Gastric cancer is the fourth most common type of cancer and the second highest leading cause of cancer-related deaths worldwide. It has already been established that miR-133a is involved in gastric cancer. In this study, we investigated the molecular mechanisms by which miR-133a inhibits the proliferation of gastric cancer cells. We analyzed the proliferative capacity of human gastric cancer cells SNU-1 using an MTT assay. Cell apoptosis was determined using flow cytometry. The expression levels of ERBB2, p-ERK1/2, and p-AKT in SNU-1 cells were determined using Western blot analysis. To confirm that ERBB2 is a direct target of miR-133a, a luciferase reporter assay was performed. Results showed that miR-133a overexpression inhibited SNU-1 cell proliferation and increased apoptosis. ERBB2 was a direct target of miR-133a, and it was negatively regulated by miR-133a. Interestingly, ERBB2 silencing has a similar impact to miR-133a overexpression, in that it significantly induced apoptosis and inhibited ERK and AKT activation. Our study showed that miR-133a inhibits the proliferation of gastric cancer cells by downregulating the expression of ERBB2 and its downstream signaling molecules p-ERK1/2 and p-AKT. Therefore, miR-133a might be used as a therapeutic target for treating gastric cancer.

Lung cancer is the most common cancer type with increasingly high incidence. MicroRNAs provide the potential biomarkers for lung cancer treatment. Thus, we aimed to investigate the function of microRNA-425-5p in lung cancer development and the underlying mechanisms. MicroRNA-425-5p overexpression inhibited A549 lung cancer cell proliferation in vitro and in vivo . On the other hand, microRNA-425-5p inhibition increased A549 proliferation. Mechanistically, the underlying mechanism by which microRNA-425-5p inhibits lung cancer cell growth was mediated through its ability in targeting and downregulating the TFIIB-related factor 2. Our results for the first time identified microRNA-425-5p as a tumor suppressor in lung cancer. Thus, microRNA-425-5p may serve as a potential therapeutic target for lung cancer. Keywords microRNA-425-5p , lung cancer , cell growth , TFIIB-related factor 2 , biomarker

Objective: To investigate the impact of human epidermal growth factor receptor 2 (HER2) gene silencing on the expression of trefoil factor 3 (TFF3), and to explore the effects of combined down-regulation of HER2 and TFF3 gene expressions on the proliferation, migration and invasion of human gastric cancer NCI-N87 cells.Methods: The data of m RNA expression levels of HER2 and TFF3 in 38 different gastric cancer cell lines were obtained from Cancer Cell Line Encyclopedia (CCLE) database, and the correlation between HER2 and TFF3 m RNA expressions was analyzed. Human gastric cancer NCI-N87 cells were transfected with HER2-si RNA and TFF3-si RNA as well as HER2 overexpression recombined plasmids using Lipofect AMINETM 2000, respectively. The expression levels of HER2 and TFF3 m RNAs and proteins were detected by real-time fluorescent quantitative PCR and Western blotting, respectively. The proliferation, migration and invasion abilities of NCI-N87 cells transfected with HER2-si RNA and TFF3-si RNA were detected by CCK-8 method and Transwell assay, respectively.Results: There was a negative correlation between the mRNA expression levels of HER2 and TFF3 in 38 different gastric cancer cell lines (γ =-0.24, P = 0.049). After transfection with HER2-siRNA, comparing with the negative control groups, the expression levels of HER2 mRNA and protein were significantly down-regulated, while the expression levels of TFF3 mRNA and protein were up-regulated (all P ＜ 0.05). After transfection with HER2 overexpression recombined plasmid, the expression levels of HER2 mRNA and protein were significantly up-regulated (both P ＜ 0.05), while the expression levels of TFF3 mRNA and protein were down-regulated, though the difference was not statistically significant (both P＞ 0.05). HER2-siRNA or TFF3-siRNA transfection could inhibit the proliferation, migration and invasion of NCI-N87 cells (all P ＜ 0.05), furthermore the combined transfection resulted in the stronger inhibition (all P ＜ 0.05).Conclusion: The expressions of HER2 and TFF3 are negatively correlated in different gastric cancer cell lines. HER 2 gene silencing induces the expression of TFF3 in NCI-N87 cells. The combined down-regulation of HER 2 and TFF 3 gene has synergistic inhibitiory effects on the proliferation, migration and invasion of NCI-N87 cells.

