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  • GENE  (14)
  • 1
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; carcinoma ; Germany ; IN-VIVO ; INHIBITION ; THERAPY ; VITRO ; GENE ; GENES ; LINES ; MICE ; PATIENT ; IMPACT ; INDUCTION ; treatment ; 5-FLUOROURACIL ; prevention ; resistance ; AGE ; NUDE-MICE ; CELL-LINE ; chemotherapy ; LINE ; CARCINOMAS ; specificity ; CISPLATIN ; pancreatic cancer ; CANCER-THERAPY ; CYTOTOXICITY ; signaling ; GEMCITABINE ; RE ; PANCREATIC-CANCER ; cancer therapy ; pancreatic ; GENDER ; dexamethasone ; GLUCOCORTICOID-INDUCED APOPTOSIS ; NAUSEA ; HISTOLOGY ; in vivo ; surgical resection
    Abstract: Background: Chemotherapy for pancreatic carcinoma often has severe side effects that limit its efficacy. The glucocorticoid (GC) dexamethasone (DEX) is frequently used as co-treatment to prevent side effects of chemotherapy such as nausea, for palliative purposes and to treat allergic reactions. While the potent pro-apoptotic properties and the supportive effects of GCs to tumour therapy in lymphoid cells are well studied, the impact of GCs to cytotoxic treatment of pancreatic carcinoma is unknown. Methods: A prospective study of DEX-mediated resistance was performed using a pancreatic carcinoma xenografted to nude mice, 20 surgical resections and 10 established pancreatic carcinoma cell lines. Antiapoptotic signaling in response to DEX was examined by Western blot analysis. Results: In vitro, DEX inhibited drug-induced apoptosis and promoted the growth in all of 10 examined malignant cells. Ex vivo, DEX used in physiological concentrations significantly prevented the cytotoxic effect of gemcitabine and cisplatin in 18 of 20 freshly isolated cell lines from resected pancreatic tumours. No correlation with age, gender, histology, TNM and induction of therapy resistance by DEX co-treatment could be detected. In vivo, DEX totally prevented cytotoxicity of chemotherapy to pancreatic carcinoma cells xenografted to nude mice. Mechanistically, DEX upregulated pro-survival factors and anti-apoptotic genes in established pancreatic carcinoma cells. Conclusion: These data show that DEX induces therapy resistance in pancreatic carcinoma cells and raise the question whether GC-mediated protection of tumour cells from cancer therapy may be dangerous for patients
    Type of Publication: Journal article published
    PubMed ID: 16539710
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  • 2
    Keywords: INHIBITOR ; Germany ; DISEASE ; RISK ; SITE ; GENE ; GENES ; PROTEIN ; ACTIVATION ; CLEAVAGE ; MUTATION ; genetics ; MUTATIONS ; Jun ; INDIVIDUALS ; heredity ; chronic pancreatitis ; RECOMBINANT ; pancreas ; VARIANT ; ENZYME ; pancreatic ; LOSSES ; odds ratio ; PROTECTS ; HEREDITARY PANCREATITIS ; HUMAN CATIONIC TRYPSINOGEN
    Abstract: Chronic pancreatitis is a common inflammatory disease of the pancreas. Mutations in the genes encoding cationic trypsinogen (PRSS1) 1 and the pancreatic secretory trypsin inhibitor (SPINK1) 2 are associated with chronic pancreatitis. Because increased proteolytic activity owing to mutated PRSS1 enhances the risk for chronic pancreatitis, mutations in the gene encoding anionic trypsinogen (PRSS2) may also predispose to disease. Here we analyzed PRSS2 in individuals with chronic pancreatitis and controls and found, to our surprise, that a variant of codon 191 (G191R) is overrepresented in control subjects: G191R was present in 220/6,459 (3.4%) controls but in only 32/2,466 (1.3%) affected individuals (odds ratio 0.37; P = 1.1 x 10(-8)). Upon activation by enterokinase or trypsin, purified recombinant G191R protein showed a complete loss of trypsin activity owing to the introduction of a new tryptic cleavage site that renders the enzyme hypersensitive to autocatalytic proteolysis. In conclusion, the G191R variant of PRSS2 mitigates intrapancreatic trypsin activity and thereby protects against chronic pancreatitis
    Type of Publication: Journal article published
    PubMed ID: 16699518
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  • 3
