ObjectiveTo review the research advances about myeloid derived suppressor cells(MDSC)and pancreatic cancer, and explore the future research trends. MethodRelated literatures in recent 5 years from abroad databases(PubMed, Web of Science, and EMBASE)and domestic databases(CNKI, WANFANG, and WEIPU)were collected and reviewed. ResultsThe MDSC was the core of tumor immune regulation network in pancreatic cancer microenvironment, it formed a complicated feedback with the pancreatic cancer and the stellate cells. MDSC could promote the cancerogensis and progression of pancreatic cancer, and the accumulation of MDSC in peripheral blood of pancreatic cancer patient could predict the poor prognosis. However up to now, the literatures about the relation between MDSC and the chemotherapy and metastasis of pancreatic cancer were limited. ConclusionsThe comprehensive therapy by targeting MDSC of pancreatic cancer is promising. However, many issues need to be further investigated.
Objective To explore changes and challenges on management of chronic pancreatitis. Methods The updated clinical guidelines and the latest research findings were collected and reviewed. Results The proposition of a new mechanistic definition and identification of an early stage give us a novel insight into chronic pancreatitis. The intraductal pancreatic calcifications has been regarded as the most reliable ultrasonography and CT features of chronic pancreatitis. In addition, the endoscopic ultrasonography is also of great value. The present surgical strategies are established on the concepts of step-up approach and damage control. The surgery perform better than the endoscopic treatment in the long-term outcome, but the timing course of surgery need to be further investigated. Conclusions Early diagnosis and treatment plays a critical role in cases of chronic pancreatitis. More patients of chronic pancreatitis should be treated in a multidisciplinary team as future perspectives.
Objective To investigate the diagnosis and treatment of the liver hydatidosis in nonpastureland. Methods Clinical features of 16 patients with liver hydatidosis were analyzed retrospectively. Results Only 8 of 16 patients possessed the clinical symptoms and 8 patients had had history of inhabitancy in epidemic area. Casoni test and indirect hemagglutination showed a sensitivity of 90% and the correct diagnostic rate of CT was higher than that of B-ultrasound examination. The main effective treatment of the liver hydatidosis was surgical, 15 out of 16 patients received surgical treatment. In this series, the curative effect was good without any death, allergic reaction and implantation. Conclusion The cystic lesion of liver should be considered as liver hydatidosis and Casoni test, indirect hemagglutination, together with CT and B-us examination can be used to comfirm the diagnosis though no clinical symptoms and history of inhabitancy in epidemic area presented. Surgical operation is the main effective treatment for liver hydatidosis.
Objective To evaluate the utility of collagen-gel droplet embedded-culture drug sensitivity test (CD-DST) in pancreatic carcinoma cell by compared with WST-8. Methods The chemosensitivity to 5-fluorouracil (5-FU), gemzar (GEM) and oxaliplatin (OXA) of pancreatic adenocarcinoma cells SW1990, PCT-3 and ASPC-1 were tested by WST-8 and CD-DST respectively. Results In a certain living cell number range (500-10 000), there was a linear correlation (r=0.991 1, P＜0.05) between the integral optical density in CD-DST and the cell number. The inhibition ratios of three kinds of cell growth tested by CD-DST were higher than those tested by WST-8 (P＜0.05). The results of drug chemosensitivity to 5-FU， GEM and OXA detected by two methods were uniform. Conclusion The CD-DST can be used to assay the drug chemosensitivity in vitro for pancreatic carcinoma.
【Abstract】Objective To investigate the possible mechanism of gemcitabine resistance in pancreatic cancer chemotherapy. Methods Recent literatures about the genes and signal pathways those play key roles in mediating gemcitabine chemotherapy resistance of pancreatic cancer were collected and reviewed.Results Oncogenes like c-Src and bcl-XL, inflammation pathway of NF-κB, cytokines like IL-1β and NO are closely related with the chemoresistance； the relationship between multiple drug resistance relevant genes like MDR1/P-gP and the resistance to gemcitabine remains to be clarified. Conclusion Genes and pathways like c-Src, bcl-XL, NF-κB, etc. might become new targets to increase the chemotherapeutic sensitivity of pancreatic cancer, however, the mechanism of pancreatic cancer chemotherapy resistance still needs further to be studied.
Objective To investigate the mechanism of the resistance of pancreatic cancer cells to tumor necrosis factor related apoptosis inducing ligand (TRAIL)mediated apoptosis. MethodsThe expression of TRAIL receptor-4 (TRAIL-R4) in normal pancreas tissue and pancreatic cancer was analyzed by using Northern blotting, Western blotting and immunohistochemistry.ResultsTRAIL-R4 mRNA and protein were expressed at moderate to high levels in human pancreatic cancer, but demonstrated weak to negative in the normal pancreas. Moreover, pancreatic cancer cells showed b TRAIL-R4 immunostaining throughout the tumor mass. Conclusion TRAIL-R4 levels are significantly different in pancreatic cancer in comparison to the normal pancreas. These findings give new insights into the resistance mechanisms of pancreatic cancer cells towards TRAILmediated apoptosis.
Objective To introduce the research progress in the effect of chemotherapeutic resistance of metabolic enzymes of gemcitabine to pancreatic cancer.Methods Recent literatures about metabolic enzymes that played key roles in mediating gemcitabine chemotherapeutic resistance of pancreatic cancer were collected and reviewed. Results The metabolic enzymes of gemcitabine, such as hENT1, dCK, RRM1 and CDA, were closely related to chemotherapeutic resistance of pancreatic cancer. The relationship between the single nucleotide polymorphism of metabolic enzymes and the resistance to gemcitabine remained to be clarified. Conclusion Multiple factors are involved in the mechanism of chemotherapeutic resistance of pancreatic cancer to gemcitabine, which needs further research.