No biologically based diagnostic criteria are in clinical use today for obsessive–compulsive disorder (OCD), schizophrenia, and major depressive disorder (MDD), which are defined with reference to Diagnostic and Statistical Manual clinical symptoms alone. However, these disorders cannot always be well distinguished on clinical grounds and may also be comorbid. A biological blood‐based dynamic genomic signature that can differentiate among OCD, MDD, and schizophrenia would therefore be of great utility. This study enrolled 77 patients with OCD, 67 controls with no psychiatric illness, 39 patients with MDD, and 40 with schizophrenia. An OCD‐specific gene signature was identified using blood gene expression analysis to construct a predictive model of OCD that can differentiate this disorder from healthy controls, MDD, and schizophrenia using a logistic regression algorithm. To verify that the genes selected were not derived as a result of chance, the algorithm was tested twice. First, the algorithm was used to predict the cohort with true disease/control status and second, the algorithm predicted the cohort with disease/control status randomly reassigned (null set). A six‐gene panel (COPS7A, FKBP1A, FIBP, TP73‐AS1, SDF4, and GOLGA8A) discriminated patients with OCD from healthy controls, MDD, and schizophrenia in the training set (with an area under the receiver‐operating‐characteristic curve of 0.938; accuracy, 86%; sensitivity, 88%; and specificity, 85%). Our findings indicate that a blood transcriptomic signature can distinguish OCD from healthy controls, MDD, and schizophrenia. This finding further confirms the feasibility of using dynamic blood‐based genomic signatures in psychiatric disorders and may provide a useful tool for clinical staff engaged in OCD diagnosis and decision making.

Gastric cancer is the fourth most common type of cancer and the second highest leading cause of cancer-related deaths worldwide. It has already been established that miR-133a is involved in gastric cancer. In this study, we investigated the molecular mechanisms by which miR-133a inhibits the proliferation of gastric cancer cells. We analyzed the proliferative capacity of human gastric cancer cells SNU-1 using an MTT assay. Cell apoptosis was determined using flow cytometry. The expression levels of ERBB2, p-ERK1/2, and p-AKT in SNU-1 cells were determined using Western blot analysis. To confirm that ERBB2 is a direct target of miR-133a, a luciferase reporter assay was performed. Results showed that miR-133a overexpression inhibited SNU-1 cell proliferation and increased apoptosis. ERBB2 was a direct target of miR-133a, and it was negatively regulated by miR-133a. Interestingly, ERBB2 silencing has a similar impact to miR-133a overexpression, in that it significantly induced apoptosis and inhibited ERK and AKT activation. Our study showed that miR-133a inhibits the proliferation of gastric cancer cells by downregulating the expression of ERBB2 and its downstream signaling molecules p-ERK1/2 and p-AKT. Therefore, miR-133a might be used as a therapeutic target for treating gastric cancer.

Colon cancer is one of the most lethal varieties of cancer. Chemotherapy remains as one of the principal treatment approaches for colon cancer. The anticancer activity of procaine (PCA), which is a local anesthetic drug, has been explored in different studies. In our study, we aimed to explore the anticancer effect of PCA on colon cancer and its underlying mechanism. The results showed that PCA significantly inhibited cell viability, increased the percentage of apoptotic cells, and decreased the expression level of RhoA in HCT116 cells in a dose-dependent manner (p < 0.05 or p < 0.01). Moreover, PCA increased the proportion of HCT116 cells in the G1 phase as well as downregulated cyclin D1 and cyclin E expressions (p < 0.05). In addition, we found that PCA remarkably inhibited cell migration in HCT116 cells (p < 0.01). However, all these effects of PCA on cell proliferation, apoptosis, and migration were significantly reversed by PCA + pc-RhoA (p < 0.05 or p < 0.01). PCA also significantly decreased the levels of p-ERK, p-p38MAPK, and p-FAK, but PCA + pc-RhoA rescued these effects. Furthermore, the ERK inhibitor (PD098059), p38MAPK inhibitor (SB203580), and FAK inhibitor (Y15) reversed these results. These data indicate that PCA inhibited cell proliferation and migration but promoted apoptosis as well as inactivated the ERK/MAPK/FAK pathways by regulation of RhoA in HCT116 cells.

