Prediction of subsolid pulmonary nodule growth rate using radiomics.

BACKGROUND: Pulmonary nodule growth rate assessment is critical in the management of subsolid pulmonary nodules (SSNs) during clinical follow-up. The present study aimed to develop a model to predict the growth rate of SSNs. METHODS: A total of 273 growing SSNs with clinical information and 857 computed tomography (CT) scans were retrospectively analyzed. The images were randomly divided into training and validation sets. All images were categorized into fast-growth (volume doubling time (VDT) ≤ 400 days) and slow-growth (VDT > 400 days) groups. Models for predicting the growth rate of SSNs were developed using radiomics and clinical features. The models' performance was evaluated using the area under the curve (AUC) values for the receiver operating characteristic curve. RESULTS: The fast- and slow-growth groups included 108 and 749 scans, respectively, and 10 radiomics features and three radiographic features (nodule density, presence of spiculation, and presence of vascular changes) were selected to predict the growth rate of SSNs. The nomogram integrating radiomics and radiographic features (AUC = 0.928 and AUC = 0.905, respectively) performed better than the radiographic (AUC = 0.668 and AUC = 0.689, respectively) and radiomics (AUC = 0.888 and AUC = 0.816, respectively) models alone in both the training and validation sets. CONCLUSION: The nomogram model developed by combining radiomics with radiographic features can predict the growth rate of SSNs more accurately than traditional radiographic models. It can also optimize clinical treatment decisions for patients with SSNs and improve their long-term management.

Endovascular Repair of Celiac Artery Aneurysm with the Use of Stent Grafts.

PURPOSE: To determine the feasibility, safety, and long-term outcome of stent-graft insertion for endovascular repair of celiac artery aneurysm (CAA). MATERIALS AND METHODS: From January 2010 to April 2015, 10 patients (three men and seven women; mean age, 51.6 y ± 12.1; age range, 39-81 y) with CAAs underwent endovascular repair via stent-graft insertion in a single center. During treatment, the stent graft was placed at the celiac and common hepatic arteries. Standard follow-up protocol included abdominal CT angiography and clinical examinations at 1, 3, 6, and 12 months and annually thereafter. Follow-up was performed every 2-3 months via telephone for the duration of the follow-up period to confirm patients' general condition. Data on patient characteristics, technical success, procedure-related complications, and follow-up were collected and analyzed retrospectively. RESULTS: CAA was successfully sealed by the stent graft in all patients. The common hepatic artery was patent after stent insertion in all patients, and no procedure-related complication occurred. All patients were followed up for 1-64 months (mean, 19.3 mo ± 18.9). Abdominal CT angiography demonstrated no endoleak, stent obstruction, or splenic infarction during follow-up. All patients experienced CAA shrinkage with formation of thrombi or increase in the quantity of thrombi in the CAA sac. CONCLUSIONS: Stent-graft insertion is a safe and effective method for endovascular repair of CAA.

Percutaneous recanalization for combined-type Budd-Chiari syndrome: strategy and long-term outcome.

PURPOSE: To investigate the feasibility, strategy, and long-term outcome of percutaneous recanalization for combined-type Budd-Chiari syndrome (BCS). METHODS: From December 2007 to August 2014, consecutive symptomatic combined-type BCS patients were treated by percutaneous recanalization in our centers. Inferior vena cava (IVC) recanalization was the first-stage treatment for all patients. Recanalization of one hepatic vein (HV) was the second-stage treatment for the selected patients. If the patient had the compensatory and patent accessory HV (AHV), we observed this patient for 7 days after IVC recanalization. If the symptoms of portal hypertension improved, HV recanalization was not needed. Otherwise, HV recanalization was performed. If the patient had no patent AHV, HV recanalization was performed 3 days after IVC recanalization. Data on technical success, clinical success, and follow-up were analyzed, respectively. RESULTS: Sixty-two symptomatic combined-type BCS patients were enrolled. Technical success of percutaneous recanalization was achieved in 60 patients. Among them, 52 patients had the patent AHV and underwent single IVC recanalization, and 8 patients had no patent AHV and underwent combined IVC and HV recanalization. Clinical success was achieved in all of the 60 patients. Three patients died during the follow-up. The cumulative 1-, 2-, and 4-year survival rates were 98.3%, 96.5%, and 92.7%, respectively. CONCLUSION: Percutaneous recanalization is suitable for most combined-type BCS patients. Treatment strategy can be made according to the situation of AHV. If the patient has the patent AHV, single IVC recanalization is enough. Otherwise, combined IVC and HV recanalization should be performed.

