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  • 1
    Keywords: CANCER ; Germany ; DIAGNOSIS ; screening ; POPULATION ; PATIENT ; MARKER ; colon ; tumour ; early detection ; AGE ; colorectal cancer ; FECAL-OCCULT-BLOOD ; COLORECTAL-CANCER ; LONG-TERM SURVIVAL ; CANCER-PATIENTS ; specificity ; CANCER PATIENTS ; ONCOLOGY ; ADULTS ; RE ; INTERVAL ; analysis ; TESTS ; rectum ; colorectal ; - ; M2 PYRUVATE-KINASE ; PERFORMANCE-CHARACTERISTICS ; stool test ; tumour M2-PK
    Abstract: Stool testing based on tumour-derived markers might offer a promising approach for non-invasive colorectal cancer (CRC) screening. The aim of this study was to estimate the potential of a new test for faecal tumour M2-PK to discriminate patients with CRC from a large sample of unselected older adults. Faecal tumour M2-PK concentrations were determined in 65 CRC patients and in a population-based sample of 917 older adults (median age: 65 and 62 years, respectively). Sensitivity and specificity of the test were calculated at different cutoff values, and receiver-operating characteristic curves (ROC) were constructed to visualise the discriminatory power of the test. The median ( interquartile range) faecal tumour M2-PK concentration was 8.6 U ml(-1) (2.8-18.0) among CRC patients and 〈 2 U ml(-1) (〈 2-3.2; P 〈 0.0001) in the population sample. At a cutoff value of 4 U ml(-1), sensitivity (95% confidence interval) was 85% ( 65 - 96%) for colon cancer and 56% (41-74%) for rectum cancer. Specificity (95% confidence interval) was estimated to be 79% (76-81%). Given the comparatively high sensitivity of the tumour M2-PK stool test (especially for colon cancer) and its simple analysis, the potential use of the test for early detection of CRC merits further investigation. Possibilities to enhance specificity of the test should be explored
    Type of Publication: Journal article published
    PubMed ID: 17406361
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  • 2
    Keywords: CANCER ; tumor ; carcinoma ; CELL ; Germany ; CT ; imaging ; DISEASE ; DIFFERENTIATION ; TISSUE ; computed tomography ; SURGERY ; PATIENT ; primary ; MRI ; MAGNETIC-RESONANCE ; magnetic resonance imaging ; NO ; DIFFERENCE ; NUMBER ; METASTASIS ; metastases ; REGION ; REGIONS ; DISSEMINATED TUMOR-CELLS ; adenocarcinoma ; COMPUTED-TOMOGRAPHY ; CELL CARCINOMA ; renal cell carcinoma ; pancreas ; ENHANCEMENT ; methods ; multidetector CT ; RENAL-CELL
    Abstract: Aims: To investigate the characteristics of metastasis to the pancreas using computed tomography (CT) and magnetic resonance imaging (MRI). Methods: Twenty-two patients with metastases to the pancreas were examined preoperatively by MRI (7/22) and/or multidetector CT (15/22). Pre- and post-contrast images were acquired and morphology, size, and contrast enhancement of the tumor analyzed. Subsequently, all patients underwent surgery, and the histopathologic findings were compared with the imaging results. Results: In 22 patients, a total of 29 metastases were found on CT and MRI. These metastases originated from renal cell carcinomas (RCC; 22/29), colorectal carcinoma (3/29), and other malignancies (4/29). The metastases differed not in size or location, but in their contrast enhancement characteristics. RCC metastases had either intense homogeneous enhancement (in small lesions) or rim enhancement (in large lesions). Outer regions of colorectal metastases showed no difference from normal pancreatic tissue, whereas the inner area showed hypo-enhancement due to central necrosis. Conclusion: Imaging features of metastases from RCC point to their primary origin. While they can be distinguished from primary adenocarcinoma of the pancreas, differentiation from endocrine carcinoma might be difficult. Differentiation of colorectal carcinoma remains to be investigated on larger numbers of cases. Copyright (C) 2008 S. Karger AG, Basel and IAP
