Galectin-1 is implicated in making tumor cells immune privileged, in part by regulating the survival of infiltrating T cells. Galectin-1 is strongly expressed in activated pancreatic stellate cells (PSCs); however, whether this is linked to tumor cell immune escape in pancreatic cancer is unknown. Galectin-1 was knocked down in PSCs isolated from pancreatic tissues using small interfering RNA (siRNA), or overexpressed using recombinant lentiviruses, and the PSCs were cocultured with T cells. CD31 , CD4 1 and CD8 1 T cell apoptosis was detected by flow cytometry; T cell IL-2, IL-4, IL-5 and INF-c production levels were quantified using ELISA. Immunohistochemical analysis showed increased numbers of PSCs expressed Galectin-1 (p < 0.01) and pancreatic cancers had increased CD3 1 T cell densities (p < 0.01) compared to normal pancreas or chronic pancreatitis samples. In coculture experiments, PSCs that overexpressed Galectin-1 induced apoptosis of CD4 1 T cells (p < 0.01) and 05). Supernatants from T cells cocultured with PSCs that overexpressedGalectin-1 contained significantly increased levels of Th2 cytokines (IL-4 and IL-5, p < 0.01) and decreased Th1 cytokines (IL-2 and INF-c, p < 0.01). However, the knockdown of PSC Galectin-1 had the opposite effect on Th1 and Th2 cytokine secretion. Our study suggests that the overexpression of Galectin-1 in PSCs induced T cell apoptosis and Th2 cytokine secretion, which may regulate PSC-dependent immunoprivilege in the pancreatic cancer microenvironment. Galectin-1 may provide a novel candidate target for pancreatic cancer immunotherapy.Pancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive malignancy, which is resistant to currently available systemic therapies. PDAC has one of the worst prognoses of all human cancers with incidence rates nearly equal to mortality rates. 1 There is evidence that excessive desmoplasia play a crucial role in the aggressive behavior of pancreatic cancer, 2 which impedes effective systemic treatments on a molecular level. Pancreatic stellate cells (PSCs) are stellate-shaped mesenchymal pancreatic cells, which have been identified as important regulators of desmoplasia in PDAC. 3In their quiescent state, PSCs can be identified by the presence of vitamin A-containing lipid droplets in the cytoplasm and the expression of desmin and glial-fibrillary-acidic protein (GFAP). 4 In response to pancreatic damage or stress, PSC are transformed into an activated myofibroblast-like phenotype. Activated PSCs express a-smooth muscle actin (a-SMA), and synthesize excessive amounts of ECM proteins, including Collagen I and III, fibronectin and matrix-degrading enzymes such as MMPs.5-7 Activated PSCs have a variety of cell functions and can promote the proliferation, migration, invasion and metastasis of pancreatic cancer cells; 1,8,9 however, the factors that PSCs secrete to advance pancreatic cancer progression remain largely unknown.Galectin-1, a member of the galectin family of b-galactosidebinding proteins, is a homodimer of 14-kDa subunits pos...

ObjectivesTo assess the efficacy and safety of propofol sedation for gastrointestinal endoscopy, we conducted a meta-analysis of randomized controlled trials (RCTs) comparing propofol with traditional sedative agents.MethodsRCTs comparing the effects of propofol and traditional sedative agents during gastrointestinal endoscopy were found on MEDLINE, the Cochrane Central Register of Controlled Trials, and EMBASE. Cardiopulmonary complications (i.e., hypoxia, hypotension, arrhythmia, and apnea) and sedation profiles were assessed.ResultsTwenty-two original RCTs investigating a total of 1,798 patients, of whom 912 received propofol only and 886 received traditional sedative agents only, met the inclusion criteria. Propofol use was associated with shorter recovery (13 studies, 1,165 patients; WMD –19.75; 95% CI –27.65, 11.86) and discharge times (seven studies, 471 patients; WMD –29.48; 95% CI –44.13, –14.83), higher post-anesthesia recovery scores (four studies, 503 patients; WMD 2.03; 95% CI 1.59, 2.46), better sedation (nine studies, 592 patients; OR 4.78; 95% CI 2.56, 8.93), and greater patient cooperation (six studies, 709 patients; WMD 1.27; 95% CI 0.53, 2.02), as well as more local pain on injection (six studies, 547 patients; OR 10.19; 95% CI 3.93, 26.39). Effects of propofol on cardiopulmonary complications, procedure duration, amnesia, pain during endoscopy, and patient satisfaction were not found to be significantly different from those of traditional sedative agents.ConclusionsPropofol is safe and effective for gastrointestinal endoscopy procedures and is associated with shorter recovery and discharge periods, higher post-anesthesia recovery scores, better sedation, and greater patient cooperation than traditional sedation, without an increase in cardiopulmonary complications. Care should be taken when extrapolating our results to specific practice settings and high-risk patient subgroups.