    Keywords: RECEPTOR ; SPECTRA ; ANGIOGENESIS ; APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; GROWTH ; GROWTH-FACTOR ; INHIBITOR ; tumor ; CELL ; FACTOR RECEPTOR ; Germany ; IN-VIVO ; INHIBITION ; KINASE ; THERAPY ; TYROSINE KINASE ; VIVO ; QUANTIFICATION ; DEATH ; DISEASE ; GENE ; PROTEIN ; cell line ; LINES ; PATIENT ; LIGAND ; FLOW ; cell cycle ; CELL-CYCLE ; CELL-LINES ; CYCLE ; protein kinase ; PROTEIN-KINASE ; TYROSINE KINASE INHIBITOR ; TARGET ; PROGRESSION ; immunohistochemistry ; ASSAY ; CELL-DEATH ; MUTATION ; CELL-LINE ; LINE ; MUTATIONS ; CANCER-PATIENTS ; POLYMERASE-CHAIN-REACTION ; PROTEIN-KINASE-C ; CHAIN-REACTION ; RECEPTORS ; CANCER PATIENTS ; point mutation ; cell lines ; pancreatic cancer ; RANDOMIZED-TRIAL ; TUMOR ANGIOGENESIS ; MANAGEMENT ; CELL-CYCLE PROGRESSION ; INHIBITORS ; CELL-GROWTH ; CHAIN ; ONCOLOGY ; PANCREATIC-CANCER ; TUMOR-GROWTH ; flow cytometry ; THERAPIES ; ACUTE MYELOID-LEUKEMIA ; polymerase chain reaction ; REAL-TIME ; POINT MUTATIONS ; MURINE MODEL ; TYROSINE KINASES ; analysis ; methods ; pancreatic ; ASSAYS ; cell death ; BIOLOGICAL-ACTIVITY ; USA ; POTENTIAL ROLE ; vascular endothelial growth factor ; COMPOUND ; in vivo ; SPECTRUM ; SPECIMENS ; KINASE INHIBITOR ; GROWTH-FACTOR-RECEPTOR ; receptor tyrosine kinase ; RECEPTOR TYROSINE KINASES ; - ; POINT ; modeling ; quantitative ; block ; ACTIVATING MUTATION ; ENDOTHELIAL GROWTH ; FLT3 ; FLT3 MUTATIONS ; INTERNATIONAL CONSENSUS ; PKC412 ; SOLID HUMAN TUMORS ; VEGF-RII
    Abstract: BACKGROUND. PKC412 is a kinase inhibitor that blocks protein kinase C (PKC), vascular endothelial growth factor receptors, platelet-derived growth factor receptor FLT3, and other class III receptor tyrosine kinases. The enthusiasm for this compound is based on its inhibitory effect even in the case of FLT3 mutations. The aim of this study was to analyze the role of FLT3 in pancreatic cancer and to study the biological activity of combined inhibition of neovascularization and mitogenesis in this disease. METHODS. FLT3 expression was analyzed in 18 pancreatic cancer specimens by real-time quantitative polymerase chain reaction (RTQ-PCR) and immunohistochemistry. Sixteen pancreatic cancer cell lines were screened for ITD and D835 point mutations of the FLT3 gene. MTT assays and anchorage-independent growth assays were used to study cell growth. Flow cytometry was used for cell cycle analysis and apoptosis quantification. In vivo AsPC-1 and HIAF-II cells were used for orthotopic tumor modeling. Immunohistochemistry was used to quantity tumor angiogenesis. RESULTS. FLT3 expression is down-regulated in pancreatic cancer. Activating FLT3 mutations (ITD, D835) were not detectable in any of the pancreatic cancer cell lines. Cell growth was significantly inhibited as cell-cycle progression was reduced and programmed cell death increased. In vivo PKC412 therapy resulted in a significant inhibition of orthotopic tumor growth with abrogation of tumor angiogenesis. CONCLUSIONS. These data highlight that PKC412 may be a new compound in target therapy of inoperable pancreatic cancer patients and suggest a potential role for the combined use of broad spectrum kinase inhibitors in the management of these patients
    Type of Publication: Journal article published
    PubMed ID: 17676584
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  • 4
    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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  • 5
    Keywords: RECEPTOR ; CANCER ; CANCER CELLS ; EXPRESSION ; tumor ; Germany ; DISEASE ; GENE ; GENES ; GENOME ; PROTEIN ; RNA ; TUMORS ; IDENTIFICATION ; LESIONS ; immunohistochemistry ; MICROARRAY DATA ; expression profiling ; pancreatic cancer ; pancreatic carcinoma ; review ; PANCREATIC-CANCER ; DUCTAL ADENOCARCINOMA ; MEDIATED APOPTOSIS ; development ; CYSTIC LESIONS ; pancreatic tumor ; EXPERIMENT ANNOTATIONS ; Fas-activated serine/threonine kinase ; PAPILLARY MUCINOUS NEOPLASMS ; siRNA silencing