    Type of Publication: Journal article published
    PubMed ID: 18434757
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  • 3
    Keywords: CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; INVASION ; carcinoma ; CELL ; Germany ; PATHWAY ; PATHWAYS ; VITRO ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; RNA ; SAMPLE ; SAMPLES ; transcription ; COMPONENTS ; TISSUE ; LINES ; TRANSDUCTION ; ACTIVATION ; TISSUES ; BIOLOGY ; CELL-LINES ; fibroblasts ; MOLECULAR-BIOLOGY ; signal transduction ; SIGNAL ; BREAST-CANCER ; PROGRESSION ; immunohistochemistry ; gene expression ; DIFFERENCE ; NUMBER ; METASTASIS ; SIGNAL-TRANSDUCTION ; CELL-LINE ; LINE ; adenocarcinoma ; TARGETS ; MICROARRAY ANALYSIS ; OVEREXPRESSION ; DIFFERENTIAL EXPRESSION ; gene expression profiling ; expression profiling ; microdissection ; pancreatic cancer ; pancreatic carcinoma ; chronic pancreatitis ; WNT ; molecular biology ; molecular ; PANCREATIC-CANCER ; fibroblast ; DUCTAL ADENOCARCINOMA ; PANCREATITIS ; PROTOCOL ; quantitative RT-PCR ; interaction ; analysis ; DIFFERENTIALLY EXPRESSED GENES ; signalling ; WNT pathway ; tumor microenvironment ; ENGLAND ; SET ; MEDICINE ; quantitative ; PROFILE ; pancreatic ductal adenocarcinoma ; response ; interactions ; SFRP1 ; expression profile ; stroma ; in vitro ; ABERRANT METHYLATION ; WNT5a
    Abstract: Pancreatic ductal adenocarcinoma (PDAC) is characterized by an abundant desmoplastic stroma. Interactions between cancer and stromal cells play a critical role in tumour invasion, metastasis and chemoresistance. Therefore, we hypothesized that gene expression profile of the stromal components of pancreatic carcinoma is different from chronic pancreatitis and reflects the interaction with the tumour. We investigated the gene expression of eleven stromal tissues from PDAC, nine from chronic pancreatitis and cell lines of stromal origin using the Affymetrix U133 GeneChip set. The tissue samples were microdissected, the RNA was extracted, amplified and labelled using a repetitive in vitro transcription protocol. Differentially expressed genes were identified and validated using quantitative RT-PCR and immuno-histochemistry. We found 255 genes to be overexpressed and 61 genes to be underexpressed within the stroma of pancreatic carcinoma compared to the stroma of chronic pancreatitis. Analysis of the involved signal transduction pathways revealed a number of genes associated with the Wnt pathway of which the differential expression of SFRP1 and WNT5a was confirmed using immunohistochemistry. Moreover, we could demonstrate that WNT5a expression was induced in fibroblasts during cocultivation with a pancreatic carcinoma cell line. The identified differences in the expression profile of stroma cells derived from tumour compared to cells of inflammatory origin suggest a specific response of the tissue surrounding malignant cells. The overexpression of WNT5a, a gene involved in the non canonical Wnt signalling and chondrocyte development might contribute to the strong desmoplastic reaction seen in pancreatic cancer
    Type of Publication: Journal article published
    PubMed ID: 18298655
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  • 4
    Keywords: CANCER ; tumor ; Germany ; KINASE ; screening ; COLORECTAL-CANCER ; STABILITY ; ADULTS ; RE
    Type of Publication: Journal article published
    PubMed ID: 16595841
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  • 5