A randomized clinical trial of nerve block to manage end-stage pancreatic cancerous pain.

Pain control is the most difficult puzzle in patients with terminal pancreatic cancerous pain. Many methods in clinical practice fail in 20 ~ 50% of patients. The present study aims to explore the effect of nerve block on patients with end-stage pancreatic cancerous pain. In this study, 100 subjects with end-stage pancreatic cancerous pain were enrolled and randomly assigned into two groups: 68 in nerve block group (N) and 32 in sham group (S). One group was treated with nerve block and the other group with sham procedure as controls. The pain score (by visual analog scale (VAS)), pain duration, reduction of other analgesic medications, and quality of life (with questionnaire QLQ) were evaluated before and 3 months after interventions. Comparisons were performed between before and after intervention in nerve block group and sham group. The results indicated that compared with sham group, the subjects in nerve block group had significant reduction with pain score, pain duration, and other analgesic medications, as well as improvement of quality of life (P < 0.05, respectively). In conclusion, nerve block is an effective method for treating patients with end-stage pancreatic cancerous pain.

Effects of miR-16 plus CA19-9 detections on pancreatic cancer diagnostic performance.

BACKGROUND: Although the detection of serum carbohydrate antigen 19-9 (CA19-9) has traditionally been used for the diagonosis of pancreatic cancer, the specific markers are lacking. The miRNAs have been used as new diagnosic markers in cancer patients. The effects of miR-16 plus CA19-9 detections on pancreatic cancer diagnostic performance were analyzed in this study. METHODS AND RESULTS: 70 pancreatic cancer patients and 70 chronic pancreatitis patients were recruited from January 2011 to August 2012 and 50 healthy volunteers for comparison. Serum CA19-9 level was measured by a chemiluminescent method. Plasma miR-16 level was measured by a real-time reverse transcription-polymerase chain reaction method. The effects of detecting miR-16, CA19-9, and their combination on pancreatic cancer diagnosis were analyzed. The plasma miR-16 content of the pancreatic cancer group was higher than that of the chronic pancreatitis group (p < 0.05), but the contents of the two groups did not differ significantly. Combining miR-16 and CA19-9 detections significantly increased the sensitivity and specificity of pancreatic cancer diagnosis (LR+ > 20, LR- < 0.2). CONCLUSIONS: The combination of miR-16 and CA19-9 detections boosted the diagnostic performance in pancreatic cancer detection.

Signature of gene aberrant alternative splicing events in pancreatic adenocarcinoma prognosis.

