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1. Cullingworth J, Hooper ML, Harrison DJ, Mason JO, Sirard C, Patek CE, Clarke AR: Carcinogen-induced pancreatic lesions in the mouse: effect of Smad4 and Apc genotypes. Oncogene; 2002 Jul 11;21(30):4696-701
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  • Mutations in the tumour suppressor genes SMAD4 (DPC4, deleted in pancreatic cancer locus 4) and adenomatous polyposis coli (APC) have been implicated in the development of pancreatic cancer in humans.
  • Treatment of wild-type, Smad4(+/-), Apc(Min/+) or Apc(Min/+)Smad4(+/-) mice with N-Nitroso-N-Methyl Urea (NMU) results in abnormal foci in pancreatic acinar cells characterized by increased levels of beta-catenin.
  • Previously such foci have been shown to be the precursors of pancreatic neoplasia.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Carcinogens / toxicity. DNA-Binding Proteins / genetics. Methylnitrosourea / toxicity. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology. Trans-Activators / genetics. Zebrafish Proteins
  • [MeSH-minor] Animals. Cell Division / drug effects. Cytoskeletal Proteins / metabolism. Genotype. Immunohistochemistry. In Situ Nick-End Labeling. Mice. Mutation. Proto-Oncogene Proteins / metabolism. Signal Transduction / drug effects. Smad4 Protein. Transforming Growth Factor beta / pharmacology. Wnt Proteins. beta Catenin

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  • (PMID = 12096346.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / CTNNB1 protein, mouse; 0 / Carcinogens; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / Smad4 Protein; 0 / Smad4 protein, mouse; 0 / Trans-Activators; 0 / Transforming Growth Factor beta; 0 / Wnt Proteins; 0 / Zebrafish Proteins; 0 / beta Catenin; 0 / smad4 protein, zebrafish; 684-93-5 / Methylnitrosourea
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2. Huynh H, Alpert L, Alaoui-Jamali MA, Ng CY, Chan TW: Co-administration of finasteride and the pure anti-oestrogen ICI 182,780 act synergistically in modulating the IGF system in rat prostate. J Endocrinol; 2001 Oct;171(1):109-18
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  • Co-administration of ICI plus finasteride reduces prostate weight by approximately 50% and causes acinar dilation with decreased luminal epithelial cell thickness.
  • The acinar epithelial cells became atrophic and inactive with minimal cytoplasm.
  • Because the IGF and IGFBP-3 system plays an important role in prostate epithelial cell proliferation, apoptosis and tumour progression, the inhibitory effects of finasteride and ICI on IGF system may contribute to their anti-proliferative activity.
  • [MeSH-minor] Animals. Blotting, Northern / methods. Cell Division / drug effects. Drug Synergism. Enzyme Inhibitors / pharmacology. Epithelial Cells / drug effects. Insulin-Like Growth Factor Binding Protein 3 / metabolism. Male. Organ Size / drug effects. Phosphorylation. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Rats. Receptor, IGF Type 1 / metabolism. Statistics, Nonparametric