    Keywords: CANCER ; tumor ; Germany ; DIAGNOSIS ; imaging ; screening ; TOOL ; DISEASE ; SITE ; GENE ; TUMORS ; MARKER ; early detection ; colorectal cancer ; COLORECTAL-CANCER ; MARKERS ; p53 ; HIGH-RISK ; COMPUTED-TOMOGRAPHY ; sensitivity ; specificity ; pathology ; pancreatic cancer ; pancreas ; review ; RE ; PANCREATIC-CANCER ; DUCTAL ADENOCARCINOMA ; P53 GENE ; aging ; biomarker ; K-RAS MUTATIONS ; FAMILY-HISTORY ; ENDOSCOPIC ULTRASOUND ; CANDIDATE ; TOOLS ; ENGLAND ; NOV ; gastrointestinal ; biological ; epigenetic ; STOOL MARKER ; stool testing ; CYCLOOXYGENASE-2 MESSENGER-RNA ; FECAL DNA ; HIGH-RISK INDIVIDUALS ; SCREENING-TEST ; stool
    Abstract: The development of effective tools for the early detection of pancreatic cancer, or its precursors, in high-risk subjects could play a key role in reducing the burden of this disease, which is the most lethal among solid gastrointestinal tumors. Given the poor accessibility of the pancreas due to its anatomic site, and given the limitations of imaging modalities, biomarker screening might be a promising diagnostic option. This review focuses on the rationale of using stool markers for the early detection of pancreatic cancer, and systematically summarizes current evidence. Despite several potential advantages of stool testing for pancreatic cancer and its biological plausibility, only six studies investigating two genetic markers in stool (the K-ras and the p53 gene) could be identified. Even though these studies were limited in size and could hardly approximate the screening setting, both markers appear to lack sensitivity and, in particular, specificity. The investigation of further marker candidates (e.g., epigenetic markers) in adequately designed studies represents an important next step to explore the potential of stool testing for pancreatic cancer. Pertinent studies could greatly benefit from recent methodological advances gained in connection with stool testing for colorectal cancer
    Type of Publication: Journal article published
    PubMed ID: 18999925
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  • 6
    Keywords: RECEPTOR ; INHIBITOR ; INVASION ; SURVIVAL ; tumor ; Germany ; IN-VIVO ; INHIBITION ; MODEL ; PATHWAY ; VIVO ; MICE ; TIME ; NF-KAPPA-B ; ACTIVATION ; MECHANISM ; animals ; mechanisms ; BINDING ; cytokines ; STIMULATION ; NO ; CARE ; DESIGN ; DIFFERENCE ; NECROSIS-FACTOR-ALPHA ; BETA ; FACTOR-KAPPA-B ; LETHALITY ; INHIBITORS ; FACTOR-ALPHA ; CYTOKINE ; PANCREATITIS ; INTERLEUKIN-1 ; NUCLEAR ; USA ; prospective ; animal ; NICOTINE ; MEDICINE ; response ; INTERVENTIONS ; LIGATION ; cecal ligation and puncture ; cholinergic anti-inflammatory pathway ; CHOLINERGIC ANTIINFLAMMATORY PATHWAY ; MURINE ENDOTOXEMIA ; neostigmine ; neutrophil ; physostigmine ; SEPTIC SHOCK ; SYSTEMIC INFLAMMATORY RESPONSE ; VAGUS NERVE
    Abstract: Objective: Lethal sepsis occurs when an excessive inflammatory response evolves that cannot be controlled by physiologic anti-inflammatory mechanisms, such as the recently described cholinergic anti-inflammatory pathway. Here we studied whether the cholinergic anti-inflammatory pathway can be activated by pharmacologic cholinesterase inhibition in vivo. Design: Prospective, randomized laboratory investigation that used an established murine sepsis model. Setting: Research laboratory in a university hospital. Subjects: Female C57BL/6 mice. Interventions: Sepsis in mice was induced by cecal ligation and puncture. Animals were treated immediately with intraperitoneal injections of nicotine (400 mu g/kg), physostigmine (80 mu g/kg), neostigmine (80 mu g/kg), or solvent three times daily for 3 days. Measurements and Main Results: Treatment with physostigmine significantly reduced lethality (p 〈= .01) as efficiently as direct stimulation of the cholinergic anti-inflammatory pathway with nicotine (p 〈= .05). Administration of cholinesterase inhibitors significantly down-regulated