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  • 1
    Keywords: CANCER CELLS ; CELLS ; EXPRESSION ; tumor ; carcinoma ; CELL ; Germany ; human ; DISEASE ; NEW-YORK ; DISTINCT ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; RNA ; cell line ; TISSUE ; validation ; LINES ; MARKER ; TISSUES ; tumour ; CELL-LINES ; BREAST-CANCER ; TARGET ; immunohistochemistry ; gene expression ; affymetrix ; CELL-LINE ; LINE ; MARKERS ; CARCINOMAS ; adenocarcinoma ; OVEREXPRESSION ; PERIPHERAL-BLOOD ; GASTRIC-CANCER ; ADAM9 ; CDNA MICROARRAYS ; cell lines ; expression profiling ; HUMAN GENES ; K-RAS ; METALLOPROTEASE-DISINTEGRIN ; microarray hybridisation ; microdissection ; OLIGONUCLEOTIDE ARRAYS ; pancreatic cancer ; pancreatic carcinoma ; SERIAL ANALYSIS
    Abstract: In a search for new molecular markers of pancreatic ductal adenocarcinoma (PDAC), we compared the gene expression profiles of seven pancreatic carcinomas and one carcinoma of the papilla Vateri with those of duct cells from three non-neoplastic pancreatic tissues. In addition, the human pancreatic duct cell line and five PDAC cell lines (AsPC-1, BxPC-3, Capan-1, Capan-2, HPAF) were examined. RNA was extracted from microdissected tissue or cultured cell lines and analysed using a custom-made Affymetrix Chip containing 3023 genes, of which 1000 were known to be tumour associated. Hierarchical clustering revealed 81 differentially expressed genes. Of all the genes, 26 were downregulated in PDAC and 14 were upregulated in PDAC. In PDAC cell lines versus normal pancreatic duct cells, 21 genes were downregulated and 20 were upregulated. Of these 81 differentially expressed genes, 15 represented human genes previously implicated in the tumourigenesis of PDAC. From the genes that were so far not known to be associated with PDAC tumorigenesis, we selected ADAM9 for further validation because of its distinct overexpression in tumour tissue. Using immunohistochemistry, the over-expressed gene, ADAM9, was present in 70% of the PDACs analysed. In conclusion, using microarray technology we were able to identify a set of genes whose aberrant expression was associated with PDAC and may be used to target the disease
    Type of Publication: Journal article published
    PubMed ID: 12942322
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  • 2
    Abstract: BACKGROUND: Initially, unresectable colorectal liver metastases can be resected after response to chemotherapy. While cetuximab has been shown to increase response and resection rates, the survival outcome for this conversion strategy needs further evaluation. PATIENTS AND METHODS: Patients with technically unresectable and/or 〉/=5 liver metastases were treated with FOLFOX/cetuximab (arm A) or FOLFIRI/cetuximab (arm B) and evaluated with regard to resectability every 2 months. Tumour response and secondary resection data have been reported previously. A final analysis of overall survival (OS) and progression-free survival (PFS) was carried out in December 2012. RESULTS: Between December 2004 and March 2008, 56 patients were randomised to arm A, 55 to arm B. The median OS was 35.7 [95% confidence interval (CI) 27.2-44.2] months [arm A: 35.8 (95% CI 28.1-43.6), arm B: 29.0 (95% CI 16.0-41.9) months, HR 1.03 (95% CI 0.66-1.61), P = 0.9]. The median PFS was 10.8 (95% CI 9.3-12.2) months [arm A: 11.2 (95% CI 7.2-15.3), arm B: 10.5 (95% CI 8.9-12.2) months, HR 1.18 (95% CI 0.79-1.74), P = 0.4]. Patients who underwent R0 resection (n = 36) achieved a better median OS [53.9 (95% CI 35.9-71.9) months] than those who did not [21.9 (95% CI 17.1-26.7) months, P 〈 0.001]. The median disease-free survival for R0 resected patients was 9.9 (95% CI 5.8-14.0) months, and the 5-year OS rate was 46.2% (95% CI 29.5% to 62.9%). CONCLUSIONS: This study confirms a favourable long-term survival for patients with initially sub-optimal or unresectable colorectal liver metastases who respond to conversion therapy and undergo secondary resection. Both FOLFOX/FOLFIRI plus cetuximab, appear to be appropriate regimens for 'conversion' treatment in patients with K-RAS codon 12/13/61 wild-type tumours. Thus, liver surgery can be considered curative or alternatively as an additional 'line of therapy' in those patients who are not cured. CLINICAL TRIAL NUMBER: NCT00153998, www.clinicaltrials.gov.