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  • (PMID = 11572795.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 5-alpha Reductase Inhibitors; 0 / Enzyme Inhibitors; 0 / Estrogen Antagonists; 0 / Insulin-Like Growth Factor Binding Protein 3; 0 / Proto-Oncogene Proteins; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol; 57GNO57U7G / Finasteride; 67763-96-6 / Insulin-Like Growth Factor I; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.1 / Akt1 protein, rat; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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3. de la Mano AM, Sevillano S, Manso MA, Pérez M, de Dios I: Cholecystokinin blockade alters the systemic immune response in rats with acute pancreatitis. Int J Exp Pathol; 2004 Apr;85(2):75-84
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  • The aim of this study was to study whether the time-course of inflammatory events during AP induced by bile-pancreatic duct obstruction (BPDO) varies after lowering the acinar enzyme content by L364,718 (0.1 mg/kg/day) administration over 7 days before inducing AP.
  • Flow cytometric immunophenotyping was used to analyse the following at different AP stages: distribution of major circulating leucocyte subsets, activation state of circulating neutrophils and monocytes as reflected by CD11b expression and tumour necrosis factor-alpha (TNF-alpha) production and the contribution of T-cell-derived pro-(TNF-alpha) and anti-(IL-10) inflammatory mediators.
  • It is concluded that lowering the acinar enzyme content through L364,718 treatment prevents earlier systemic immune events in BPDO-induced AP.
  • [MeSH-major] Devazepide / therapeutic use. Hormone Antagonists / therapeutic use. Pancreatitis / drug therapy. Receptors, Cholecystokinin / drug effects
  • [MeSH-minor] Acute Disease. Animals. Antigens, CD11b / analysis. Flow Cytometry / methods. Interleukin-10 / immunology. Lung / immunology. Lymphocyte Activation. Male. Neutrophil Infiltration. Neutrophils / immunology. Pancreas / immunology. Rats. Rats, Wistar. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 15154913.001).
  • [ISSN] 0959-9673
  • [Journal-full-title] International journal of experimental pathology
  • [ISO-abbreviation] Int J Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Hormone Antagonists; 0 / Receptors, Cholecystokinin; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; JE6P7QY7NH / Devazepide
  • [Other-IDs] NLM/ PMC2517463
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4. Haas M, Laubender RP, Stieber P, Holdenrieder S, Bruns CJ, Wilkowski R, Mansmann U, Heinemann V, Boeck S: Prognostic relevance of CA 19-9, CEA, CRP, and LDH kinetics in patients treated with palliative second-line therapy for advanced pancreatic cancer. Tumour Biol; 2010 Aug;31(4):351-7
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  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. C-Reactive Protein / metabolism. CA-19-9 Antigen / blood. Carcinoembryonic Antigen / blood. L-Lactate Dehydrogenase / blood. Palliative Care. Pancreatic Neoplasms / blood
  • [MeSH-minor] Adenocarcinoma / blood. Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adult. Aged. Biomarkers, Tumor / blood. Bone Neoplasms / blood. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Carcinoma, Acinar Cell / blood. Carcinoma, Acinar Cell / drug therapy. Carcinoma, Acinar Cell / pathology. Female. Humans. Kinetics. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lung Neoplasms / blood. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Male. Middle Aged. Neoplasm Staging. Peritoneal Neoplasms / blood. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / secondary. Prognosis. Retrospective Studies. Survival Rate

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  • (PMID = 20480409.001).
  • [ISSN] 1423-0380
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen; 9007-41-4 / C-Reactive Protein; EC 1.1.1.27 / L-Lactate Dehydrogenase
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5. Elcombe CR, Elcombe BM, Foster JR, Farrar DG, Jung R, Chang SC, Kennedy GL, Butenhoff JL: Hepatocellular hypertrophy and cell proliferation in Sprague-Dawley rats following dietary exposure to ammonium perfluorooctanoate occurs through increased activation of the xenosensor nuclear receptors PPARα and CAR/PXR. Arch Toxicol; 2010 Oct;84(10):787-98
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  • [Title] Hepatocellular hypertrophy and cell proliferation in Sprague-Dawley rats following dietary exposure to ammonium perfluorooctanoate occurs through increased activation of the xenosensor nuclear receptors PPARα and CAR/PXR.
  • Although non-genotoxic, chronic dietary treatment of Sprague-Dawley (S-D) rats with APFO produced an increase in benign tumours of the liver, acinar pancreas, and testicular Leydig cells.
  • The present study evaluates the potential roles for APFO-induced activation of PPARα and CAR/PXR with respect to liver tumour production in the S-D rat and when compared to the specific PPARα agonist, 4-chloro-6-(2,3-xylidino)-2-pyrimidinylthioacetic acid (Wy 14,643).
  • Responses to treatment with Wy 14,643 were consistent with increased activation of PPARα, specifically: increased CYP4A1 and peroxisomal β-oxidation; increased hepatocellular hypertrophy and cell proliferation; decreased apoptosis; and hypolipidaemia.
  • [MeSH-major] Caprylates / toxicity. Cell Proliferation / drug effects. Environmental Pollutants / toxicity. Fluorocarbons / toxicity. Hepatocytes / drug effects. Receptors, Cytoplasmic and Nuclear / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Body Weight / drug effects. Cytochrome P-450 Enzyme System / metabolism. DNA / metabolism. Hepatomegaly / chemically induced. Hypertrophy. Liver / enzymology. Liver / metabolism. Liver / pathology. Male. Organ Size / drug effects. PPAR alpha / metabolism. Peroxisomes / metabolism. Rats. Rats, Sprague-Dawley. Receptors, Steroid / metabolism