Human epidermal growth factor receptor 2 (HER2), if activated abnormally, can promote tumor progression. The correlation of overexpression of HER2 and the prognosis of breast cancer is clear, but the effect of HER2 overexpression on the prognosis of pancreatic cancer is still controversial. The present study aimed to evaluate the prognostic role of HER2 in pancreatic cancer. PubMed, EMBASE, Ovid, CNKI (China National Knowledge Infrastructure) and Web of Science (Jan 2001 to Jun 2015) were searched to identify eligible studies assessing the correlation between expression of HER2 and pancreatic cancer. Data were extracted from studies and computed into hazard ratios (HRs) with 95% confidence intervals (CIs). A total of 19 eligible studies comprising 2,123 patients were included in the analysis. The univariate analysis results showed that HER2 overexpression was not significantly associated with patients' overall survival (pooled HRs, 1.09, 95% CI, 0.88-1.34, P=0.44), which are maintained in three studies of multivariate analysis (HR 0.93, 95% CI, 0.49-1.78, P=0.823). It also had no correlation with clinicopathological factors such as gender, tumor size, lymph node metastasis, and tumor stage. Our results indicated that overexpression of HER2 may not predict poor outcomes in pancreatic cancer.

BACKGROUND:Previous studies have shown that human epidermal growth factor receptor 2 (HER2) may play an important role in the invasion and metastasis of pancreatic cancer, but the relationship between HER2 amplification level and prognosis of pancreatic cancer patients is still controversial. Therefore, we performed a meta-analysis to determine the prognostic significance of HER2 amplification based on fluorescence in situ hybridization (FISH) in patients with pancreatic cancer.METHODS:PubMed, EMBASE, and Web of Science (Jan 2001 to Jun 2015) were searched. Only articles that detect the HER2 amplification by FISH method were included. RevMan 5.3 and STATA version 12 were used to perform this meta-analysis. Pooled calculations were carried out on hazard ratio (HR) and 95% confidence interval (CI) to assess the risk of disease.RESULTS:A total of six eligible studies were enrolled in meta-analysis. The univariate analysis results showed that HER2 amplification was not significantly associated with patients' overall survival (pooled HR, 1.87, 95% CI, 0.64-5.46, P=0.25), which are maintained in one study of multivariate analysis (HR 0.51, 95% CI, 0.12-2.14, P=0.358). HER2 amplification also had no correlation with clinicopathological factors such as age, gender, lymph node metastasis, and tumor stage.CONCLUSIONS:Our results showed that HER2 amplification based on FISH may not be a good prognostic factor for survival in patients with pancreatic cancer.

Objective To investigate the correlation of CD 44 and clinicopathological parameters in pancreatic head ca-ner,and its correlation with survival and prognosis .Methods 48 pancreatic head cancer samples were collected .Immunohisto-chemistry was applied to test the expression of CD 44 in pancreatic head cancer .The clinical data of the patients were collected in-cluding their gender,age,the histology and location,lymph node metastasis.The correlation between the CD44 expression and the clinicopathological factors of patients with pancreatic head cancer was analyzed by the software SPSS 13.0.Furthermore,the rele-vance among these markers was also detected .Results The positive rate of CD44 expression in the samples were 64.6%(31/48 ) .Univariate analysis showed that there were significant differences between the CD 44 expression and the pancreatic cancer ' T staging,TNM staging,lymph node metastasis(P<0.05).There was no significant difference between the expression of CD 44 and age,gender,vascular invasion,nerve invasion,and differentiation degree (P>0.05).The Cox proportional hazards model showed that CD44 and lymph node metastasis were independent prognostic factors .Conclusion CD44 is related to the distant metastasis and aggressive malignant behaviors of pancreatic head cancer .