    Type of Publication: Journal article published
    PubMed ID: 24585720
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  • 3
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; INVASION ; tumor ; carcinoma ; CELL ; Germany ; human ; DEATH ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; cell line ; TISSUE ; LINES ; DNA ; CARCINOGENESIS ; CELL-LINES ; IDENTIFICATION ; immunohistochemistry ; gene expression ; EXPRESSION ANALYSIS ; CELL-LINE ; LINE ; MUTATIONS ; BENIGN ; adenocarcinoma ; REVEALS ; gene expression profiling ; cell lines ; expression profiling ; pancreatic cancer ; pancreatic carcinoma ; CDNA MICROARRAY ; E-cadherin ; pancreas ; PANCREATIC-CANCER ; DUCTAL ADENOCARCINOMA ; ARRAY ; development ; SWITZERLAND ; analysis ; CANCER DEVELOPMENT ; carcinoma cell ; DUCT CELLS ; methods ; pancreatic ; pancreatic adenocarcinoma ; primary isolates ; REGULATED GENE ; thymosin ; THYMOSIN BETA-10 GENE ; TUMOR-CELL
    Abstract: Background: Pancreatic cancer is one of the leading causes of cancer-related death. Using DNA gene expression analysis based on a custom made Affymetrix cancer array, we investigated the expression pattern of both primary and established pancreatic carcinoma cell lines. Methods: We analyzed the gene expression of 5 established pancreatic cancer cell lines (AsPC-1, BxPC-3, Capan-1, Capan-2 and HPAF II) and 5 primary isolates, 1 of them derived from benign pancreatic duct cells. Results: Out of 1,540 genes which were expressed in at least 3 experiments, we found 122 genes upregulated and 18 downregulated in tumor cell lines compared to benign cells with a fold change 〉3. Several of the upregulated genes (like Prefoldin 5, ADAM9 and E-cadherin) have been associated with pancreatic cancer before. The other differentially regulated genes, however, play a so far unknown role in the course of human pancreatic carcinoma. By means of immunohistochemistry we could show that thymosin beta-10 (TMSB10), upregulated in tumor cell lines, is expressed in human pancreatic carcinoma, but not in non-neoplastic pancreatic tissue, suggesting a role for TMSB10 in the carcinogenesis of pancreatic carcinoma. Conclusion: Using gene expression profiling of pancreatic cell lines we were able to identify genes differentially expressed in pancreatic adenocarcinoma, which might contribute to pancreatic cancer development. Copyright (C) 2005 S. Karger AG, Basel and IAP
    Type of Publication: Journal article published
    PubMed ID: 15983444
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  • 4
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    German Medical Science; Düsseldorf, Köln
    In:  123. Kongress der Deutschen Gesellschaft für Chirurgie; 20060502-20060505; Berlin; DOC06dgch5444 /20060502/
    Publication Date: 2006-05-09
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 5
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    German Medical Science; Düsseldorf, Köln
    In:  122. Kongress der Deutschen Gesellschaft für Chirurgie; 20050405-20050408; München; DOC05dgch3569 /20050615/
    Publication Date: 2005-06-16
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 6
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    German Medical Science; Düsseldorf, Köln
    In:  121. Kongress der Deutschen Gesellschaft für Chirurgie; 20040427-20040430; Berlin; DOC04dgch1408 /20041007/
    Publication Date: 2004-10-07
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 7