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  • (PMID = 20614104.001).
  • [ISSN] 1432-0738
  • [Journal-full-title] Archives of toxicology
  • [ISO-abbreviation] Arch. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Caprylates; 0 / Environmental Pollutants; 0 / Fluorocarbons; 0 / PPAR alpha; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Steroid; 0 / constitutive androstane receptor; 0 / pregnane X receptor; 9007-49-2 / DNA; 9035-51-2 / Cytochrome P-450 Enzyme System; 947VD76D3L / perfluorooctanoic acid
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6. Bozem M, Kuhlmann S, Blum R, Feick P, Schulz I: Hormone-stimulated calcium release is inhibited by cytoskeleton-disrupting toxins in AR4-2J cells. Cell Calcium; 2000 Aug;28(2):73-82
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  • We have studied the role of the actin cytoskeleton in bombesin-induced inositol 1,4,5-trisphosphate (IP(3))-production and Ca(2+)release in the pancreatic acinar tumour cell line AR4-2J.
  • Intracellular and extracellular free Ca(2+)concentrations were measured in cell suspensions, using Fura-2.
  • In latrunculin B-pretreated cells inhibition of both, bombesin-stimulated IP(3)- production and Ca(2+)release was partly suspended in the presence of aluminum fluoride, an activator of G-proteins.
  • [MeSH-major] Bacterial Proteins. Calcium / metabolism. Cytoskeleton / drug effects. Hormones / pharmacology. Pancreas / cytology. Pancreas / metabolism
  • [MeSH-minor] Aluminum Compounds / pharmacology. Animals. Bacterial Toxins / pharmacology. Bicyclo Compounds, Heterocyclic / pharmacology. Bombesin / metabolism. Bombesin / pharmacology. Cell Membrane Permeability / drug effects. Cytochalasin D / pharmacology. Cytosol / drug effects. Cytosol / metabolism. Fluorides / pharmacology. GTP-Binding Proteins / drug effects. GTP-Binding Proteins / metabolism. Inositol 1,4,5-Trisphosphate / metabolism. Pancreatic Neoplasms. Rats. Thiazoles / pharmacology. Thiazolidines. Tumor Cells, Cultured. Type C Phospholipases / drug effects. Type C Phospholipases / metabolism