Alternative splicing (AS), as an effective and universal mechanism of transcriptional regulation, is involved in the development and progression of cancer. Therefore, systematic analysis of alternative splicing in pancreatic adenocarcinoma (PAAD) is warranted. The corresponding clinical information of the RNA-Seq data and PAAD cohort was downloaded from the TCGA data portal. Then, a java application, SpliceSeq, was used to evaluate the RNA splicing pattern and calculate the splicing percentage index (PSI). Differentially expressed AS events (DEAS) were identified based on PSI values between PAAD cancer samples and normal samples of adjacent tissues. Kaplan-Meier and Cox regression analyses were used to assess the association between DEAS and patient clinical characteristics. Unsupervised cluster analysis used to reveal four clusters with different survival patterns. At the same time, GEO and TCGA combined with GTEx to verify the differential expression of AS gene and splicing factor. After rigorous filtering, a total of 45,313 AS events were identified, 1,546 of which were differentially expressed AS events. Nineteen DEAS were found to be associated with OS with a five-year overall survival rate of 0.946. And the subtype clusters results indicate that there are differences in the nature of individual AS that affect clinical outcomes. Results also identified 15 splicing factors associated with the prognosis of PAAD. And the splicing factors ESRP1 and RBM5 played an important role in the PAAD-associated AS events. The PAAD-associated AS events, splicing networks, and clusters identified in this study are valuable for deciphering the underlying mechanisms of AS in PAAD and may facilitate the establishment of therapeutic goals for further validation.

[GM-CSF gene-modified dendritic cell vaccine enhances antitumor immunity in vitro].

OBJECTIVE: To investigate if granulocyte-macrophage colony stimulating factor (GM-CSF) gene-modified dendritic cells (DC) enhance antitumor immunity in vitro. METHODS: Mice were injected with chemokine ligand 3 (CCL3) via the tail vein. Fresh B220(-)CD11c(+) cells were sorted from the peripheral blood mononuclear cells (PBMCs) and cultured into DCs by cytokines.DCs were transfected with AdGM-CSF gene at different ratios of multiplicity of infection (MOI) to determine the optimal gene transfection conditions, and the expression of GM-CSF was detected after transfection. The variation of GM-CSF gene-modifiedDCs were analyzed by morphological examination, phenotype analysis, and mixed lymphocyte reaction (MLR).DCs were loaded with gastric cancer antigen obtained by freezing and thawing method. The killing effect of DCs vaccine-stimulated T lymphocytes on gastric cancer cells was assessed by MTT assay. INF-gamma production was determined with the INF-gamma ELISA kit. RESULTS: B220(-)CD11c(+) cells increased obviously after CCL3 injection. The ELISA results showed that after GM-CSF gene modification, DCs could produce high level of GM-CSF. When DCs were transfected with AdGM-CSF gene at MOI equal to 100, the GM-CSF level in culture supernatants reached saturation [(130.00 +/- 12.61) pg/ml]. After GM-CSF gene-modification, DCs tend to be more maturated as detected by morphological observation and phenotype analysis. At the same time, the capacity of activating the proliferation of allogeneic T lymphocytes was enhanced greatly. T lymphocytes stimulated by DCs transfected with GM-CSF gene showed a specific killing effect on gastric carcinoma cells and produced high level of INF-gamma [(1245.00 +/- 13.75) pg/ml]. CONCLUSION: After GM-CSF gene modification, DCs can produce high level of GM-CSF, which tend to be more maturated, and the capacity of activating the proliferation of allogeneic T lymphocytes is enhanced greatly. GM-CSF gene modified DCs can induce specific CTL to target tumor cells in vitro.

Effects of lorglumide on growth and invasion of human pancreatic cancer cell line Mia PaCa-2 in vitro through the cholecystokinin-cholecystokinin-1 receptor pathway.

