ObjectiveTo explore the values of CA19-9, CA242, CEA, and CA125 single or combined detection on clinical diagnosis and prognosis for patients with pancreatic cancer. MethodsSerum tumor markers CA199, CA242, CEA, and CA125 of 63 patients with pancreatic cancer, 33 patients with cancer of bile duct, and 27 patients with benign pancreatic disease were detected, and those patients were followed up after operation. ResultsThe levels of CA19-9, CA242, CEA, and CA125 in patients with pancreatic cancer were significantly higher than those in patients with benign pancreatic disease and cancer of bile duct (Plt;0.05). The sensitivity of CA19-9 alone was the highest in the four tumor markers for the patients with pancreatic cancer 〔79.4% (50/63)〕, but the specificity (61.9%) was lower than that of CA242 (83.3%) and CEA (80.0%). The specificity of combined detection of CA199+CA242+CEA was the highest 〔93.3% (56/60)〕. The level of CA19-9 in carcinoma of body/tail of pancreas was significantly higher than that of carcinoma of pancreas head or whole pancreas (Plt;0.05). The serum levels of CA19-9 and CA242 in patients with stage Ⅳ were significantly higher than those in stage Ⅰ or Ⅱ/Ⅲ (Plt;0.05). Fifteen patients were lost to follow up, 48 patients were followed up 2－12 months with an average 6 months. The levels of CA242 and CA199 in patients with pancreatic cancer on 0.5 month and 3 months after operation were lower than those before operation (Plt;0.05). ConclusionsSingle detection of CA19-9 can improve the diagnostic sensitivity, and combined detection of tumor markers CA199+CA242+CEA can improve the diagnostic specificity. CA19-9 or CA242 is a valuable marker for evaluating treatment effects and estimating prognosis.
【 Abstract 】 Objective Overexpressions of epidermal growth factor (EGF) and EGF receptor have been associated with progression and invasive phenotype of pancreatic cancer. However, the underlying molecular mechanism by which EGF worked in pancreatic cancer cells has not been completely understood. In this study, effect of EGF on the invasion and metastasis of pancreatic cancer cells and its regulatory mechanism were investigated. Methods The effects of EGF on the proliferation, adhesion and invasion of pancreatic cancer cells were detected by WST-1 proliferation assay, adhesion assay and invasive assay, respectively. The activity and expression of MMP-2 and MMP-9 were examined by zymography, Western blot and RT-PCR, respectively. The activity of NF- κ B was examined by EMSA. Results EGF could significantly promote the invasiveness of pancreatic cancer cells but did not affect cell proliferation or adhesion. The expressions of NF- κ B and MMP-9 were significantly increased by EGF, but EGF did not affect the activity and expression of MMP-2. Furthermore, EGF stimulated the NF- κ B binding activity. Pretreatment with NF- κ B inhibitors, pyrrolidine dithiocarbamate (PDTC), could significantly inhibit the activity of NF- κ B induced by EGF. Meanwhile, the EGF-induced expression and activity of MMP-9, as well as cell invasiveness were also inhibited by NF- κ B inhibitor. Conclusion EGF could increase the expression and promote the invasiveness of MMP-9 via the activation of NF- κ B in pancreatic cancer cells, which implies that NF- κ B inhibitant, such as PDTC, may diminish the invasiveness of pancreatic cancer cells.
【Abstract】ObjectiveTo establish adriamycin (ADM) resistant pancreatic cancer cell line SW1990/ADM and to investigate its drug resistance mechanism.MethodsADM-resistant pancreatic cancer cell line SW1990/ADM was obtained by culture of pancreatic cancer cell line SW1990 in vitro with intermittently increasing the concentration of ADM in the culture medium for ten months. After two months of drug free culture, its biological characteristics, drug sensitivity as well as the expression and function of multidrug resistant gene 1 (mdr1) were detected, respectively. ResultsCompared with the parental cell line, SW1990/ADM showed great changes in biological characteristics and developed a cross resistance to various chemotherapy drugs. The drug resistance indexes of cell line SW1990/ADM to ADM, mitomycin, fluorouracil and gemcitabine were 49.60, 7.25, 3.80 and 1.25, respectively. The level of mdr1 mRNA expression in cell line SW1990/ADM was much higher than that of the parental cell line（P＜0.01). ConclusionWe have established adriamycin resistant pancreatic cancer cell line SW1990/ADM with multidrug resistance phenotype, its multidrug resistance is positively relevant to the expression of mdr1.