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  • (PMID = 10970764.001).
  • [ISSN] 0143-4160
  • [Journal-full-title] Cell calcium
  • [ISO-abbreviation] Cell Calcium
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] SCOTLAND
  • [Chemical-registry-number] 0 / Aluminum Compounds; 0 / Bacterial Proteins; 0 / Bacterial Toxins; 0 / Bicyclo Compounds, Heterocyclic; 0 / Hormones; 0 / Thiazoles; 0 / Thiazolidines; 0 / toxB protein, Clostridium difficile; 22144-77-0 / Cytochalasin D; 76343-94-7 / latrunculin B; 85166-31-0 / Inositol 1,4,5-Trisphosphate; EC 3.1.4.- / Type C Phospholipases; EC 3.6.1.- / GTP-Binding Proteins; PX9AZU7QPK / Bombesin; Q80VPU408O / Fluorides; SY7Q814VUP / Calcium; Z77H3IKW94 / aluminum fluoride
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7. Dimitriou ID, Kapsogeorgou EK, Moutsopoulos HM, Manoussakis MN: CD40 on salivary gland epithelial cells: high constitutive expression by cultured cells from Sjögren's syndrome patients indicating their intrinsic activation. Clin Exp Immunol; 2002 Feb;127(2):386-92
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  • CD40 has been identified in an expanding list of haematopoietic and non-haematopoietic cells and has received an increased interest based on its role in a variety of cell-mediated responses and its potential to participate in the pathogenesis of chronic inflammatory disorders.
  • We studied the expression of CD40 protein in cultured non-neoplastic salivary gland epithelial cell (SGEC) lines as well as in minor SG biopsies obtained from 17 SS patients and 12 controls.
  • Immunocytochemical and flow cytometric analyses had revealed the occurrence of constitutively expressed CD40 molecules on the surface of long-term cultured SGEC lines, which could be further induced by interferon-gamma (IFN-gamma) and IL-1beta cytokines, but not tumour necrosis factor-alpha (TNF-alpha), IL-4, IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF) or IFN-alpha.
  • In SG biopsies, CD40 was constitutively expressed by lymphocytes, ductal epithelial cells and endothelial cells but not by other glandular cell types, such as acinar cells, myoepithelial cells and fibroblasts.
  • Our findings indicate the immunoregulatory potential of SGEC and lend further support to a model of intrinsic activation in salivary epithelia in SS, whereby these cells actively participate in the induction and maintenance of lymphocytic infiltrates of patients.
  • [MeSH-minor] Biopsy. CD40 Ligand / biosynthesis. CD40 Ligand / genetics. Cells, Cultured / drug effects. Cells, Cultured / metabolism. Cytokines / pharmacology. Endothelium / drug effects. Endothelium / metabolism. Endothelium / pathology. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Epithelial Cells / pathology. Female. HLA Antigens / biosynthesis. HLA Antigens / genetics. Humans. Intercellular Adhesion Molecule-1 / biosynthesis. Intercellular Adhesion Molecule-1 / genetics. Lymphocytes / drug effects. Lymphocytes / metabolism. Lymphocytes / pathology. Male

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  • (PMID = 11876766.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Cytokines; 0 / HLA Antigens; 126547-89-5 / Intercellular Adhesion Molecule-1; 147205-72-9 / CD40 Ligand
  • [Other-IDs] NLM/ PMC1906327
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8. Qi T, Han J, Cui Y, Zong M, Liu X, Zhu B: Comparative proteomic analysis for the detection of biomarkers in pancreatic ductal adenocarcinomas. J Clin Pathol; 2008 Jan;61(1):49-58
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  • METHODS: Eight pairs of matched PDAC and non-cancerous pancreas tissues were profiled with two-dimensional electrophoresis; differentially expressed proteins were identified by mass spectrometry.
  • RESULTS: A total of 48 differentially expressed proteins were identified; 30 of them are novel potential biomarkers.
  • Immunohistochemistry showed that TBX4 expression could be seen in both centroacinar cells and small ducts in normal pancreas and tumour cells in 5/5 (100%) well differentiated, 35/38 (92.1%) moderately differentiated, and 11/18 (61.1%) poorly differentiated PDAC tissues with different staining intensity.
  • However, in normal acinar cells and tumour cells in the other 3/38 (7.9%) moderately differentiated and 7/18 (38.9%) poorly differentiated PDAC tissues, there was no visible TBX4 expression.
  • In addition, there was obvious morphology difference between TBX4 negatively stained and positively stained tumour cells, which suggests different cellular origins.
  • Strong expression of HSP60 could be seen in both acinar cells and small ducts in normal pancreas tissues and tumour cells in PDAC tissues except for islets and tumour stoma; no correlation was found between HSP60 expression and differentiation of PDAC tissues.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Cell Differentiation. Female. HSP40 Heat-Shock Proteins / metabolism. Humans. Male. Middle Aged. Neoplasm Proteins / metabolism. Pancreas / metabolism. Proteomics. T-Box Domain Proteins / metabolism. Trypsin / metabolism