    Abstract: Aim: The diversity in the aggressiveness of cystic tumors of the pancreas - ranging from the usually benign serous cystadenoma to lesions of variable degrees of malignancy - was utilized for the identification of molecular factors that are involved in the occurrence of malignancy. Methods: We analyzed the transcript profiles of different cystic tumor types. The results were confirmed at the protein level by immunohistochemistry. Also, functional studies with siRNA silencing were performed. Results: Expression variations at the RNA and protein level were identified that are closely correlated with the degree of malignancy. Besides, all tumors could be classified effectively by this means. Many of the identified factors had not previously been known to be associated with malignant cystic lesions. siRNA silencing of the gene with the most prominent variation - the anti-apoptotic factor FASTK (Fas-activated serine/threonine kinase) - revealed a regulative effect on several genes known to be relevant to the development of tumors. Conclusion: By a molecular analysis of rare types of pancreatic cancer, which are less frequent in terms of disease, variations could be identified that could be critical for the regulation of malignancy and thus relevant to the treatment of also the majority of pancreatic tumors. Copyright (C) 2008 S. Karger AG, Basel and IAP
    Type of Publication: Journal article published
    PubMed ID: 19077453
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  • 6
    Keywords: EXPRESSION ; tumor ; carcinoma ; Germany ; NEW-YORK ; GENE ; TISSUE ; TUMORS ; TISSUES ; DELETION ; LESIONS ; MICROARRAY DATA ; MUTATION ; METASTASIS ; inactivation ; MUTATIONS ; HEAD ; adenocarcinoma ; ADENOCARCINOMAS ; beta-catenin ; MICROARRAY ANALYSIS ; point mutation ; CLUSTER ; MASSES ; molecular ; FEATURES ; pancreas ; DUCTAL ADENOCARCINOMA ; ACINAR-CELL-CARCINOMA ; AUTOPSY ; CLUSTER-ANALYSIS ; DPC4/SMAD4 ; p16(INK4A)
    Abstract: An unusual pancreatic tumor with microcystic and tubulopapillary features was observed in a 53-year-old woman. The tumor presented as a large, focally cystic mass in the head of the pancreas, which compressed the surrounding structures. The histological and immunohistochemical analysis revealed a neoplasm that could not be assigned to any of the known pancreatic tumor types. At the molecular level, the tumor showed inactivation of the DPC4/SMAD4 gene, deletion of exon 1 of the p16(INK4A) gene and a point mutation at codon 34 (GGA〉AGA) of beta-catenin. Transcriptional profiling analyses and subsequent correspondence cluster analysis demonstrated that the transcriptional profile of the tumor differed distinctly from that of ductal adenocarcinomas, pancreatic cystic tumors and normal pancreatic tissues. These data suggest that the neoplasm most likely represents a new pancreatic tumor entity, which we would like to refer to as microcystic tubulopapillary tumor
    Type of Publication: Journal article published
    PubMed ID: 15014986
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  • 7
    Keywords: radiotherapy ; BLOOD ; CANCER ; imaging ; Germany ; GENE ; PATIENT ; BIOMARKERS ; radiology ; PANCREATIC-CANCER ; GEMCITABINE ; IMRT ; pancreatic cancer ; biomarker ; SIGNATURES ; cetuximab
    Type of Publication: Meeting abstract published
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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: ENVIRONMENT ; RECEPTOR ; ANGIOGENESIS ; CANCER ; CELLS ; ENDOTHELIAL-CELLS ; EXPRESSION ; GROWTH ; INHIBITOR ; tumor ; AGENTS ; CELL ; Germany ; human ; NETWORK ; RISK ; GENE ; GENES ; PROTEIN ; PROTEINS ; DRUG ; COMPONENTS ; MICE ; PATIENT ; knockout ; STAGE ; PROGRESSION ; DESIGN ; INDUCED APOPTOSIS ; METASTASIS ; COLORECTAL-CANCER ; COMPONENT ; cancer risk ; RECURRENCE ; COLON-CANCER ; CANCER-PATIENTS ; STRATEGIES ; REVEALS ; systems biology ; CANCER PATIENTS ; pancreatic cancer ; pancreatic carcinoma ; chronic pancreatitis ; ACQUIRED-RESISTANCE ; INHIBITORS ; signaling ; AGENT ; RE ; PANCREATIC-CANCER ; PATTERN ; TUMOR-GROWTH ; cancer therapy ; PANCREATITIS ; regulation ; antiangiogenic therapy ; LEVEL ; pancreatic ; USA ; DRUGS ; INCREASED RISK ; CANCER-RISK ; ENDOTHELIAL-CELL ; HOMEOSTASIS ; SPECIMENS ; peroxisome ; EGFR INHIBITORS ; GLUCOSYLCERAMIDE SYNTHASE ; homeostatic balance ; PPAR-DELTA