BACKGROUND: Cholecystokinin (CCK) has been found to be a growth stimulant through its special receptor pathway, especially for gastrointestinal malignancies. Although the CCK-1 receptor has been shown to be highly expressed in resected human pancreatic cancer samples, its role is less clear. OBJECTIVE: The aim of this in vitro study was to investigate the CCK-1 receptor expression and the function of the CCK-CCK-1 receptor pathway in the human pancreatic adenocarcinoma cell line, Mia PaCa-2. METHODS: The expression of the CCK-1 receptor in Mia PaCa-2 cells was detected by reverse-transcriptase polymerase chain reaction and flow cytometry. CCK-1 receptor agonist CCK-8S (the major transmitter form of CCK) and antagonist lorglumide were cultured respectively with Mia PaCa-2. Three groups were created for this study: CCK-8S group (Mia PaCa-2 cells treated with CCK-8S), lorglumide group (Mia PaCa-2 cells treated with lorglumide), and the control group (Mia PaCa-2 cells alone). Investigators were blinded to group designation. 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry were used to detect the cell growth, cell cycle, and apoptosis. Apoptosis index rate was measured by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling. Cell invasion ability was observed by invasion assay. Expression of matrix metalloproteinase-2 (MMP-2) was measured by Western blotting. RESULTS: Mia PaCa-2 cells were found to express the CCK-1 receptor. Compared with the control group (70.2% [1.5%]), CCK-8S was associated with significant mean (SD) cell proliferation (85.1% [1.7%]; P = 0.039), and the ratio in the S stage of the cell cycle increased significantly (50.5% [1.7%] vs 42.2% [1.4%]; P = 0.021). CCK-8S was also associated with increased Mia PaCa-2 cell invasion ability (123.8 [1.7] vs 102.1 [5.8]; P = 0.005 vs control). Compared with the control group, lorglumide was associated with significantly inhibited cell growth (52.1% [1.8%]; P = 0.002) and cell invasion (77.6% [1.2%]; P = 0.003). Lorglumide also induced G0/G1 cell cycle arrest and apoptosis (27.1% [3-5%] vs 3-7% [0.6%]; P = 0.003 vs control). The change of invasion ability appeared to be mediated by MMP-2 expression, which was upregulated by CCK-8S and downregulated by lorglumide. CONCLUSION: The findings of this in vitro study suggest that CCK may exert a trophic action on the Mia PaCa-2 cell line, while lorglumide inhibited the cell growth and invasion.

Preoperative Colonic Decompression With Decompression Tube Insertion Versus Stent Insertion in Patients With Malignant Left Colonic Obstruction.

PURPOSE: To compare the clinical effectiveness of preoperative colonic decompression (PCD) performed with stent or decompression tube insertion in patients with malignant left colonic obstruction (MLCO). MATERIALS AND METHODS: Between September 2014 and September 2018, 63 patients with MLCO underwent PCD (decompression tube: 35; stent: 28) in our center. Elective surgery was performed for patients with clinical success of PCD. RESULTS: The rates of technical success for PCD with tube and stent insertion were 91.4% (32/35) and 96.4% (27/28), respectively (P=0.773). Clinical success rates for PCD with tube and stent insertion were 90.6% (29/32) and 85.2% (23/27), respectively (P=0.811). Tumor resection with primary anastomosis was performed in all patients with clinical success in both groups. No significant differences were found between 2 groups regarding the duration of surgery and rates of postoperative complications. CONCLUSION: Decompression tube and stent insertion had similar effectiveness for PCD in patients with MLCO.

miR-557 inhibits the proliferation and invasion of pancreatic cancer cells by targeting EGFR.

Deregulation of microRNA has been suggested as a critical event in pancreatic cancer development and progression. Thus far, very little is known about the role of miR-557; therefore, the goal of this study was to investigate the potential role of miR-557 in pancreatic cancer. In the present study, we discovered that miR-557 expression was lowered in cancerous pancreatic tissue samples relative to non-cancerous adjacent controls, and when miR-557 was overexpressed we found that this promoted the apoptotic death of pancreatic cancer cells, suppressing their proliferation, invasion, and migration. Using western blotting and luciferase reporter assays, we further found evidence that this miRNA may directly suppress expression of the epidermal growth factor receptor via suppressing its translation through 3'-UTR binding. When EGFR was overexpressed in our pancreatic cancer cells, this was sufficient to reverse the effects of miR-557 inhibition. In summary, miR-557 acts as a tumor suppressor in pancreatic cancer cells, impairing their ability to grow and invade surrounding tissues due at least in part to EGFR inhibition. Harnessing this targeting of EGFR via this miRNA may therefore be a viable strategy useful for patient suffering from this deadly disease.