the binding activity of nuclear factor-kappa B (p 〈= .05) and significantly reduced the concentration of circulating proinflammatory cytokines tumor necrosis factor-alpha., interleukin-1 beta, and interleukin-6 (p 〈= .001), and pulmonary neutrophil invasion (p 〈= .05). Animals treated with the peripheral cholinesterase inhibitor neostigmine showed no difference compared with physostigmine-treated animals. Conclusions: Our results demonstrate that cholinesterase inhibitors can be used successfully in the treatment of sepsis in a murine model and may be of interest for clinical use
    Type of Publication: Journal article published
    PubMed ID: 18091537
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  • 7
    Keywords: CANCER ; CELLS ; tumor ; TUMOR-CELLS ; BLOOD ; carcinoma ; CELL ; Germany ; IN-VIVO ; DIAGNOSIS ; screening ; SYSTEM ; RISK ; PROTEIN ; PROTEINS ; MARKER ; BINDING ; CARCINOMA CELLS ; PLASMA ; COLORECTAL-CANCER ; inactivation ; MARKERS ; RECURRENCE ; adenocarcinoma ; IMMUNE-RESPONSE ; LUNG-CANCER CELLS ; ONCOLOGY ; PHASE ; COMPLEMENT ACTIVATION ; diagnostic marker ; FACTOR-H ; REGULATORY PROTEINS ; adjuvant treatment ; BENEFIT ; RANK STATISTICS ; 2 PARTS ; complement system pancreatic carcinoma ; iC3b
    Abstract: Pancreatic adenocarcinoma as an aggressive tumor still lacks specific markers. Resection offers the only potential cure, and earlier diagnosis could benefit many patients. Here, we analyzed siC3b as a potential diagnostic marker. Soluble iC3b is generated in the fluid phase after binding of autoantibodies to tumor cells and subsequent inactivation of the complement cascade by interaction with complement regulatory proteins. Two hundred thirty-two plasma samples from patients with adjuvant treatment after resection, from healthy volunteers, and from vulnerable patients were collected prospectively and analyzed for siC3b. Every 3 months, the patients underwent imaging and the results from siC3b enzyme-linked immunosorbent assay were categorized according to radiologically defined recurrence within 4 months after blood withdrawal. Furthermore, the regulatory factors of the complement system were analyzed in tumor cells and in urine. The most important finding was that up to 4 months before radiologically defined recurrence, siC3b plasma level is increased with a sensitivity and specificity resulting in an area under the curve of 0.85, which could be further increased by combining it with CA19.9 ( area under the curve = 0.92). Complement regulatory proteins are highly expressed in pancreatic carcinoma cells and detectable in the patient's urine. In summary, screening for siC3b in patients with an increased risk for pancreatic ductal adenocarcinoma ( patients with chronic pancreatitis, hereditary pancreatitis, after curative resection, and patients with a variety of familial cancer syndromes) allows for early detection with high sensitivity, as siC3b plasma levels are increased up to 4 months before radiologic evidence. Sensitivity could be further increased by combining this approach with CA19.9
    Type of Publication: Journal article published
    PubMed ID: 20139773
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  • 8
    Keywords: CANCER ; CANCER CELLS ; CELLS ; ENDOTHELIAL-CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; INVASION ; proliferation ; tumor ; TUMOR-CELLS ; Germany ; VITRO ; DISEASE ; GENE ; GENES ; TISSUE ; TUMORS ; PATIENT ; prognosis ; INDUCTION ; CONTRAST ; fibroblasts ; GLYCOPROTEIN ; PROGRESSION ; immunohistochemistry ; ASSAY ; CANCER-CELLS ; EXTRACELLULAR-MATRIX ; NEOPLASTIC PROGRESSION ; POLYMERASE-CHAIN-REACTION ; adenocarcinoma ; OVEREXPRESSION ; POOR-PROGNOSIS ; pancreatic cancer ; chronic pancreatitis ; HUMAN BREAST-CANCER ; SERUM ; MATRIX ; quantitative polymerase chain reaction ; PANCREATIC-CANCER ; DUCTAL ADENOCARCINOMA ; extracellular matrix ; OLIGONUCLEOTIDE ; interaction ; TARGET GENE ; TARGET GENES ; ANTISENSE OLIGONUCLEOTIDE ; MALIGNANT-TUMORS ; EXTRACELLULAR-MATRIX PROTEINS ; DISEASE PROGRESSION ; CYSTEINE SPARC ; DEGRADING PROTEASES ; ESOPHAGEAL-CARCINOMA ; I COLLAGEN ; MATRICELLULAR PROTEIN ; SPARC EXPRESSION