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  124. Kongress der Deutschen Gesellschaft für Chirurgie; 20070501-20070504; München; DOC07dgch7361 /20071001/
    Publication Date: 2007-10-02
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 8
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    German Medical Science; Düsseldorf, Köln
    In:  123. Kongress der Deutschen Gesellschaft für Chirurgie; 20060502-20060505; Berlin; DOC06dgch5452 /20060502/
    Publication Date: 2006-05-09
    Keywords: ddc: 610
    Language: German
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  • 9
    ISSN: 1433-0385
    Keywords: Key words: Pancreatitis ; Early complication ; Interleukin-6 ; Interleukin-8. ; Schlüsselwörter: Pankreatitis ; Frühkomplikation ; Interleukin-6 ; Interleukin-8.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung. Die akute Pankreatitis (AP) induziert abhängig von ihrer Verlaufsform ödematös oder nekrotisierend systemische Komplikationen, deren Pathogenese ungeklärt ist. Der Nachweis von Cytokinen im Blut dieser Patienten könnte einen Beitrag zur Pathophysiologie der systemischen Frühkomplikationen der AP liefern. Weiterhin kann der Anstieg der Cytokine im Blut einen Hinweis auf den Schweregrad der Pankreatitis geben. Im Zeitraum von Oktober 1992 bis August 1993 wurden 23 Patienten mit einer AP im Rahmen einer prospektiven Beobachtungsstudie dokumentiert und Serum für die Messung der Cytokine in einem gewerblichen ELISA und des C-reaktiven-Proteins (CRP) nephelometrisch gewonnen. Sechs der 11 Patienten mit nekrotisierender AP sind früh (n = 1) oder an späten septischen Komplikationen gestorben. Keiner der 12 Patienten mit ödematöser AP verstarb. Es wurde jeweils das Maximum der Cytokin- bzw. CRP-Konzentration in den ersten drei Tagen zur Bewertung herangezogen. Die IL-6-Werte im Plasma reichten von 0 bis 2664 pg/ml. Im Verlauf der Erkrankung fielen die Werte unabhängig von weiteren Komplikationen gegen 0. Das Maximum der IL-6-Konzentration in den ersten 3 Tagen klassifizierte – bei einem Grenzwert von 600 pg/ml – bei 20 Patienten richtig die ödematöse oder nekrotisierende AP (Sensitivität: 82 %, Spezifität: 91 %, p 〈 0,001). Die Plasmawerte für IL-8 reichten von 〈 100 bis 1381 pg/ml und zeigten zwar während der ersten Tage die höchsten Werte, wiesen aber im Gegensatz zum IL-6 mehrere Anstiege im weiteren Verlauf auf. Das Maximum der IL-8-Konzentration korrelierte – bei einem Grenzwert von 200 pg/ml – nur bei 18 Patienten mit der Form der AP (Sensitivität 82 %, Spezifität 75 %, p 〈 0,01). Das CRP im Serum der Patienten lag zwischen 0 und 535 mg/l. Bei der nekrotisierenden AP fanden sich entsprechend den Cytokinen deutlich höhere Werte im Vergleich zur ödematösen AP. Bei einem Grenzwert von 200 mg/l für das CRP-Maximum in den ersten 3 Tagen wurden 18 von 22 Patienten richtig klassifiziert, entsprechend einer Sensitivität und Spezifität von 82 % (p 〈 0,01). Es fand sich keine Korrelation zwischen den Plasmawerten der Cytokine und der Letalität. Das Cytokin TNF-α war im Verlauf der Proben von 5 Patienten mit ödematöser oder nekrotisierender AP nicht nachweisbar. Die Konzentration vor allem des Cytokins IL-6 und weniger des Cytokins IL-8 sowie des CRP gibt Hinweise auf den Verlauf der AP in der Frühphase. Da ihnen eine zentrale Rolle in der immunologischen Reaktion zukommt, kann eine zum Teil exzessive Stimulation der spezifischen Zellen (Makrophagen, Lymphocyten und Endothelien) im Verlauf der AP angenommen werden. Hieraus folgen die systemischen Frühkomplikationen der AP.
    Notes: Summary. The detection of cytokines may elucidate the pathophysiological mechanisms that produce early systemic complications in acute interstitial (i) or necrotizing (n) pancreatitis (AP). The increase in the level of cytokines in the blood of patients with AP may correlate with the severity of the disease. In a prospective clinical trial from October 1992 to August 1993, 23 patients with AP were recruited and blood samples taken for cytokine detection by commercially available Elisa kits and C-reactive protein (CRP) by laser nephelometry. Six of 11 patients with nAP died either early (n = 1) or of late septic complications. None died of iAP. The peak of cytokine and CRP level in the first 3 days of hospitalization was used for calculation. The IL-6 concentration in the blood reached up to 2600 pg/ml in the 1st few days, depending on the severity of AP, and dropped to almost zero in the next days, independently of the clinical course. The differentiation of i- versus nAP, using a cutoff line of 600 pg/ml, was correct in 20 patients [87 %, sensitivity (SE): 82 %, specificity (SP): 91 %, P 〈 0.001]. The blood levels of IL-8 reached a maximum of 1381 pg/ml in the 1st few days, depending on the severity of AP, and showed a correlation with the clinical course in the following days. The peak of IL-8 blood levels indicated correctly the severity of AP in 18 out of 23 patients using a cutoff level of 200 pg/ml (accuracy: 78 %, SE: 82 %, SP: 75 %, P 〈 0.01). The CRP levels increased up to a maximum of 535 mg/l and indicated the course of AP correctly in 18 out of 22 patients (SE and SP 82 %, P 〈 0.01). There was no correlation between cytokine blood levels and mortality. In the blood samples of five patients with i- or nAP, no TNF-α was detectable. The blood levels of IL-6, and to a lesser extent of IL-8 and CRP, can predict the severity and early systemic complications of AP. The excessive rise in cytokines can be explained by the stimulation of immunological cells (macrophages, lymphocytes and endothelial cells) in the course of AP, inducing early systemic complications.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1433-0385
    Keywords: Key words: Hepatic artery aneurysm ; Gastrointestinal bleeding ; Embolization. ; Schlüsselwörter: Hepaticaaneurysma ; Gastrointestinalblutung ; Embolisation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung. Wir berichten über ein intrahepatisches Aneurysma in einem peripheren Ast der A. hepatica dextra bei einer 64 jährigen Patientin. Nach zunächst uncharakteristischer Oberbauchsymptomatik war es zu wiederholten akuten oberen Gastrointestinalblutungen bis zur Schocksymptomatik gekommen, deren Ursachenfindung bei Zustand nach Billroth-II-Magenresektion erschwert war. Erst die verzögert diagnostizierte Hämobilie führte zur Cöliacographie. Bei Nachweis eines intrahepatischen Aneurysmas der A. hepatica dextra gelang noch in gleicher Sitzung die angiographische superselektive Embolisation. Obere Gastrointestinalblutungen ohne den sicheren Nachweis einer entsprechenden Blutungsquelle sollten immer an ein Aneurysma im Bereich der Visceralarterien denken lassen und eine ätiologisch unklare Hämobilie stets Anlaß zur Cöliacographie sein. Die superselektive angiographische Embolisation intrahepatischer Aneurysmen ist eine risikoarme und erfolgversprechende Therapiemöglichkeit.
    Notes: Summary. We report the case of a 64-year-old female with an intrahepatic aneurysm of the right hepatic artery. Initially uncharacteristic upper abdominal symptoms were followed by repeated upper gastrointestinal bleeding and, eventually, hemorrhagic shock. Finding the cause of severe hematemesis was challenging due to a previous Billroth-II gastric resection. Delayed diagnosis of hemobilia necessitated coeliacography, whereby an intrahepatic aneurysm of the right hepatic artery was found and, during the same session, superselective embolization was achieved. If the cause of upper abdominal complaints remains unknown after routine diagnostic measures and the origin of bleeding in the upper gastrointestinal tract cannot be identified, aneurysms of abdominal arteries should be considered. Hemobilia of unknown etiology should always be an indication for coeliacography. The superselective angiographic embolization of intrahepatic aneurysms is a promising form of treatment with low risk.
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