A Panel of Three Biomarkers Identified by iTRAQ for the Early Diagnosis of Pancreatic Cancer.

PURPOSE: Due to a lack of early diagnostic markers, pancreatic cancer (PC) remains a lethal disease. Proteomic approaches are now being applied to identify novel PC biomarkers. EXPERIMENTAL DESIGN: In this study, iTRAQ and LC-MS/MS are used to perform comparative analyses of serum from PC patients and healthy controls (HC), to identify specific serum biomarkers for PC. Serum levels of candidate proteins are determined using ELISA. RESULTS: Among 869 proteins identified, 55 are potential biomarkers; Vitamin K-dependent protein Z (PROZ) and tumor necrosis factor receptor superfamily member 6b (TNFRSF6B) are selected for further analysis. Serum levels of PROZ and TNFRSF6B are significantly higher in PC patients than in HC or pancreatic benign controls (BC) (p < 0.01). The AUCs range from 0.816 to 0.971 for PROZ, TNFRSF6B, and carbohydrate antigen 19-9, either individually or in combination, in PC versus HC+BC, and from 0.711 to 0.932 in PC Stage I versus HC+BC. CONCLUSIONS AND CLINICAL RELEVANCE: It is demonstrated that PROZ and TNFRSF6B are novel serum biomarkers for detecting early stage PC, and for distinguishing PC from pancreatic benign tumor and healthy individuals. Additional large cohort studies are needed to develop PROZ and TNFRSF6B as clinical PC biomarkers.

Inhibition of pancreatic carcinoma cell growth in vitro by DPC4 gene transfection.

AIM: To detect the expression of DPC4 in malignant and non-malignant specimens of human pancreas, and observe the inhibition of retroviral pLXSN containing DPC4 on pancreatic carcinoma cells in vitro. METHODS: The expression of DPC4 was determined in 40 pancreatic adenocarcinoma and 36 non-malignant pancreatic specimens by reverse-transcriptase polymerase chain reaction (RT-PCR) and immunohisto-chemistry. Furthermore, we constructed retroviral vectors containing DPC4, which then infected the pancreatic carcinoma cell line BxPC-3. Cell growth in vitro after being infected was observed, and the vascular endothelial growth factor (VEGF) mRNA level in the daughter cells was determined by semi-quantitative PCR assay. RESULTS: The RT-PCR assay showed a positive rate of DPC4 mRNA in 100% (36/36) of normal specimens, compared to 40% (16/40) in adenocarcinoma specimens. The regional and intense positive cases of DPC4 expression in adenocarcinoma detected by immunohistochemistry were 10 and four, whereas it was all positive expression in normal tissues. There was a significant difference of DPC4 expression between them. The stable expression of DPC4 in the pancreatic carcinoma cells BxPC-3 could be resumed by retroviral vector pLXSN transfection, and could inhibit cell growth in vitro. Rather, DPC4 could decrease VEGF mRNA transcription levels. CONCLUSION: The deletion of DPC4 expression in pancreatic carcinoma suggests that loss of DPC4 may be involved in the development of pancreatic carcinoma. The retroviral vector pLXSN containing DPC4 can inhibit the proliferation of pancreatic carcinoma cells, and down-regulate the level of VEGF.

Effect of recombinant adenovirus vector mediated human interleukin-24 gene transfection on pancreatic carcinoma growth.