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  • (PMID = 17412869.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HSP40 Heat-Shock Proteins; 0 / Neoplasm Proteins; 0 / T-Box Domain Proteins; 0 / TBX4 protein, human; EC 3.4.21.4 / Trypsin
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9. Sorscher SM: Metastatic acinar cell carcinoma of the pancreas responding to gemcitabine, 5-fluorouracil and leucovorin therapy: a case report. Eur J Cancer Care (Engl); 2009 May;18(3):318-9
Hazardous Substances Data Bank. LEUCOVORIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastatic acinar cell carcinoma of the pancreas responding to gemcitabine, 5-fluorouracil and leucovorin therapy: a case report.
  • Acinar cell carcinoma of the pancreas is rare tumour with a generally poor prognosis.
  • There are very few reports of tumour regression following chemotherapy.
  • In this case report, a patient with metastatic acinar cell carcinoma in the liver developed progressive disease after cisplatin/etoposide and then had progressive disease after weekly paclitaxel chemotherapy.
  • However, his tumour then responded to gemcitibine/5-flourouracil/leucovorin chemotherapy.
  • Herein, previously described chemotherapy regimens used for this rare tumour are reviewed.
  • This case represents the first reported metastatic acinar cell carcinoma responding to this regimen.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Liver Neoplasms / drug therapy. Pancreatic Neoplasms
  • [MeSH-minor] Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Drug Resistance, Neoplasm. Fluorouracil / administration & dosage. Humans. Leucovorin / administration & dosage. Male. Middle Aged. Treatment Outcome. Vitamin B Complex / administration & dosage

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  • (PMID = 19445023.001).
  • [ISSN] 1365-2354
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; 12001-76-2 / Vitamin B Complex; B76N6SBZ8R / gemcitabine; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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10. Chan TW, Mark G, Huynh H: Induction of mammary epithelial cell differentiation and inhibition of dimethylbenz(A)anthracene-induced mammary tumour by co-administration of a pure antiestrogen ICI 182,780 and testosterone enanthate. Int J Oncol; 2001 Aug;19(2):263-9
Hazardous Substances Data Bank. TESTOSTERONE .

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  • [Title] Induction of mammary epithelial cell differentiation and inhibition of dimethylbenz(A)anthracene-induced mammary tumour by co-administration of a pure antiestrogen ICI 182,780 and testosterone enanthate.
  • TE increased the Ki-67 labelling index, stimulated lobuloalveolar and ductal growth, as well as the secretory activity of acinar cells.
  • Unlike TE, ICI caused a significant reduction in DMBA-induced tumour incidence, number of tumour bearing and tumour size.
  • Tumour incidence was reduced to 8% when both ICI and TE were co-administered.
  • These observations may give insight into novel actions of ICI and TE on breast differentiation and protection against carcinogenesis which may be useful in designing novel strategies for cancer prevention and/or treatment based on maximizing mammary epithelial cell differentiation.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Differentiation / drug effects. Epithelial Cells / drug effects. Estradiol / pharmacology. Mammary Neoplasms, Experimental / prevention & control. Testosterone / pharmacology
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene / administration & dosage. Animals. Cell Division / drug effects. Drug Therapy, Combination. Female. Immunohistochemistry. Ki-67 Antigen / analysis. Mammary Glands, Animal / chemistry. Mammary Glands, Animal / cytology. Mammary Glands, Animal / drug effects. Rats. Rats, Sprague-Dawley. Time Factors

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  • (PMID = 11445837.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ki-67 Antigen; 22X328QOC4 / fulvestrant; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; 7Z6522T8N9 / testosterone enanthate
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11. Ebert C, Nebe B, Walzel H, Weber H, Jonas L: Inhibitory effect of the lectin wheat germ agglutinin (WGA) on the proliferation of AR42J cells. Acta Histochem; 2009;111(4):335-42
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  • The rat pancreatic acinar tumour cell line AR42J is a widely used model to study the secretion, proliferation and differentiation of cells under the influence of hormones.
  • They possess both subtypes of the highly glycosylated cholecystokinin (CCK) receptor which are important for the regulation of secretion and for cell growth.
  • [MeSH-major] Cell Proliferation / drug effects
  • [MeSH-minor] Animals. Cell Line, Tumor. Flow Cytometry. Galectin 1 / pharmacology. Glycosylation / drug effects. Humans. Microscopy, Electron, Transmission. Pancreas / pathology. Pancreas / ultrastructure. Plant Lectins / pharmacology. Rats. Receptors, Cholecystokinin / chemistry. Secretory Vesicles / ultrastructure. Wheat Germ Agglutinins / pharmacology. alpha-Amylases / pharmacology