The purpose of this study was to verify the efficacy and safety of high intensity focused ultrasound therapy (HIFU) combined with S-1 in the treatment of metastatic pancreatic cancer after failure of gemcitabine (GEM). In total, 120 patients with GEM-refractory PC who received HIFU and S-1 between Aug 2012 and December 2014 were randomly assigned to 2 groups. The patients in group A (n = 61) received HIFU in combination with S-1 and those in group B (n = 59) were given S-1 alone. S-1 was administered orally twice a day on days 1-14. Cycles were repeated every 21 days. The follow up time was 3~19 months in both groups. The median overall survival (OS) time and progression free survival (PFS) were analysed by Kaplan-Meier method and Logrank test. The pain remission rate of the two groups was compared by χ(2) test. Patient characteristics and prognostic factors were compared. Patient characteristics did not significantly differ between the 2 groups. Median OS was significantly longer in group A (10.3 months) than in group B (6.6 months, P = 0.000). Median PFS was also significantly longer in group A than in group B (5.1 months vs 2.3 months, P = 0.000). Meanwhile, the pain remission rate was markedly higher in group A than in group B (57% vs. 20%, P = 0.000). There were mild side effects and no significant difference was observed between the two groups. The treatment effect was independently associated with a good outcome. HIFU in combination with S-1 might be effective and well tolerated as salvage chemotherapy in the treatment for metastatic pancreatic cancer.

Background CD44 and phosphorylated AKT (p-AKT) is a potentially interesting prognostic marker and therapeutic target in pancreatic cancer. The expression of CD44 and p-AKT has been reported to correlate with poor prognosis of pancreatic cancer in most literatures. The purpose of this study is to investigate the roles of CD44 and p-AKT in pancreatic head cancer and their correlation with the prognosis of pancreatic head cancer patients. Methods Forty-eight pancreatic head cancer samples were collected dating from Jan. 2010 to Dec. 2012. Immunohistochemistry was applied to test the expression of CD44 and p-AKT in pancreatic head cancer. The clinical data of the patients were collected including their gender, age, the histology and location, lymph node metastasis, and so on. The correlation between the CD44 expression and the clinicopathological factors of patients with pancreatic head cancer was analyzed by the software SPSS 13.0. Results The positive rates of CD44 and p-AKT expression in the samples were 64.6 and 29.2 %, respectively. There was a significant difference between the CD44 expression and the pancreatic cancer’ T staging, tumor node metastasis (TNM) staging, lymph node metastasis ( P < 0.05). The Cox proportional hazard model showed that CD44 and lymph node metastasis were independent prognostic factors. Conclusions CD44 was related to the distant metastasis and aggressive malignant behaviors of pancreatic head cancer.

目的 探讨CD44在人类胰腺癌发生、发展中可能的作用以及与胰腺癌各临床病理参数、生存期和预后的关系.方法 选取2010年1月-2012年12月在上海交通大学医学院附属新华医院胰腺癌手术标本共67例,记录患者性别、年龄、组织学分型、肿瘤所在部位和淋巴结转移等情况,采用免疫组织化学法检测CD44的表达.结果 CD44在67例胰腺癌阳性表达率为73.1％ (49/67).单因素分析显示,胰腺癌患者的T分期、TNM分期、淋巴结转移情况、分化程度、肿瘤部位与CD44的阳性率表达相关(P＜0.05).而年龄、性别、血管侵犯、神经侵犯等与CD44的阳性率表达差别无统计学意义(P＞0.05).Cox模型分析显示:分化程度、CD44的表达情况、神经侵犯可作为独立的预后因子.结论 胰腺癌中CD44呈高表达,其与胰腺癌的恶性程度有关.分化程度、CD44的表达情况、神经侵犯为胰腺癌的独立预后因子.

