel-Haenszel method was used. When considerable heterogeneity was found (p<0.1, or I2>50%), further analysis (subgroup analysis, sensitivity analysis or random-effect model) was performed to identify potential cause. Results Results reported from 5 RCTs involving 2284 patients were included in the analysis. Compared to chemotherapy alone, the addition of vandetanib resulted in a significant longer PFS (HR 0.79 [0.72–0.87], p<0.00001) and a higher ORR (RR 1.75 [1.43–2.15], p<0.00001), but failed to show advantage on OS (HR 0.96 [0.87–1.06], p = 0.44). Conclusion Vandetanib has activity in NSCLC. Identification of predictive biomarkers is warranted in future trials to select a subset of patients with advanced NSCLC who may benefit from vandetanib.