Objective To summarize the domestic and abroad articles related to the research on the relation between microRNA （miRNA） and pancreatic cancer，and explore the important effects of miRNA expression patterns in diagnosis of pancreatic cancer. Methods “microRNA and pancreatic cancer” were searched as key words by PubMed and CNKI series full-text database retrieval systems from 2000 to 2012. Totally 60 English papers and 15 Chinese papers were obtained. Choice criteria：the basic research of miRNA and pancreatic cancer，the clinical research of miRNA and pancreatic cancer， and the prospect of miRNA in pancreatic cancer diagnosis and treatment. According to the choice criteria，31 papers were finally analyzed. Results The miRNA expression spectrum and specific miRNA expression such as miR-21，miR-34，miR-217，miR-196a，miR-10a，miR-155，miR-221，miR-222，miR-181a，miR-181b，miR-181d， and the family members of miR-200 and let-7 might be used as tumor markers to differentiate pancreatic cancer from normal pancreas，chronic pancreatitis or pancreatic endocrine tumors，and might be used as prognostic factor to predict the outcome. Conclusions miRNA expression spectrum are not only related to diagnosis of pancreatic cancer， but also have provided a new research direction and method for gene therapy of pancreatic cancer．
ObjectiveTo investigate the indications and clinical effect of pancreatoduodenectomy with extended lymphadenectomy for pancreatic head carcinoma. MethodsThe clinical data of 21 patients with pancreatic head carcinoma that performed pancreatoduodenectomy with extended lymphadenectomy between June 2010 to June 2011 in Union Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology were retrospective analyzed. The 21 patients included 15 men and 6 women with an age range of 36-57 years and an average age of 47.8 years. ResultsThere were 3 cases(14.3%), 9 cases(42.9%), 8 cases(38.1%), and 1 case(4.8%) in stageⅠ, ⅡA, ⅡB, andⅢ, respectively. Eighteen cases had a R0 resection(85.7%) and 3 cases had a R1 resection. The total number of resected lymph nodes were 14-43 with an average of 27.4. Lymph node invasion occurred in 10 cases(47.6%). The average operative time was 6.8 h(5-8.5 h) and the average amount of blood transfusion was 5.6 U(3-8 U). There was no death in this group and 5 cases(23.8%) had postoperative complications. Tree cases(14.3%) developed pancreatic fistula, 1 case(4.8%) developed bile leakage, 1 case(4.8%) developed abdominal hemorrhage, 1 case(4.8%) developed gastrointestinal bleeding, and 2 cases(9.5%) developed intractable diarrhea. Postoperative pathological results in high, medium, and low differentiated adenocarcinoma was 6 cases(28.6%), 10 cases(47.6%), and 5 cases(23.8%), respec-tively. Twenty one cases were followed-up, the follow-up time ranged from 5 to 40 months with a median time of 19 months. 1-, 2-, and 3-year cumulative survival rates was 66.7%, 38.1%, and 19%, respectively. ConclusionSelective application of pancreatoduodenectomy with extended lymphadenectomy in resectable pancreatic head carcinoma is conducive to increase the proportion of the radical resection and improve the prognosis, but the postoperative complications is higher.
Objective To search for the significant gene indicators in the diagnosis of pancreatic cancer. Methods Literatures about genetic diagnosis of pancreatic cancer were collected and reviewed. Results K-ras, p53, DPC4 and telomerase genes were considered to play important roles in the diagnosis of pancreatic cancer. Conclusion Detection of the genes related to pancreatic cancer may be of helpful in early diagnosis of pancreatic cancer.