    Abstract: A shift of the angiogenic balance to the proangiogenic state, termed the "angiogenic switch," is a hallmark of cancer progression. Here we devise a strategy for identifying genetic participants of the angiogenic switch based on inverse regulation of genes in human endothelial cells in response to key endogenous pro- and antiangiogenic proteins. This approach reveals a global network pattern for vascular homeostasis connecting known angiogenesis-related genes with previously unknown signaling components. We also demonstrate that the angiogenic switch is governed by simultaneous regulations of multiple genes organized as transcriptional circuitries. In pancreatic cancer patients, we validate the transcriptome-derived switch of the identified "angiogenic network:" The angiogenic state in chronic pancreatitis specimens is intermediate between the normal (angiogenesis off) and neoplastic (angiogenesis on) condition, suggesting that aberrant proangiogenic environment contributes to the increased cancer risk in patients with chronic pancreatitis. In knockout experiments in mice, we show that the targeted removal of a hub node (peroxisome proliferative-activated receptor delta) of the angiogenic network markedly impairs angiogenesis and tumor growth. Further, in tumor patients, we show that peroxisome proliferative-activated receptor 8 expression levels are correlated with advanced pathological tumor stage, increased risk for tumor recurrence, and distant metastasis. Our results therefore also may contribute to the rational design of antiangiogenic cancer agents; whereas "narrow" targeted cancer drugs may fail to shift the robust angiogenic regulatory network toward antiangiogenesis, the network may be more vulnerable to multiple or broad-spectrum inhibitors or to the targeted removal of the identified angiogenic "hub" nodes
    Type of Publication: Journal article published
    PubMed ID: 17652168
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  • 10
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; GROWTH ; tumor ; TUMOR-CELLS ; CELL ; Germany ; human ; PATHWAY ; PATHWAYS ; PROSTATE ; DIAGNOSIS ; GENE ; transcription ; cell line ; LINES ; PATIENT ; COMPLEX ; COMPLEXES ; prognosis ; CARCINOGENESIS ; INDUCTION ; CELL-LINES ; treatment ; ACID ; TARGET ; NO ; LESIONS ; NEOPLASIA ; prevention ; INDUCED APOPTOSIS ; PROMOTER ; COLORECTAL-CANCER ; metastases ; CELL-LINE ; LINE ; CANCER-CELLS ; CANCER-PATIENTS ; POLYMERASE-CHAIN-REACTION ; intraepithelial neoplasia ; CHAIN-REACTION ; chemoprevention ; CANCER PATIENTS ; OVEREXPRESSION ; cell lines ; pancreatic cancer ; ARACHIDONIC-ACID ; TUMOR CELLS ; chronic pancreatitis ; ACTIVATED RECEPTOR-GAMMA ; TRANSCRIPTIONAL REGULATION ; METABOLITE ; HUMAN COLON-CANCER ; CELL-GROWTH ; targeting ; CHAIN ; ONCOLOGY ; pancreas ; PANCREATIC-CANCER ; TUMOR-SUPPRESSOR ; SUPPRESSOR GENE ; polymerase chain reaction ; development ; CYCLOOXYGENASE-2 ; analysis ; pancreatic ; TUMOR-CELL ; SUPPRESSOR ; USA ; LOSSES ; lymph node metastases ; LYMPH-NODE ; pancreatic intraepithelial neoplasia ; INHIBIT ; PRECURSOR ; NOV ; TUMOR-DEVELOPMENT ; - ; pancreatic carcinogenesis ; 15-lipoxygenase-1 ; cell growth ; tubular complexes
    Abstract: Pancreatic cancer patients have an abysmal prognosis because of late diagnosis and lack of therapeutic options. Pancreatic intraepithelial neoplasias (PanINs), the precursor lesions, are a potential target for chemoprevention. Targeting eicosanoid pathways is an obvious choice because 5-lipoxygenase (5-LOX) has been suggested as a tumor promoter in pancreatic carcinogenesis. Here we provide evidence that 15-lipoxygenase- 1 (15-LOX-1) expression and activity may exert antitumorigenic effects in pancreatic cancer. Reverse transcription - polymerase chain reaction ( RTPCR) and Western blot analysis showed absence or very weak expression of 15-LOX-1 in all pancreatic cancer cell lines tested. 15-LOX-1 was strongly stained in normal ductal cells, tubular complexes, and centroacinar cells, but no staining was seen in islets, cancer cells, PanIN lesions, or in tumor cells in lymph node metastases, indicating that 15-LOX-1 expression is lost during tumor development in human pancreas. Overexpression of 15-LOX-1 in pancreatic tumor cells or treatment with its arachidonic acid - derived metabolite resulted in decreased cell growth. These findings provide evidence that loss of 15-LOX-1 may play an important role in pancreatic carcinogenesis, possibly as a tumor suppressor gene. Thus, induction of 15-LOX-1 expression may be an attractive option for the prevention and treatment of pancreatic cancer
    Type of Publication: Journal article published
    PubMed ID: 18030360
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