CD133 is one of the most commonly used markers of pancreatic cancer stem cells (CSCs), which are characterized by their ability for self-renewal and tumorigenicity. Although the expression of CD133 has been reported to correlate with poor prognosis of PDAC in most literatures, some controversies still exist. In this study, we aimed to investigate the correlation between CD133 expression and prognosis and clinicopathological features in PDAC. A search in the Medline, EMBASE and Chinese CNKI (China National Knowledge Infrastructure) database (up to 1 March 2015) was performed using the following keywords pancreatic cancer, CD133, AC133, prominin-1 etc. Data from eligible studies were extracted and included into meta-analysis using a random effects model. Outcomes included overall survival and various clinicopathological features. We performed a final analysis of 723 patients from 11 evaluable studies for prognostic value and 687 patients from 12 evaluable studies for clinicopathological features. Our study shows that the pooled hazard ratio (HR) of overexpression CD133 for overall survival in PDAC was 0.58 (95% confidence interval (CI): 0.49-0.67) by univariate analysis and 0.73 (95% CI: 0.52-1.03) by multi-variate analysis. With respect to clinicopathological features, CD133 overexpression by immunohistochemistry (IHC) method was closely correlated with clinical TNM stage (TNM stage III+IV, OR=0.32, 95% CI: 0.19-0.54), tumor differentiation (poor differentiation, OR=0.56, 95% CI: 0.37-0.83), and lymph node metastasis (N1, 3.15, 95% CI: 1.56-6.36) in patients with PDAC. Our meta-analysis results suggest that CD133 is an efficient prognostic factor in PDAC. Overexpression of CD133 was significantly associated with clinical TNM stage, tumor differentiation and lymph node metastasis.

Objective:We investigated the potential functions of shRNA in CD44 targeting in pancreatic cancer cells.Methods:To devise and synthesis of effectively interference of shRNA sequence of CD44,which was transefect-ed to the pancreatic cancer cells.Results:After the transfection,pancreatic cancer cells'proliferation and invasion a-bilities were obviously inhibited by the colony formation assay,soft agar colony formation test,Transwell chamber inva-sion assay.Western Blot showed that p -ERK,p -AKT was reduced and the AKT were gradually raised in protein levels.Conclusion:shRNA targets CD44 in pancreatic cancer cells and suppresses pancreatic cancer cell growth and metastasis in vitro.This project may provide highly effective targeted therapy for pancreatic cancer and provide a new idea and method for targeting CD44.

Previous studies have suggested that the glutathione S -transferases M1 (GSTM1) null genotype is associated with the risk of gastric cancer. However, the interaction between GSTM1 null genotype and smoking for the risk of gastric cancer is still elusive. Therefore, we performed a meta-analysis to ascertain this issue. Databases of PubMed, EMBASE, and China National Knowledge Infrastructure were searched to retrieve relevant studies. Smokers were categorized as “ever-smokers” and “non-smokers.” Odds ratios (ORs) and 95 % confidence intervals (95 % CIs) were calculated to estimate the association strength. Subgroup analyses according to ethnicity, source of control, and sample size were also conducted. A total of 15 eligible studies, including 4,687 gastric cancer cases and 7,002 controls, were identified. We found that the GSTM1 null genotype was associated with increased risk of gastric cancer among ever-smokers (OR = 1.460, 95 % CI 1.064–2.003, heterogeneity: P = 0.019). The null genotype also significantly increased the risk of gastric cancer among non-smokers (OR = 1.777, 95 % CI 1.301–2.426, heterogeneity: P < 0.01). Stratified analysis according to ethnicity showed that the GSTM1 null genotype was associated with increased risk of gastric cancer among Asians both in ever-smokers (OR = 1.841, 95 % CI 1.184–2.861) and non-smokers (OR = 1.773, 95 % CI 1.382–2.275). In conclusion, the GSMT1 null genotype significantly increased the risk of gastric cancer both in ever-smokers and non-smokers.