CAF-derived galectin-1 significantly promotes angiogenesis in gastric cancer and may be a target for angiostatic therapy.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most common malignant tumors with poor prognosis due to extremely high malignancy, low rate of eligibility for surgical resection and chemoradiation resistance. Increasing evidence indicate that the interaction between activated pancreatic stellate cells (PSCs) and PDAC cells plays an important role in the development of PDAC. By producing high levels of cytokines, chemotactic factors, growth factors and excessive extracellular matrix (ECM), PSCs create desmoplasia and a hypoxic microenvironment that promote the initiation, development, evasion of immune surveillance, invasion, metastasis and resistance to chemoradiation of PDAC. Therefore, targeting the interaction between PSCs and PDAC cells may represent a novel therapeutic approach to advanced PDAC, especially therapies that target PSCs of the pancreatic tumor microenvironment.Pancreatic ductal adenocarcinoma (PDAC) is the most common and lethal malignant tumors in humans with very poor prognosis, due to a variety of causes including the insidious onset, absence of efficient screening methods for early detection, low rate of surgical resection at the time of clinical presentation and chemoradiation resistance. 1 Although scholars have been committed during the last three decades to studying genetic and/or epigenetic molecular changes of PDAC cells and chemotherapy with a combination of cytotoxic drugs have been implemented, the survival of patients with PDAC has not yet significantly improved.2,3 Until recently, an encouraging FOLFIRINOX scheme was reported to provide a statistically and clinically significant benefit over single-agent gemcitabine in patients with advanced PDAC but Key words: pancreatic ductal adenocarcinoma, pancreatic stellate cells, tumor microenvironment Abbreviations: ADMR: adrenomedullin receptor; AM: adrenomedullin; ATRA: all-trans retinoic acid; CTGF: connective tissue growth factor; DCs: dendritic cells; ECM: extracellular matrix; EGF: epidermal growth factor; EMMPRIN: extracellular matrix metalloproteinase inducer; EMT: epithelial-mesenchymal transition; ET-1: endothelin-1; FGF: fibroblast-growth-factor; GFAP: glial-fibrillary-acidic protein; HGF: hepatocyte growth factor; HPDE: human pancreatic duct epithelial; HSCs: hepatic stellate cells; HUVEC: endothelial cells; IGF-1: insulin-like growth factor-1; IL: interleukin; MMPs: matrix metalloproteinases; NADPH: nicotinamide adenine dinucleotide phosphate; NO: nitric oxide; PAEE: palmitic acid ethyl ester; PCLMs: pancreatic cancer liver metastases; PDAC: pancreatic ductal adenocarcinoma; PDGF: platelet-derived growth factor; PEDF: pigment epithelium-derived factor; PK: prokineticin; PKR: prokineticin receptor; PSCs: pancreatic stellate cells; ROS: oxygen species; Runx-2: Runt-related transcription factor-2; SDF-1: stromal cell-derived factor-1; sFRP4: secreted frizzled-related protein 4; SMO: smoothened; a-SMA: a-smooth muscle actin; SPARC: secreted protein acidic and rich in cysteine; TFF1: trefoil factor 1; TGF-b: transforming gr...

The occurrence of in-hospital postoperative complications was an independent predictor of worse 5-year overall survival rate after radical resection of gastric cancer.

Colorectal cancer is the third largest cancer in worldwide and has been proven to be closely related to the intestinal microbiota. Many reports and clinical studies have shown that intestinal microbial behavior may lead to pathological changes in the host intestines. The changes can be divided into epigenetic changes and carcinogenic changes at the gene level, which ultimately promote the production and development of colorectal cancer. This article reviews the pathways of microbial signaling in the intestinal epithelial barrier, the role of microbiota in inflammatory colorectal tumors, and typical microbial carcinogenesis. Finally, by gaining a deeper understanding of the intestinal microbiota, we hope to achieve the goal of treating colorectal cancer using current microbiota technologies, such as fecal microbiological transplantation.

BackgroundGalectin-1, a member of carbohydrate-binding proteins with a polyvalent function on tumor progression, was found strongly expressed in pancreatic satellite cells (PSCs), which partner in crime with cancer cells and promote the development of pancreatic ductal adenocarcinoma (PDAC). We evaluated the effects of PSCs derived Galectin-1 on the progression of PDAC, as well as the tumor establishment and development in mouse xenografts.MethodsThe relationship between immunohistochemistry staining intensity of Galectin-1 and clinicopathologic variables were assessed in 66 PDAC tissues, 18 chronic pancreatitis tissues and 10 normal controls. The roles of PSCs isolated from PDAC and normal pancreas on the proliferative activity, MMP2 and MMP9 expression, and the invasion of CFPAC-1 in the co-cultured system, as well as on the tumor establishment and development in mouse xenografts by mixed implanting with CFPAC-1 subcutaneously were evaluated.ResultsGalectin-1 expression was gradually increased from normal pancreas (negative), chronic pancreatitis (weak) to PDAC (strong), in which Galectin-1 expression was also increased from well, moderately to poorly differentiated PDAC. Galectin-1 staining intensity of pancreatic cancer tissue was associated with increase in tumor size, lymph node metastasis, perineural invasion and differentiation and UICC stage, and served as the independent prognostic indicator of poor survival of pancreatic cancer. In vitro and in vivo experiments indicated that TGF-β1 upregulated Galectin-1 expression in PSCs, which could further promotes the proliferative activity, MMP2 and MMP9 expression, and invasion of pancreatic cancer cells, as well as the tumor establishment and growth.ConclusionGalectin-1 expression in stromal cells of pancreatic cancer suggests that this protein plays a role in the promotion of cancer cells invasion and metastasis and provides a therapeutic target for the treatment of pancreatic cancer.

Diagnostic and prognostic value of the methylation status of secreted frizzledrelated protein 2 in colorectal cancer AbstractPurpose: e aim of this study was to investigate the diagnostic and prognostic signicance of the methylation status of secreted frizzled-related protein 2 (SFRP2) in colorectal cancer (CRC).Methods: Methylation-speci c PCR assay was performed to analyze SFRP2 promoter methylation in solid tissue, stool and serum samples collected from 169 CRC patients, 63 patients with advanced adenomas, 46 patients with non-adenomatous polyps and 30 normal healthy controls.