Objective To investigate the invasion ability of Panc-1 cells in vivo and in vitro af ter being t ransfected with tissue factor pathway inhibitor 2 gene ( TFPI-2) . Methods The expression vector pEGFP-C1-TFPI-2 was transfected into human pancreatic cancer line Panc-1 cells by using liposome. TFPI-2 mRNA and protein of transfected and nontransfected cells were detected by reverse t ranscription-polymerase chain reaction (RT-PCR) and Western blot respectively. The tumor cells invasive behavior of t ransfected ( Panc-1-TFPI-2) and nontransfected ( Panc-1-V and Panc-1-P) cells were assessed in vitro through Boyden Chamber method. The transfected and nontransfected cells were implanted into nude mice to observe it s growth and metastasis in vivo. Results Expressions of mRNA and protein of TFPI-2 were confirmed in transfected cells. Af ter TFPI-2 t ransfection , the number of Panc-1-TFPI-2 , Panc-1-V and Panc-1-P cells passing through membrane of Boyden Chamber were 24. 4 ±3. 5 ,61. 3 ±4. 1 and 60. 2 ±3. 9 , respectively. The number of TFPI-2-expressing cells to t raverse a Matrigel-coated membrane was obviously decreased compared with that of non-expressing cells , the invasion ability was lower than that before transfection in vitro. The subcutaneous tumor volume of the Panc-1-TFPI-2 group was (438. 0 ±69. 8) mm3 , the Panc-1-V group was (852. 0 ±102. 9) mm3 and the Panc-1-P group was (831. 0 ±78. 1) mm3 , P lt; 0. 05. The metastasis to liver and lung and muscular invasion occurred in the Panc-1-V group and the Panc-1-P group. There were no muscular invasion and metastatic lesions in the Panc-1-TFPI-2 group. Conclusion TFPI-2 gene expression may obviously inhibit the invasion ability of pancreatic cancer cells in vitro and in vivo , which provides an experimental basis for the treatment of human pancreatic cancer by gene therapy.
bjectiveTo study the therapeutic effect and mechanism of photodynamic therapy (PDT) to the nude mice model of pancreatic cancer by intratumoral injecting photosensitizers hematoporphyrin derivatives (HpD), hypocrellin A (HA) and 2butylamino2demethoxyhypocrellin A (2BA2DMHA).MethodsThe animal model of human pancreatic cancer was developed by injecting human pancreatic cancer cells SW1990 into the back of the nude mice. After photosensitizers HpD, HA and 2BA2DMHA was given by the intratumoral injection, the 632.8 nm HeNe laser was used to irradiate the tumor. The curative effect was recorded and factorⅧ was used in the immunohistochemical staining to study the vessel change. ResultsPDT can destroy the pancreatic neoplasm, the tumor growth rate was significantly reduced after PDT. The immunohistochemical staining showed PDT could make injury to vessel endothelial cell.ConclusionPDT can induce injuries of pancreatic cancer; vascular injury is an important way to exert function.
【Abstract】Objective To analyze the function of BAG3 in antiapoptosis and chemotherapy resistance induction process of pancreatic cancer.Methods The expressions of BAG-3 in pancreatic cancerous tissues of patients with chemotherapy and those without chemotherapy before resection were determined by immunohistochemistry. The expression difference of BAG-3 protein 18 hours after cultured with chemotherapy drugs (concentration of drugs: 5-FU 50 μg/ml, MMC 0.5 μg/ml, EADM 1.5 μg/ml) of 3 pancreatic cancer cell lines （MIACaPa-2, PANC-1, SW1990） was measured through Western blotting method.Results The median positive rate of pancreatic cancer tissue from patients accepted chemotherapy before resection was higher than those not accepted chemotherapy, but there wasn’t significant difference. Eighteen hours after cultured with drugs, the level of BAG-3 of this three cell lines had significant increased compared with control group (P＜0.05). Conclusion Chemotherapy induces elevation of BAG-3 expression of pancreatic cancer. The upregulate of BAG-3 may associate with the chemotherapy resistance induced by drugs.
【Abstract】Objective To investigate the relationship between the development of pancreatic cancer and inflammation, and the therapy strategy.Methods Related articles were reviewed.Results The pathogenesis of inflammation in pancreatic cancer development involves cytokines, NF-κB, COX-2, PPAR-γ, DNA damage, gene changes，etc. Based on these mechanisms some medications are under developing. Conclusion Accumulative effects of pancreatic inflammation may lead to DNA changes, and even pancreatic cancer development. Medications aimed at suppressing pancreatic inflammation may help with prevention and treatment of pancreatic cancer.