BACKGROUND: Pancreatic cancer is a highly malignant tumor affecting an ever increasing number of patients with a mean 5-year survival rate below 4%. Therefore, gene therapy for cancer has become a potential novel therapeutic modality. In this study we sought to determine the inhibitory effects of adenovirus-mediated human interleukin-24 (AdhIL-24) on pancreatic cancer. METHODS: Human interleukin-24 gene was cloned into replication-defective adenovirus specific for patu8988 tumor cells by virus recombination technology. Reverse transcription-polymerase chain reaction and Western blotting analysis were used to determine the expression of human interleukin-24 mRNA in patu8988 cells in vitro. Induction of apoptosis by overexpression of human interleukin-24 in patu8988 cells was determined by flow cytometry. In vivo efficacy of adenoviral delivery of human interleukin-24 was assessed in nude mice (n = 10 for each group) bearing patu8988 pancreatic cancer cell lines by determining inhibition of tumor growth, endothelial growth factor and CD34 expression, and intratumoral microvessel density (MVD). RESULTS: The recombinant adenovirus vector AdVGFP/IL-24 was constructed with a packaged recombinant retrovirus titer of 1.0 x 10(10) pfu/ml and successfully expressed of both mRNA and protein in patu8988 cells. The AdVGFP/IL-24 induced apoptosis of patu8988 tumor cells in vitro and significantly inhibited tumor growth in vivo (P < 0.05). The intratumoral MVD decreased significantly in the treated tumors (P < 0.05). CONCLUSION: The recombinant adenovirus AdGFP/IL-24 can effectively express biologically active human interleukin-24, which results in inhibition of pancreatic cancer growth.

SP1 reduces autophagic flux through activating p62 in gastric cancer cells.

Gastric cancer is the most common type of gastrointestinal cancer, causing mortality worldwide. However, the underlying molecular mechanism in gastric cancer progression remains unclear. The autophagic flux was determined in gastric cancer cells overexpressing or inhibiting Sp1 transcription factor (SP1) using western blotting, reverse transcription­polymerase chain reaction and immunofluorescence staining. Luciferase and ChIP assays were performed to detect the potential underlying mechanism of SP1 in gastric cancer cells. Lastly, immunohistochemistry was also performed on SP1 and p62 expression levels in human gastric cancer specimens. It was demonstrated that SP1 diminished autophagic flux via activating p62 in gastric cancer. Moreover, SP1 deficiency increased the rate of autophagy of gastric cancer cells. Notably, it was observed that SP1 enhanced the expression levels of p62 by directly binding to the promoter of p62. Analysis of gastric cancer specimen staining established that p62 expression levels were increased in SP1­positve gastric tissues. The present study provided evidence for a novel mechanism regulating autophagy in gastric cancer cells.

DNM1L, a key prognostic predictor for gastric adenocarcinoma, is involved in cell proliferation, invasion, and apoptosis.

Dynamin-1-like protein (DNM1L) encodes a member of the dynamin superfamily of GTPases. It mediates mitochondrial and peroxisomal division and is involved in the regulation of apoptosis. However, its role in gastric cancer remains unclear. MKN-45 gastric cancer cells were transfected with short hairpin RNA (shRNA) to suppress DNM1L expression. MTT, flow cytometry, and Transwell assays were used to detect the changes in cell proliferation, apoptosis, and invasion, respectively. Immunohistochemistry was used to detect DNM1L expression in gastric adenocarcinoma specimens, and the association of DNM1L expression with clinicopathological features and prognosis was analyzed. After the suppression of endogenous DNM1L expression in MKN-45 cells with shRNA, cell proliferation and invasion rates were significantly reduced, whereas apoptosis was significantly increased (all P<0.01). The expression of DNM1L was significantly higher in gastric adenocarcinoma specimens compared with that in pericarcinoma tissues (P<0.001). The expression of DNM1L increased with increasing infiltration depth, lymphatic metastasis, and higher tumor node metastasis stage (P<0.05). The expression of DNM1L associated negatively with prognosis (P<0.01). DNM1L plays a critical role in the proliferation, invasion and apoptosis of human gastric adenocarcinoma. DNM1L expression has prognostic significance for the survival of patients with gastric adenocarcinoma.

HIF-2α promotes the formation of vasculogenic mimicry in pancreatic cancer by regulating the binding of Twist1 to the VE-cadherin promoter.

