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1. Pijpe J, Meijer JM, Bootsma H, van der Wal JE, Spijkervet FK, Kallenberg CG, Vissink A, Ihrler S: Clinical and histologic evidence of salivary gland restoration supports the efficacy of rituximab treatment in Sjögren's syndrome. Arthritis Rheum; 2009 Nov;60(11):3251-6
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  • [Title] Clinical and histologic evidence of salivary gland restoration supports the efficacy of rituximab treatment in Sjögren's syndrome.
  • OBJECTIVE: To assess the effect of rituximab (anti-CD20 antibody) therapy on the (immuno)histopathology of parotid tissue in patients with primary Sjögren's syndrome (SS) and the correlation of histologic findings with the flow rate and composition of parotid saliva.
  • METHODS: In a phase II study, an incisional parotid biopsy specimen was obtained from 5 patients with primary SS before and 12 weeks after rituximab treatment (4 infusions of 375 mg/m(2)).
  • Immunohistochemical characterization was performed to analyze the B:T cell ratio of the lymphocytic infiltrate (CD20, CD79a, CD3) and cellular proliferation in the acinar parenchyma (by double immunohistologic labeling for cytokeratin 14 and Ki-67).
  • Following rituximab treatment, the lymphocytic infiltrate was reduced, with a decreased B:T cell ratio and (partial) disappearance of germinal centers.
  • The initially increased proliferation of acinar parenchyma in response to inflammation was reduced in all patients.
  • CONCLUSION: Sequential parotid biopsy specimens obtained from patients with primary SS before and after rituximab treatment demonstrated histopathologic evidence of reduced glandular inflammation and redifferentiation of lymphoepithelial duct lesions to regular striated ducts as a putative morphologic correlate of increased parotid flow and normalization of the salivary sodium content.
  • These histopathologic findings in a few patients underline the efficacy of B cell depletion and indicate the potential for glandular restoration in SS.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antirheumatic Agents / therapeutic use. Salivary Glands / pathology. Sjogren's Syndrome / drug therapy. Sjogren's Syndrome / pathology
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Murine-Derived. Biopsy. Cell Proliferation. Female. Humans. Middle Aged. Parotid Gland / drug effects. Parotid Gland / pathology. Rituximab. Saliva. Treatment Outcome. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 19877054.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antirheumatic Agents; 0 / Tumor Necrosis Factor-alpha; 4F4X42SYQ6 / Rituximab
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2. Distler M, Rückert F, Dittert DD, Stroszczynski C, Dobrowolski F, Kersting S, Grützmann R: Curative resection of a primarily unresectable acinar cell carcinoma of the pancreas after chemotherapy. World J Surg Oncol; 2009;7:22
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  • [Title] Curative resection of a primarily unresectable acinar cell carcinoma of the pancreas after chemotherapy.
  • BACKGROUND: Acinar cell carcinoma (ACC) represents only 1-2% of pancreatic cancers and is a very rare malignancy.
  • At the time of diagnosis only 50% of the tumors appear to be resectable.
  • Reliable data for an effective adjuvant or neoadjuvant treatment are not available.
  • CASE PRESENTATION: A 65-year old male presented with obstructive jaundice and non-specific upper abdominal pain.
  • MRI-imaging showed a tumor within the head of the pancreas concomitant with Serum-Lipase and CA19-9.
  • During ERCP, a stent was placed.
  • Endosonographic fine needle biopsy confirmed an acinar cell carcinoma.
  • Laparotomy presented an locally advanced tumor with venous infiltration that was consequently deemed unresectable.
  • Chemotherapy was well tolerated, and no severe complications were observed.
  • Twelve months later, the patient was in stable condition, and CT-scanning showed an obvious reduction in the size of the tumor.
  • Histopathological examination gave evidence of a diffuse necrotic ACC-tumor, all resection margins were found to be negative.
  • Eighteen months later, the patient showed no signs of recurrent disease.
  • Therefore, neoadjuvant chemotherapy could be an option to reduce a primarily unresectable ACC to a point where curative resection can be achieved.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Carcinoma, Acinar Cell / surgery. Fluorouracil / therapeutic use. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Aged. Combined Modality Therapy. Humans. Magnetic Resonance Imaging. Male. Neoplasm Staging. Prognosis. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 19239719.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2657786
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3. Letoha T, Somlai C, Takacs T, Szabolcs A, Jarmay K, Rakonczay Z Jr, Hegyi P, Varga I, Kaszaki J, Krizbai I, Boros I, Duda E, Kusz E, Penke B: A nuclear import inhibitory peptide ameliorates the severity of cholecystokinin-induced acute pancreatitis. World J Gastroenterol; 2005 Feb 21;11(7):990-9
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  • AIM: To assess the effect of our novel cell-permeable nuclear factor-kappaB (NF-kappaB) inhibitor peptide PN50 in an experimental model of acute pancreatitis.
  • PN50 was produced by conjugating the cell-penetrating penetratin peptide with the nuclear localization signal of the NF-kappaB p50 subunit.
  • METHODS: Pancreatitis was induced in male Wistar rats by administering 2X100 mug/kg body weight of cholecystokinin-octapeptide (CCK) intraperitoneally (IP) at an interval of 1 h.
  • PN50-treated animals received 1 mg/kg of PN50 IP 30 min before or after the CCK injections.
  • RESULTS: All the examined laboratory (the pancreatic weight/body weight ratio, serum amylase activity, pancreatic levels of TNF-alpha and IL-6, degree of lipid peroxidation, reduced glutathione levels, NF-kappaB binding activity, pancreatic and lung myeloperoxidase activity) and morphological parameters of the disease were improved before and after treatment with the PN50 peptide.
  • According to the histological findings, PN50 protected the animals against acute pancreatitis by favoring the induction of apoptotic, as opposed to necrotic acinar cell death associated with severe acute pancreatitis.
  • [MeSH-major] Pancreatitis / drug therapy. Pancreatitis / pathology. Peptides / pharmacokinetics
  • [MeSH-minor] Active Transport, Cell Nucleus. Acute Disease. Amino Acid Sequence. Amylases / blood. Animals. Body Weight. Cell Line, Transformed. Electrophoretic Mobility Shift Assay. Glutathione / metabolism. Interleukin-6 / metabolism. Lipid Peroxidation / drug effects. Lung / metabolism. Male. Mice. Molecular Sequence Data. NF-kappa B / metabolism. Organ Size. Pancreas / metabolism. Pancreas / pathology. Peroxidase / metabolism. Rats. Rats, Wistar. Sincalide. Transcription, Genetic / drug effects. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 15742402.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / NF-kappa B; 0 / Peptides; 0 / SN50 peptide; 0 / Tumor Necrosis Factor-alpha; EC 1.11.1.7 / Peroxidase; EC 3.2.1.- / Amylases; GAN16C9B8O / Glutathione; M03GIQ7Z6P / Sincalide
  • [Other-IDs] NLM/ PMC4250791
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4. Noji T, Nan-ya K, Mizutani M, Katagiri C, Sano J, Takada C, Nishikawa S, Karasawa A, Kusaka H: KF24345, an adenosine uptake inhibitor, ameliorates the severity and mortality of lethal acute pancreatitis via endogenous adenosine in mice. Eur J Pharmacol; 2002 Nov 1;454(1):85-93
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  • In this study, we examined the effects of 3-[1-(6,7-diethoxy-2-morpholinoquinazolin-4-yl)piperidin-4-yl]-1,6-dimethyl-2,4(1H,3H)-quinazolinedione hydrochloride (KF24345), an adenosine uptake inhibitor, on experimental acute pancreatitis induced by choline-deficient and ethionine-supplemented diet in mice.
  • KF24345, administered with the diet onset and every 24 h thereafter, prevented hyperamylasemia, acinar cell injury and serum tumor necrosis factor-alpha elevation and ultimately decreased mortality.
  • Therapeutic treatment with KF24345, which started 32 h after the diet onset, also decreased mortality.
  • The adenosine uptake inhibition could be a new therapeutic approach for acute pancreatitis.
  • [MeSH-major] Adenosine / antagonists & inhibitors. Neurotransmitter Uptake Inhibitors / pharmacology. Pancreatitis / drug therapy. Pyrimidinones / pharmacology. Quinazolines / pharmacology
  • [MeSH-minor] Acute Disease. Amylases / blood. Animals. Choline Deficiency / complications. Diet. Female. L-Lactate Dehydrogenase / blood. Mice. Organ Size. Pancreas / drug effects. Time Factors. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 12409009.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 3-(1-(6,7-diethoxy-2-morpholinoquinazolin-4-yl)piperidin-4-yl)-1,6-dimethyl-2,4-(1H,3H)-quinazolinedione; 0 / Neurotransmitter Uptake Inhibitors; 0 / Pyrimidinones; 0 / Quinazolines; 0 / Tumor Necrosis Factor-alpha; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 3.2.1.- / Amylases; K72T3FS567 / Adenosine
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5. Shet T, Ramadwar M, Sharma S, Laskar S, Arora B, Kurkure P: An eyelid sialoblastoma-like tumor with a sarcomatoid myoepithelial component. Pediatr Dev Pathol; 2007 Jul-Aug;10(4):309-14
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  • [Title] An eyelid sialoblastoma-like tumor with a sarcomatoid myoepithelial component.
  • Nonround cell tumors are rare in children and often difficult to diagnose.
  • This article describes an 18-month-old child who presented with a mass on the outer aspect of the left eyelid.
  • Histologically, the tumor had nests of basaloid and relatively round cells with immature acinar or ductular structures similar to those seen in a conventional sialoblastoma, but these nests were embedded in a malignant spindle cell stroma.
  • This stroma on immunohistochemistry was marked with S-100 and cytokeratin, which, in combination with the pertinent ultrastructural evidence, indicated a myoepithelial differentiation.
  • Overall histologic features suggested a tumor similar to a sialoblastoma with sarcomatoid transformation of the myoepithelial component, hitherto not described in literature.
  • This tumor probably arose from the palpebral lobe of the lacrimal gland.
  • Postsurgery, the patient received chemotherapy (6 cycles of ifosfamide, vincristine, and doxorubicin hydrochloride [Adriamycin]) and local radiotherapy in view of residual disease.
  • Three months after completion of the treatment (1 year after surgery), the patient is well, without any local disease.
  • Awareness of this unusual histology of sialoblastoma will help in avoiding misdiagnosis and also refine treatment-related issues on this rare tumor.
  • [MeSH-major] Eyelid Neoplasms / pathology. Myoepithelioma / pathology. Sarcoma / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Combined Modality Therapy. Desmosomes / ultrastructure. Disease-Free Survival. Humans. Immunohistochemistry. Infant. Treatment Outcome

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  • (PMID = 17638426.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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6. Way D, Smith S, Sivendran S, Chie L, Kanovsky M, Brandt-Rauf PW, Chung DL, Michl J, Pincus MR: A protein kinase C inhibitor induces phenotypic reversion of ras-transformed pancreatic cancer cells and cooperatively blocks tumor cell proliferation with an anti- ras peptide. Cancer Chemother Pharmacol; 2002 Jun;49(6):429-37
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  • [Title] A protein kinase C inhibitor induces phenotypic reversion of ras-transformed pancreatic cancer cells and cooperatively blocks tumor cell proliferation with an anti- ras peptide.
  • We sought to determine whether CGP 41 251 blocks proliferation of ras-transformed mammalian cells and whether it synergistically exerts this effect with a ras-p21 peptide (residues 96-110) that interferes with the interaction of ras-p21 with JNK.
  • METHODS: We incubated ras-transformed rat pancreatic cancer TUC-3 cells and their normal counterpart pancreatic acinar BMRPA1 cells with CGP 42 251 alone and in the presence of the ras-p21 96-110 peptide, both in pre- and post-monolayer phases and determined cell counts and morphology and, for TUC-3 cells, their ability to grow on soft agar.
  • RESULTS: CGP 41 251, but not its inactive analogue, CGP 42 700, blocked pre-monolayer growth and reduced post-monolayer cell counts of both TUC-3 and BMRPA1 cells (IC(50) 0.28 and 0.35 micro M, respectively).
  • After 2 weeks of treatment, all the remaining TUC-3 cells exhibited the untransformed phenotype.
  • CONCLUSIONS: CGP 41 251 strongly blocks growth of ras-transformed pancreatic cancer cells by causing cell death and by induction of phenotypic reversion.
  • These findings suggest the possibility of using these two agents in anticancer therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Acinar Cell / pathology. Cell Transformation, Neoplastic / drug effects. Enzyme Inhibitors / pharmacology. Mitogen-Activated Protein Kinases / physiology. Oncogene Protein p21(ras) / physiology. Pancreatic Neoplasms / pathology. Peptide Fragments / pharmacology. Protein Kinase C / physiology. Staurosporine / pharmacology
  • [MeSH-minor] Cell Division / drug effects. Cells, Cultured / cytology. Cells, Cultured / drug effects. Humans. JNK Mitogen-Activated Protein Kinases. Phenotype. Protein Binding. Signal Transduction

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  • (PMID = 12107546.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 42500
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Peptide Fragments; 120685-11-2 / 4'-N-benzoylstaurosporine; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.2 / Oncogene Protein p21(ras); H88EPA0A3N / Staurosporine
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7. Yao E, Zhou W, Lee-Hoeflich ST, Truong T, Haverty PM, Eastham-Anderson J, Lewin-Koh N, Gunter B, Belvin M, Murray LJ, Friedman LS, Sliwkowski MX, Hoeflich KP: Suppression of HER2/HER3-mediated growth of breast cancer cells with combinations of GDC-0941 PI3K inhibitor, trastuzumab, and pertuzumab. Clin Cancer Res; 2009 Jun 15;15(12):4147-56
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  • PURPOSE: Oncogenic activation of the phosphatidylinositol 3-kinase (PI3K) signaling pathway is prevalent in breast cancer and has been associated with resistance to HER2 inhibitors in the clinic.
  • We therefore investigated the combinatorial activity of GDC-0941, a novel class I PI3K inhibitor, with standard-of-care therapies for HER2-amplified breast cancer.
  • EXPERIMENTAL DESIGN: Three-dimensional laminin-rich extracellular matrix cultures of human breast cancer cells were utilized to provide a physiologically relevant approach to analyze the efficacy and molecular mechanism of combination therapies ex vivo.
  • Combination studies were done using GDC-0941 with trastuzumab (Herceptin), pertuzumab, lapatinib (Tykerb), and docetaxel, the principal therapeutic agents that are either approved or being evaluated for treatment of early HER2-positive breast cancer.
  • RESULTS: Significant GDC-0941 activity (EC(50) <1 micromol/L) was observed for >70% of breast cancer cell lines that were examined in three-dimensional laminin-rich extracellular matrix culture.
  • Combined treatment of GDC-0941, trastuzumab, and pertuzumab resulted in growth inhibition, altered acinar morphology, and suppression of AKT mitogen-activated protein kinase (MAPK) / extracellular signed-regulated kinase (ERK) kinase and MEK effector signaling pathways for HER2-amplified cells in both normal and heregulin-supplemented media.
  • The GDC-0941 and lapatinib combination further showed that inhibition of HER2 activity was essential for maximum combinatorial efficacy.
  • PI3K inhibition also rendered HER2-amplified BT-474M1 cells and tumor xenografts more sensitive to docetaxel.
  • The addition of GDC-0941 to HER2-directed treatment could augment clinical benefit in breast cancer patients.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Breast Neoplasms / drug therapy. Enzyme Inhibitors / therapeutic use. Indazoles / therapeutic use. Receptor, ErbB-2 / antagonists & inhibitors. Receptor, ErbB-3 / antagonists & inhibitors. Sulfonamides / therapeutic use
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols. Cell Line, Tumor. Humans. Mice. Mice, Nude. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Quinazolines / pharmacology. Signal Transduction / drug effects. Signal Transduction / physiology. Taxoids / pharmacology. Trastuzumab. Xenograft Model Antitumor Assays

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  • (PMID = 19509167.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(1H-indazol-4-yl)-6-(4-methanesulfonylpiperazin-1-ylmethyl)-4-morpholin-4-ylthieno(3,2-d)pyrimidine; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Indazoles; 0 / Quinazolines; 0 / Sulfonamides; 0 / Taxoids; 0VUA21238F / lapatinib; 15H5577CQD / docetaxel; 380610-27-5 / pertuzumab; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.1 / Receptor, ErbB-3; P188ANX8CK / Trastuzumab
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8. Diegel CR, Cho KR, El-Naggar AK, Williams BO, Lindvall C: Mammalian target of rapamycin-dependent acinar cell neoplasia after inactivation of Apc and Pten in the mouse salivary gland: implications for human acinic cell carcinoma. Cancer Res; 2010 Nov 15;70(22):9143-52
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  • [Title] Mammalian target of rapamycin-dependent acinar cell neoplasia after inactivation of Apc and Pten in the mouse salivary gland: implications for human acinic cell carcinoma.
  • Cross-talk between the canonical Wnt and mammalian target of rapamycin (mTOR) signaling pathways occurs at multiple levels in the cell and likely contributes to the oncogenic effects of these pathways in human cancer.
  • To gain more insight into the interplay between Wnt and mTOR signaling in salivary gland tumorigenesis, we developed a mouse model in which both pathways are constitutively activated by the conditional inactivation of the Apc and Pten tumor suppressor genes.
  • Loss of either Apc or Pten alone did not cause tumor development.
  • However, deletion of both genes resulted in the formation of salivary gland tumors with 100% penetrance and short latency that showed a remarkable morphologic similarity to human acinic cell carcinoma.
  • Treatment of tumor-bearing mice using the mTOR inhibitor rapamycin led to complete regression of tumors, indicating that tumor growth was dependent on continued mTOR signaling.
  • Importantly, we found that human salivary gland acinic cell carcinomas also express markers of activated mTOR signaling.
  • Together, these results suggest that aberrant activation of mTOR signaling plays a pivotal role in acinar cell neoplasia of the salivary gland.
  • Because rapamycin analogues are approved for treating other types of human malignancies, our findings suggest that rapamycin therapy should be evaluated for treating patients with salivary gland acinic cell carcinoma.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / deficiency. Carcinoma, Acinar Cell / metabolism. PTEN Phosphohydrolase / deficiency. Salivary Glands / metabolism. TOR Serine-Threonine Kinases / metabolism
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Female. Flow Cytometry. Humans. Immunohistochemistry. Male. Mice. Mice, 129 Strain. Mice, Knockout. Salivary Gland Neoplasms / genetics. Salivary Gland Neoplasms / metabolism. Salivary Gland Neoplasms / pathology. Signal Transduction / drug effects. Sirolimus / pharmacology. Tumor Burden / drug effects


9. Satoh A, Gukovskaya AS, Edderkaoui M, Daghighian MS, Reeve JR Jr, Shimosegawa T, Pandol SJ: Tumor necrosis factor-alpha mediates pancreatitis responses in acinar cells via protein kinase C and proline-rich tyrosine kinase 2. Gastroenterology; 2005 Aug;129(2):639-51
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  • [Title] Tumor necrosis factor-alpha mediates pancreatitis responses in acinar cells via protein kinase C and proline-rich tyrosine kinase 2.
  • BACKGROUND & AIMS: Although tumor necrosis factor alpha is implicated as an important mediator of the inflammatory response in acute pancreatitis, its role in other pathologic features of the disease remains unknown.
  • We investigated the role for tumor necrosis factor alpha in cytoskeletal responses and the underlying signaling mechanisms in pancreatic acinar cells.
  • METHODS: In isolated rat pancreatic acini and AR42J cells, we determined the effect of tumor necrosis factor alpha on the actin cytoskeleton by rhodamine-phalloidin.
  • Using pharmacological and molecular approaches, we assessed the involvement of protein kinase C, Src kinases, and proline-rich tyrosine kinase 2 in the process.
  • We also studied the involvement of these signaling pathways in tumor necrosis factor-alpha-induced nuclear factor-kappaB activation and apoptosis.
  • RESULTS: Tumor necrosis factor-alpha increased the tyrosine phosphorylation of proline-rich tyrosine kinase 2 in acinar cells.
  • The broad-spectrum protein kinase C inhibitor and the Src kinase inhibitor both inhibited tumor necrosis factor-alpha-induced proline-rich tyrosine kinase 2 phosphorylation, but at different tyrosine residues.
  • Tumor necrosis factor-alpha caused disorganization of the actin cytoskeleton by a mechanism dependent on protein kinase C, Src kinases, and proline-rich tyrosine kinase 2.
  • Inhibition of protein kinase C, but not Src kinases, decreased tumor necrosis factor-alpha-induced apoptosis.
  • Furthermore, with antisense transfections, we showed that protein kinase C delta and , but not proline-rich tyrosine kinase 2, mediate tumor necrosis factor alpha-induced nuclear factor-kappaB activation.
  • CONCLUSIONS: Tumor necrosis factor-alpha activates proline-rich tyrosine kinase 2 to cause cytoskeletal disorganization and nuclear factor-kappaB to cause inflammatory response, and it triggers cell death signaling through divergent mechanisms mediated by protein kinase C.
  • The results provide insights into the mechanisms in pancreatic acinar cells that link tumor necrosis factor alpha to critical processes in acute pancreatitis.
  • [MeSH-major] Pancreas / cytology. Pancreatitis / drug therapy. Pancreatitis / enzymology. Protein Kinase C / metabolism. Protein-Tyrosine Kinases / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Acute Disease. Analysis of Variance. Animals. Apoptosis / drug effects. Apoptosis / physiology. Base Sequence. Blotting, Western. Cells, Cultured. Disease Models, Animal. Female. Focal Adhesion Kinase 2. Male. Molecular Sequence Data. Polymerase Chain Reaction / methods. Probability. Protein Kinase C-delta. Rats. Rats, Sprague-Dawley. Sensitivity and Specificity

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  • (PMID = 16083718.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NIAAA NIH HHS / AA / 1 U56 AA 0114643; United States / NIDDK NIH HHS / DK / DK-59508; United States / PHS HHS / / P50-A11999
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; EC 2.7.1.- / Prkcd protein, rat; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Focal Adhesion Kinase 2; EC 2.7.10.2 / Ptk2b protein, rat; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C-delta
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10. Holen KD, Klimstra DS, Hummer A, Gonen M, Conlon K, Brennan M, Saltz LB: Clinical characteristics and outcomes from an institutional series of acinar cell carcinoma of the pancreas and related tumors. J Clin Oncol; 2002 Dec 15;20(24):4673-8
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  • [Title] Clinical characteristics and outcomes from an institutional series of acinar cell carcinoma of the pancreas and related tumors.
  • PURPOSE: Acinar cell carcinoma is a rare tumor of the exocrine pancreas.
  • Clinical features such as prognostic information, survival, and treatment outcomes are unknown.
  • PATIENTS AND METHODS: Thirty-nine patients with pathologically confirmed acinar neoplasms of the pancreas were identified between August 1981 and January 2001.
  • Demographic data, tumor characteristics, and treatment information were obtained by chart review.
  • On the basis of a univariate analysis, the patients' stage of disease correlated significantly with survival.
  • The median survival of patients with localized disease was 38 months, versus 14 months for those presenting with metastases (P = 0.03).
  • Patients who could be treated with surgery as first-line therapy had a longer survival time (36 months) compared with those who did not have surgery (14 months).
  • Two of 18 patients who received chemotherapy and three of eight patients who received radiation had a major response.
  • CONCLUSION: The survival curves suggest a more aggressive cancer than pancreatic endocrine neoplasms but one that is less aggressive than ductal adenocarcinoma of the pancreas.
  • Those patients who present with localized disease have a much better prognosis than those who present with metastases.
  • There is a high recurrence rate after complete surgical resection, suggesting that micrometastases are present even in localized disease and that adjuvant therapies may be indicated.
  • Chemotherapy and radiation afford disappointing results, however, and novel therapies are needed.
  • [MeSH-major] Carcinoma, Acinar Cell / therapy. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Retrospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 12488412.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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11. 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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  • [Title] Prognostic relevance of CA 19-9, CEA, CRP, and LDH kinetics in patients treated with palliative second-line therapy for advanced pancreatic cancer.
  • The objective of this study was to define prognostic serum biomarkers that could serve as surrogate survival endpoints during second-line treatment for advanced pancreatic cancer.
  • This retrospective single-center study included patients treated with second-line therapy for advanced exocrine pancreatic cancer.
  • A pretreatment value and at least one serial measurement during the first two cycles of second-line chemotherapy for CA 19-9, CEA, CRP, and LDH had to be available in order to evaluate the prognostic role of kinetics on overall survival.
  • A cutoff of a >20% increase from baseline during treatment was defined in order to form groups with suspected different outcomes.
  • The effect of serial biomarker changes on survival was modeled by Cox proportional hazards regression in univariate and multivariate analyses.
  • Overall, 70 patients treated with second-line therapy for advanced disease were included; 94% had distant metastases at treatment initiation.
  • Median time to progression was 2.7 months and median survival 5.4 months.
  • