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  • ddc: 610  (18)
  • CELL  (15)
  • pancreatic cancer  (15)
  • PANCREATIC-CANCER  (13)
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  • 1
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  124. Kongress der Deutschen Gesellschaft für Chirurgie; 20070501-20070504; München; DOC07dgch7574 /20071001/
    Publication Date: 2007-10-02
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 2
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    German Medical Science; Düsseldorf, Köln
    In:  122. Kongress der Deutschen Gesellschaft für Chirurgie; 20050405-20050408; München; DOC05dgch3365 /20050615/
    Publication Date: 2005-06-16
    Keywords: ddc: 610
    Language: German
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  • 3
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    German Medical Science; Düsseldorf, Köln
    In:  121. Kongress der Deutschen Gesellschaft für Chirurgie; 20040427-20040430; Berlin; DOC04dgch0695 /20041007/
    Publication Date: 2004-10-07
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 4
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  132. Kongress der Deutschen Gesellschaft für Chirurgie; 20150428-20150501; München; DOC15dgch551 /20150424/
    Publication Date: 2015-04-25
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 5
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  128. Kongress der Deutschen Gesellschaft für Chirurgie; 20110503-20110506; München; DOC11dgch620 /20110520/
    Publication Date: 2011-05-20
    Keywords: ddc: 610
    Language: German
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  • 6
    Keywords: CANCER ; EXPRESSION ; SURVIVAL ; tumor ; CELL ; Germany ; human ; COHORT ; PROTEIN ; PROTEINS ; cell line ; TISSUE ; TUMORS ; LINES ; PATIENT ; FAMILY ; CARCINOGENESIS ; TISSUES ; CELL-LINES ; LESIONS ; PROGRESSION ; immunohistochemistry ; CELL-LINE ; LINE ; LOCALIZATION ; POLYMERASE-CHAIN-REACTION ; adenocarcinoma ; ADENOCARCINOMAS ; pathology ; OVEREXPRESSION ; cell lines ; pancreatic cancer ; protein expression ; chemoresistance ; SUBCELLULAR-LOCALIZATION ; SUBSET ; pancreas ; PANCREATIC-CANCER ; FAMILIES ; DUCTAL ADENOCARCINOMA ; polymerase chain reaction ; TUMOR TISSUE ; LEVEL ; analysis ; methods ; pancreatic ; RARE ; SURVIVAL-DATA ; Reverse Transcriptase Polymerase Chain Reaction
    Abstract: AIMS: To determine the role of two antiapoptotic proteins of the IAP family, cIAP1 and cIAP2, in human pancreatic carcinogenesis. METHODS: mRNA levels were measured in pancreatic tissues and pancreatic cancer cell lines by quantitative reverse-transcriptase polymerase chain reaction (QRT-PCR). Protein expression was assessed in pancreatic cancer cell lines by immunoblotting and in pancreatic tissues by immunohistochemistry and correlated with pathological and survival data. RESULTS: cIAP1 expression was constantly high in non-neoplastic pancreatic tissues, in PanIN lesions, as well as in a subset of primary and metastatic pancreatic ductal adenocarcinomas (PDAC), and a preferential cytoplasmatic localization was observed in the tumor tissues. cIAP1 expression was rare in a cohort of cystic tumors. cIAP2 mRNA levels were significantly higher (2.4 fold) in PDAC than in the normal tissues. cIAP2 protein was overexpressed in PDAC and was detectable in low-grade and high-grade PanIN lesions. Moreover, cIAP2 was frequently expressed in pancreatic cystic tumors. cIAP1 and cIAP2 mRNA and protein were detected in all the examined cell lines. Survival analysis revealed a shorter survival in patients with cIAP1/cIAP2-positive tumors. CONCLUSIONS: cIAP1 might contribute to the regulation of the apoptotic process in the normal and in the neoplastic pancreas, depending on its subcellular localization. cIAP2 overexpression is a frequent and early event in pancreatic cancer progression and could therefore potentially influence important pathophysiological aspects of PDAC, such as anoikis or chemoresistance
    Type of Publication: Journal article published
    PubMed ID: 16775116
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  • 7
    Keywords: RECEPTOR ; CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; GROWTH ; GROWTH-FACTOR ; CELL ; Germany ; TISSUE ; LINES ; TIME ; FAMILY ; INDUCTION ; TISSUES ; CONTRAST ; CELL-LINES ; DOWN-REGULATION ; MEMBER ; MEMBERS ; PHOSPHORYLATION ; BREAST-CANCER ; antibodies ; antibody ; immunohistochemistry ; ASSAY ; CARCINOMA CELLS ; CELL-LINE ; LINE ; CANCER-CELLS ; BETA ; RT-PCR ; adenocarcinoma ; p21 ; CELL-SURFACE ; RECEPTORS ; DIFFERENTIAL EXPRESSION ; cell lines ; pancreatic cancer ; CELL-GROWTH ; signaling ; PANCREATIC-CANCER ; FAMILIES ; DUCTAL ADENOCARCINOMA ; independent growth ; ENHANCED EXPRESSION ; TGF-beta 1 ; HEPARAN-SULFATE PROTEOGLYCANS ; LEVEL ; pancreatic ; ASSAYS ; SULFATE ; downregulation ; lymph node ; LYMPH-NODE ; correlation ; VIEW ; DECREASED SURVIVAL ; activin ; bone morphogenic protein ; CONTROLS CELLULAR-RESPONSES ; glypican ; heparan sulfate proteoglycans ; SMAD PROTEINS
    Abstract: Glypican 1 (GPC1) is a cell surface heparan sulfate proteoglycan that acts as a co-receptor for heparin-binding growth factors as well as for members of the TGF-beta family. GPC1 plays a role in pancreatic cancer by regulating growth factor responsiveness. In view of the importance of members of the TGF-beta family in pancreatic cancer, in the present study, the role of GPC1 in TGF-beta, BMP and activin signaling was analyzed. Quantitative RT-PCR and immunohistochemistry were utilized to analyze GPC1 and TGF-beta, BMP and activin receptor expression levels. Panc-1 and T3M4 pancreatic cancer cells were transfected in a stable manner with a GPC1 antisense expression construct. Anchorage-dependent and -independent growth was determined by MTT and soft agar assays. TGF-beta 1, activin-A and BMP-2 responsiveness was determined by MTT assays and immunoblotting with p21, p-Smad1, and p-Smad2 antibodies. QRT-PCR demonstrated increased GPC1 mRNA levels in pancreatic ductal adenocarcinoma (PDAC) compared to normal pancreatic tissues (NPT), as described previously. There was a significant correlation between GPC1 mRNA levels and T beta RII, act-R1a, act-R1b, act-R2a, BMP-R1a, and BMP-R2 mRNA expression in NPT. In contrast, GPC1 mRNA expression correlated directly with act-R1a and BMP-R1a in NO PDAC cases and with act-R2a and BMP-R1a in lymph node positive cases. Down-regulation of GPC1 resulted in increased doubling time in Panc-1 but not in T3M4 cells, and decreased anchorage-independent growth in both cell lines. GPC1 down-regulation resulted in a slightly altered response towards TGF-beta 1, activin-A and BMP-2 in terms of growth, p21 induction and Smad2 phosphorylation. In conclusion, enhanced GPC1 expression correlates with BMP and activin receptors in pancreatic cancer. GPC1 down-regulation suppresses pancreatic cancer cell growth and slightly modifies signaling of members of the TGF-beta family of growth factors
    Type of Publication: Journal article published
    PubMed ID: 17016645
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  • 8
    Keywords: CANCER ; CELLS ; EXPRESSION ; tumor ; TUMOR-CELLS ; carcinoma ; CELL ; Germany ; neoplasms ; DIAGNOSIS ; NEW-YORK ; microarray ; transcription ; TISSUE ; DNA ; MICROARRAY DATA ; MUTATIONS ; Jun ; PHENOTYPE ; vimentin ; HEAD ; adenocarcinoma ; pathology ; BEHAVIOR ; MICROARRAY ANALYSIS ; expression profiling ; TUMOR CELLS ; DIFFERENTIAL-DIAGNOSIS ; CELL CARCINOMA ; OF-THE-LITERATURE ; pancreas ; review ; DUCTAL ADENOCARCINOMA ; AUTOPSY ; analysis ; pancreatic ; TUMOR-CELL ; GENOTYPE ; DNA-MICROARRAY ; USA ; pancreatic ductal adenocarcinoma ; MYOEPITHELIAL CARCINOMA ; pancreatic neoplasm ; PSEUDOPAPILLARY TUMORS
    Abstract: Pancreatic neoplasms have been reliably classified on the basis of their histopathology and immunophenotype. In this study, we report on a pancreatic tumor whose phenotype and genotype could not be assigned to any known tumor entity. The tumor was observed in the pancreatic head of a 54-year-old woman. It was found to be a solid infiltrating carcinoma with abundant clear cells. Apart from cytokeratin, the tumor cells expressed vimentin, S100, and MUC-1. DNA microarray analysis revealed a transcription profile clearly differing from that of normal pancreatic tissue and pancreatic ductal adenocarcinoma. Despite metastatic behavior, the tumor displayed a more favorable course than conventional pancreatic ductal adenocarcinoma. We suggest that this tumor be called solid type clear cell carcinoma of the pancreas
    Type of Publication: Journal article published
    PubMed ID: 17453235
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  • 9
    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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  • 10
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; GROWTH ; proliferation ; tumor ; carcinoma ; CELL ; Germany ; human ; IN-VIVO ; HEPATOCELLULAR-CARCINOMA ; DISTINCT ; GENE ; GENE-EXPRESSION ; GENES ; TUMORS ; ACTIVATION ; DNA ; INFECTION ; MECHANISM ; prognosis ; mechanisms ; BREAST-CANCER ; TARGET ; virus ; TRANSGENIC MICE ; COMPARATIVE GENOMIC HYBRIDIZATION ; gene expression ; NUMBER ; etiology ; RATES ; REGION ; ONCOGENE ; ALCOHOL ; OVEREXPRESSION ; gene expression profiling ; ALCOHOL-CONSUMPTION ; CONSUMPTION ; molecular ; RE ; ARRAY ; CANDIDATE GENES ; USA ; CANDIDATE ; CANCERS ; viral ; CHROMOSOME-ABERRATIONS ; ELONGATION-FACTOR EEF1A2
    Abstract: Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide and is characterized by aggressive tumor behavior coupled with poor prognosis. Various etiologies have been linked to HCC development, most prominently chronic hepatitis B and C virus infections as well as chronic alcohol consumption. In approximately 10% of HCCs, the etiology remains cryptic; however, recent epidemiological data suggest that most of these cryptogenic HCCs develop due to nonalcoholic steatohepatitis. To identify etiology-dependent DNA copy number aberrations and genes relevant to hepatocarcinogenesis, we performed array based comparative genomic hybridization of 63 HCCs of well-defined etiology and 4 HCC cell lines followed by gene expression profiling and functional analyses of candidate genes. For a 10-megabase chromosome region on 8q24, we observed etiology-dependent copy number gains and MYC overexpression in viral and alcohol-related HCCs, resulting in up-regulation of MYC target genes. Cryptogenic HCCs showed neither 8q24 gains, nor MYC overexpression, nor target gene activation, suggesting that tumors of this etiology develop by way of a distinct MYC-independent pathomechanism. Furthermore, we detected several etiology-independent small chromosome aberrations, including amplification of MDM4 on 1q32.1 and frequent gains of EEF1A2 on 20q13.33. Both genes were overexpressed in approximately half the HCCs examined, and gene silencing reduced cell viability as well as proliferation and increased apoptosis rates in HCC cell fines. Conclusion: Our findings suggest that MDM4 and EEF1A2 act as etiology-independent oncogenes in a significant percentage of HCCs
    Type of Publication: Journal article published
    PubMed ID: 18161050
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