Vasculogenic mimicry (VM) is a blood supply modality that occurs independently of endothelial cell angiogenesis. Hypoxia and the epithelial-mesenchymal transition (EMT) induce VM formation by remodeling the extracellular matrix. Our previous study demonstrated that hypoxia-inducible factor-2 alpha (HIF-2α) promotes the progress of EMT in pancreatic cancer; however, whether HIF-2α promotes VM formation in pancreatic cancer remains unknown. In this study, we investigated HIF-2α expression and VM by immunohistochemistry in 70 pancreatic cancer patients as well as the role of Twist1and Twist2 in HIF-2α-induced VM in vitro and in vivo. We found that the overexpression of HIF-2α and VM were correlated with poor tumor differentiation, late clinical stage and lymph node metastasis, and a poor prognosis in pancreatic cancer. Moreover, the upregulation of HIF-2α in SW1990 cells induced VM formation, whereas the opposite results were found after silencing HIF-2α in AsPC-1 cells. A mechanistic study indicated that HIF-2α might regulate the binding of twist1 to vascular endothelial cadherin (VE-cadherin) to promote VM formation in pancreatic cancer cells, and that the P1 (-421bp) and P4 (-2110bp) regions of the Twist1 binding sequences are positive regulatory elements for VE-cadherin. In addition, we confirmed that the overexpression of HIF-2α increased Twist1 expression and promoted tumor growth and VM formation in pancreatic cancer xenografts in nude mice. These findings indicated that HIF-2α might play a critical role in VM and that HIF-2α and the pathway of HIF-2α inducing VM formation are potential therapeutic targets for pancreatic cancer.

Role of CD80 in stimulating T lymphocyte activation.

AIM: To observe biological characteristics of hepatocarcinoma cells before and after CD80 transfection and to compare the effect of CD80-transfected hepatocarcinoma cells on T lymphocyte activation. METHODS: Retro virus vector carrying CD80 gene was transfected into HepG2 cells to establish CD80-transfected hepatocarcinoma cells (HepG2/hCD80). Flow cytometry (FCM) was performed to detect CD80 expression in the transfected cells. RT-PCR was used to evaluate CD80 expression at mRNA level. In the presence of anti-CD3 mAb, the proliferation of T lymphocyte was observed by MTT. Meanwhile, the expression of activated molecule marker CD25 was analyzed through FCM. RESULTS: A stable cell line HepG2/hCD80 expressing the human CD80 was established. Growth curve showed that the molecule CD80 could obviously decrease the growth of tumor cells. HepG2/hCD80 was evidenced to have a potency to enhance T cell proliferation and upregulate CD25 expression. CONCLUSION: CD80 transfection can lower malignant phenotype of hepatocarcinoma cells. CD80 transfection has a down-regulatory effect to activated T cells in vitro.

Percutaneous recanalization for hepatic vein-type Budd-Chiari syndrome: long-term patency and survival.

OBJECTIVE: To determine the long-term patency and survival of percutaneous recanalization for hepatic vein (HV)-type Budd-Chiari syndrome (BCS). METHODS: From March 2009 to November 2014, consecutive symptomatic HV-type BCS patients were treated by percutaneous recanalization in our centers. These patients underwent main HV (MHV) or accessory HV (AHV) recanalization. Data on patient characteristics, technical success, clinical success, long-term patency, and survival were collected and analyzed. RESULTS: During the enrolled periods, a total of 143 symptomatic HV-type BCS patients were treated by percutaneous recanalization in our centers. Technical success was achieved in 140 of 143 patients. One hundred eleven patients underwent MHV recanalization, and 29 underwent AHV recanalization. Clinical success was achieved in 136 of 140 patients. The mean MHV/AHV pressure decreased from 33.5 ± 4.1 mmHg before treatment to 12.5 ± 3.1 mmHg after treatment (p = 0.000). The 136 patients were followed for 7-75 months (mean 33.9 ± 15.3 months). Twenty-eight patients experienced re-obstruction of MHV (n = 24) or AHV (n = 4) at 3 to 36 months (mean 18.0 ± 11.5 months) after treatment. The cumulative 1-, 3-, and 6-year primary patency rates were 91.1, 77.4, and 74.0%, respectively. The cumulative 1-, 3-, and 6-year secondary patency rates were 97.0, 92.4, and 88.8%, respectively. The cumulative 1-, 3-, and 6-year survival rates were 97.7, 92.2, and 90.0%, respectively. CONCLUSION: Percutaneous recanalization can provide good long-term patency and survival in HV-type BCS patients.

Expression and clinical significance of glucose transporter-1 in pancreatic cancer.

Increasing evidence has demonstrated that malignant cells exhibit increased glucose uptake, which facilitates survival and growth in a hypoxic environment. The glucose transporter-1 (GLUT-1) is overexpressed in a variety of malignant tumors. However, the association between GLUT-1 expression and clinicopathological factors, 18F-fluorodeoxyglucose uptake and tumor proliferation in pancreatic cancer has not been investigated to date. In the present study, the expression of GLUT-1 in 53 pancreatic cancer tissues was analyzed, which revealed that GLUT-1 was overexpressed in pancreatic tissue and correlated with poor prognosis and clinicopathological characteristics, including increased tumor size, clinical stage and lymph node metastasis, maximum standardized uptake value (SUVmax) and Ki-67 expression. The receiver operating characteristic curve analysis indicated that a cut-off SUVmax value of 4.830 was associated with optimal sensitivity (88%) and specificity (71.4%) for the detection of strong positive GLUT-1 expression. In addition, as the expression of GLUT-1 was found to correlate with Ki-67 expression, GLUT-1 may exhibit a significant effect on cell proliferation in pancreatic cancer. Overall, these findings indicate that GLUT-1 may represent a prognostic indicator, and a potential therapeutic target for pancreatic cancer.

Anti-gastric cancer active immunity induced by FasL/B7-1 gene-modified tumor cells.

AIM: To study the activation of cytotoxic T lymphocytes (CTLs) against gastric cancer cells induced by FasL/B7-1 (FB-11) gene-modified tumor cells, and to explore whether co-expression of FasL and B7-1 in SGC-7901 tumor cells could initiate synergistic antitumor effect. METHODS: FasL and B7-1 genes were transfected into human SGC-7901 gastric cancer cells with adenovirus vectors. The positive clones were selected by G418. FasL and B7-1 genes were detected by flow cytometry and RT-PCR. Abdominal infiltrating lymphocytes and sensitized spleen cells were obtained from mice that were immunized with SGC-7901/FB-11 or wild type SGC-7901 cells intraperitoneally, and cytotoxicity of these CTLs against tumor cells was determined by MTT assay. RESULTS: Flow cytometry and RT-PCR showed that FasL and B7-1 genes were highly expressed. FasL and B7-1 transfected cancer cells had a high apoptosis index. DNA laddering suggested that FasL and B7-1 genes induced gastric cancer cell apoptosis. FasL(+)/B7-1(+)SGC-7901 cells (SGC-7901/FB-11) were inoculated subcutaneously in the dorsal skin of C57BL/6 mice and then decreased their tumorigenicity greatly (z = 2.15-46.10, P<0.01). SGC-7901/FB-11 cell-sensitized mice obtained protective immune activity against the rechallenge of wild type SGC-7901 cells (z = 2.06-44.30, P<0.05). The cytotoxicity of CTLs induced by SGC-7901/FB-11 cells against SGC-7901 was significantly higher than that of CTLs activated by wild-type SGC-7901 cells (84.1+/-2.4% vs 30.5+/-2.3%, P<0.05). CONCLUSION: FasL and B7-1 genes can effectively promote the activity of CTLs against gastric cancer cells. FasL/B7-1 molecules play an important role in CTL cytotoxicity.