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  • (PMID = 19195686.001).
  • [ISSN] 1618-0372
  • [Journal-full-title] Acta histochemica
  • [ISO-abbreviation] Acta Histochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Galectin 1; 0 / Plant Lectins; 0 / Receptors, Cholecystokinin; 0 / Ulex europaeus lectins; 0 / Wheat Germ Agglutinins; EC 3.2.1.1 / alpha-Amylases
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12. Wu H, Bhopale KK, Ansari GA, Kaphalia BS: Ethanol-induced cytotoxicity in rat pancreatic acinar AR42J cells: role of fatty acid ethyl esters. Alcohol Alcohol; 2008 Jan-Feb;43(1):1-8
Hazardous Substances Data Bank. ETHANOL .

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  • [Title] Ethanol-induced cytotoxicity in rat pancreatic acinar AR42J cells: role of fatty acid ethyl esters.
  • METHODS: A time- and concentration-dependent synthesis of FAEEs and the cytotoxicity of ethanol and its predominant fatty acid esters were studied in rat pancreatic tumour (AR42J) cells in cultures.
  • RESULTS: The levels of FAEEs synthesized in cell cultures incubated with 800 mg% ethanol for 6 h were approximately 10-fold higher (60 nmol/25 x 10(6) cells) than those in cells incubated with 100 mg% ethanol (5.4 nmol/25 x 10(6) cells).
  • Ethanol exposure resulted in a concentration-dependent apoptosis (10, 12 and 13% at 200, 400 and 800 mg% ethanol, respectively, vs 5% in controls).
  • A similar concentration-dependent apoptosis was also found in the cells incubated with ethyl oleate (one of the predominant FAEEs reported in alcoholic patients).
  • [MeSH-major] Cytotoxins / toxicity. Ethanol / toxicity. Fatty Acids / toxicity. Pancreas, Exocrine / drug effects. Pancreas, Exocrine / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / physiology. Cell Line, Tumor. Dose-Response Relationship, Drug. Esters. Humans. Rats

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  • (PMID = 17942438.001).
  • [ISSN] 1464-3502
  • [Journal-full-title] Alcohol and alcoholism (Oxford, Oxfordshire)
  • [ISO-abbreviation] Alcohol Alcohol.
  • [Language] eng
  • [Grant] United States / NIAAA NIH HHS / AA / AA13171; United States / NIEHS NIH HHS / ES / P30ES06676
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytotoxins; 0 / Esters; 0 / Fatty Acids; 3K9958V90M / Ethanol
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13. Qiu X, Valentijn JA, Jamieson JD: Carboxyl-methylation of Rab3D in the rat pancreatic acinar tumor cell line AR42J. Biochem Biophys Res Commun; 2001 Jul 20;285(3):708-14
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  • [Title] Carboxyl-methylation of Rab3D in the rat pancreatic acinar tumor cell line AR42J.
  • We have previously shown that rab3D undergoes reversible carboxyl-methylation in adult rat pancreatic acinar cells, and that carboxyl-methylation of rab3D is developmentally regulated concomitantly with the maturation of the regulated secretory apparatus in rat pancreas.
  • We also observed that dexamethasone treatment of the rat pancreatic acinar tumor cell line, AR42J, led to a significant increase in the size of the unmethylated pool of a rab3-like protein.
  • Treatment of AR42J cells with N-acetyl-S-geranylgeranyl-l-cysteine, an inhibitor of carboxyl-methylation, led to a decrease in the basic form of rab3D and a proportional increase in the acidic form.
  • In contrast, N-acetyl-S-farnesyl-l-cysteine, which inhibits carboxyl-methylation of farnesylated proteins, had no effect.
  • Our data, along with previous studies done on developing rat pancreas, indicate that the tumor cell line AR42J represents a good model system for studying the regulated secretory pathway, and that carboxyl-methylation of rab3D may play a role in the acquisition of stimulus-secretion coupling.
  • [MeSH-major] Pancreas / metabolism. Pancreatic Neoplasms / metabolism. Protein Methyltransferases / metabolism. rab3 GTP-Binding Proteins / metabolism
  • [MeSH-minor] Acetylcysteine / analogs & derivatives. Acetylcysteine / pharmacology. Animals. Antibody Specificity. Cysteine / analogs & derivatives. Cysteine / pharmacology. Dexamethasone / pharmacology. Diterpenes / pharmacology. Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology. Immunoblotting. Isoelectric Focusing. Lovastatin / pharmacology. Methylation / drug effects. Protein Isoforms / metabolism. Protein Prenylation / drug effects. Rats. Subcellular Fractions / chemistry. Tumor Cells, Cultured. rab3A GTP-Binding Protein / metabolism

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  • [Copyright] Copyright 2001 Academic Press.
  • (PMID = 11453651.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA46128
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diterpenes; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / N-acetyl-S-geranylgeranyl-cysteine; 0 / Protein Isoforms; 7S5I7G3JQL / Dexamethasone; 9LHU78OQFD / Lovastatin; EC 2.1.1.- / Protein Methyltransferases; EC 3.6.1.- / RAB3B protein, human; EC 3.6.1.- / RAB3D protein, human; EC 3.6.1.- / Rab3b protein, rat; EC 3.6.1.- / Rab3c protein, mouse; EC 3.6.1.- / Rab3c protein, rat; EC 3.6.1.- / Rab3d protein, rat; EC 3.6.5.2 / rab3 GTP-Binding Proteins; EC 3.6.5.2 / rab3A GTP-Binding Protein; K848JZ4886 / Cysteine; KK6984C8O3 / N-acetyl-S-farnesylcysteine; WYQ7N0BPYC / Acetylcysteine
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14. Nagy K, Pálfia Z, Réz G: Quantitative microvascular changes during azaserine-initiated pancreatic carcinogenesis. Acta Biol Hung; 2001;52(4):403-9
Hazardous Substances Data Bank. AZASERINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although angiogenesis is considered to be indispensable for continuous tumour growth, only very few studies have been published performing microvessel quantification during tumour progression.
  • We measured the tumour vascularity in different stages of rat pancreatic carcinogenesis induced by azaserine and promoted by raw soya flour-containing pancreatotrophic diet.
  • Besides the tumour samples taken at 6 (atypical acinar cell nodules), 15 (adenomas) and 20 (localised adenocarcinomas) months after carcinogen initiation, we also investigated 3 control groups: tumour-bearing host tissue of azaserine-treated rats and normal tissue of untreated rats kept on standard or pancreatotrophic diet.
  • These results may indicate comparable growth rate of tumour and new microvessels in the premalignant stages of carcinogenesis while a more intense angiogenesis than tumour growth afterwards.
  • [MeSH-major] Azaserine / toxicity. Pancreatic Neoplasms / blood supply. Pancreatic Neoplasms / chemically induced
  • [MeSH-minor] Adenocarcinoma / blood supply. Adenocarcinoma / chemically induced. Animals. Male. Microcirculation / drug effects. Microcirculation / pathology. Neovascularization, Pathologic / chemically induced. Rats. Rats, Wistar. Time Factors

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  • (PMID = 11693990.001).
  • [ISSN] 0236-5383
  • [Journal-full-title] Acta biologica Hungarica
  • [ISO-abbreviation] Acta. Biol. Hung.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Hungary
  • [Chemical-registry-number] 87299V3Q9W / Azaserine
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