    Abstract: Objective: We sought to examine the expression and functional role of osteonectin in primary and metastatic pancreatic ductal adenocarcinoma (PDAC). Background: The glycoprotein osteonectin plays a vital role in cell-matrix interactions and is involved in various biologic processes. Overexpression of osteonectin is present in malignant tumors and correlates with disease progression and poor prognosis. Methods: Expression of osteonectin was analyzed by quantitative polymerase chain reaction and immunohistochemistry in pancreatic tissues and by enzyme-linked immunosorbent assay in the serum of patients and donors. Recombinant osteonectin and specific antisense oligonucleotides were used to examine the effects of osteonectin on induction of target genes, and on proliferation and invasiveness of pancreatic cancer cells. Results: There was a 31-fold increase in osteonectin mRNA levels in PDAC and a 16-fold increase in chronic pancreatitis as compared with the normal pancreas (P 〈 0.01). By immunohistochemistry, faint immunoreactivity was detected in the normal pancreas. In contrast, strong staining of the cancer cells was observed in addition to extensive osteonectin immunoreactivity in surrounding fibroblasts and in the extracellular matrix. In metastatic tissues, strong immunoreactivity was observed in fibroblasts and in extracellular matrix surrounding metastatic cancer cells, whereas the signal was absent in most tumor cells. In vitro studies showed that osteonectin was able to inhibit cancer cell growth while promoting invasiveness of pancreatic tumor cells. Conclusion: Osteonectin is markedly overexpressed in pancreatic cancer and has the potential to increase the invasiveness of pancreatic cancer cells
    Type of Publication: Journal article published
    PubMed ID: 16041213
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  • 9
    Keywords: Germany ; PERFUSION ; CT ; FOLLOW-UP ; imaging ; TOOL ; liver ; SURGERY ; PATIENT ; DONOR ; TRANSPLANTATION ; ANGIOGRAPHY ; CHILDREN ; RECONSTRUCTION ; MANAGEMENT ; function ; liver transplantation ; BILIARY ATRESIA ; DEXTROCARDIA ; POLYSPLENIA SYNDROME ; situs inversus
    Abstract: Liver transplantation (LT) in an adult with situs inversus (SI) is extremely rare and requires precise pre-operative management. A 48-yr-old male with SI suffering from alcoholic liver cirrhosis underwent LT at our institution in March 2003. Pre-operatively, liver anatomy was determined by CT scan, three-dimensional liver reconstruction and angiography. LT was performed using the Belghiti technique with side-to-side cavo-caval anastomosis, transplanting a graft from a donor with normal anatomy. Post-operatively, the patient recovered without major complications, except an epileptic event because of a central pontine myelinolysis, and he was discharged on the 25th post-operative day. Three months after surgery, the T-drain placed intra-operatively into the donor bile duct was removed; transplant perfusion and function were stable with an actual follow-up period of 24 months. LT in patients with SI is feasible. Pre-operative imaging with three-dimensional reconstruction is a beneficial tool for operation planning in patients with rare anatomic variations
    Type of Publication: Journal article published
    PubMed ID: 16640519
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