The prognostic significance of HER2 expression in patients with gastric cancer remains controversial, partially due to the significant heterogeneity of the approaches and criteria used for HER2 assessment among different studies. We therefore conducted a meta-analysis enrolling only studies defining HER2 status by trastuzumab for gastric cancer (ToGA) criteria. Published studies investigating the association between HER2 expression and survival were identified. Only publications that defined HER2 expression using ToGA criteria were enrolled. Meta-analyses were performed by Revman 5.2. Pooled hazard ratio (HR) and its 95 % confidence interval (CI) were calculated to evaluate the risk of disease. A total of 11 studies were enrolled in meta-analyses. Pooled data of nine studies using univariate analysis showed that HER2 expression is not associated with overall survival (OS; pooled HR, 0.97; 95 % CI, 0.84-1.12; P = 0.63), which are maintained in six studies of multivariate analysis (pooled HR, 1.01; 95 % CI, 0.75-1.35; P = 0.95). The Q statistic test for nine studies of univariate analysis and for six studies of multivariate analysis showed no and low heterogeneity (I (2) = 22 % and P = 0.25; I (2) = 41 % and P = 0.13, respectively). Furthermore, pooled data of four studies without heterogeneity (I (2) = 0 %, P = 0.74) showed that HER2 expression were not associated with relapse-free survival as well, with a pooled HR of 1.08 (95 % CI, 0.84-1.37; P = 0.55) in patients with HER2 expression. In conclusion, this meta-analysis indicated that HER2 expression based on ToGA criteria is not related to the survival in patients with gastric cancer.

The molecular biomarkers human epidermal growth factor receptor-2 (HER2) and trefoil factor 3 (TFF3) are reported to play important roles in the pathogenesis of gastric cancer (GC). In this study, we investigated the clinicopathological and prognostic significance of TFF3 and HER2 expression in GC and explored the correlation between these two biomarkers. Ninety-two patients who were diagnosed with GC were enrolled. TFF3 and HER2 expression was determined on tumor tissues. The results showed that TFF3 and HER2 were positively expressed in 42.7 and 10.9 % of the cases, respectively. There were significantly higher rates of TFF3 positivity in patients with deep invasive tumors and advanced stage ones. Patients with negative TFF3 staining survived longer than those with the presence of TFF3, with 5-year overall survival (OS) rates of 57.1 ± 7.1 and 39.5 ± 7.5 %, respectively ( P = 0.033). However, HER2 positivity was not significantly associated with OS ( P = 0.262). Multivariate analysis demonstrated TFF3 expression to be an independent indicator for short-term survival, with a hazard ratio of 2.327 (95 % confidence interval (CI), 1.202–4.507, P = 0.012). There was a trend that the expression of TFF3 was more frequent in HER2 negative tumors than in HER2 positive ones (positive rates: 16.3 vs. 4.7 %, P = 0.098). Patients with HER2-negative/TFF3-negative GC presented higher OS than those with other phenotypes ( P = 0.009). This study suggests that TFF3 is an independent indicator for survival in GC, while HER2 is not associated with the outcome. Patients with HER2-negative/TFF3-negative GC have the best outcome.

BACKGROUND:Gastric cancer remains a major health issue and a leading cause of death worldwide. This study presented a long-term survival data of gastric cancer registered in Shanghai of China from 1972-2003, with aims to describe the trends as well as the age, sex, stage and tumor sites specific characteristics.METHODS:The main source of information on cancer cases was the notification card sending to the registry. The residential status of cancer cases was confirmed by home-visits. The methods of follow-up have been a mixture of both active and passive ones.RESULTS:We observed an increased trend of survival probability during the last decades. Patients diagnosed during 1972-1976 had a 5-years relative survival rate at 12% for males and 11% for females, respectively, which had dramatically increased to 30% for male and 32% for female patients respectively during the period of 2002-2003. Among the patients diagnosed in 2002-2003, the overall survival probability declined with patient's age at the time of diagnosis. The lowest survival rate was observed among the oldest group, with the median survival time of 0.8 years. Patients diagnosed with stage I had a higher relative survival rate. Patients with cardia cancer had the worst prognosis, with the 5-year relative survival rate of 29%.CONCLUSIONS:The survival probability of patients with gastric cancer in Shanghai has improved significantly during the last decades. Age, stage and site of tumor have an impact on prognosis.

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

High intensity focused ultrasound (HIFU) is a novel therapeutic modality. Several preclinical and clinical studies have investigated the safety and efficacy of HIFU for treating solid tumours, including pancreatic cancer. Preliminary studies suggest that HIFU may be useful for the palliative therapy of cancer-related pain in patients with unresectable pancreatic cancer. This review provides a brief overview of HIFU, describes current clinical applications of HIFU for pancreatic cancer, and discusses future applications and challenges.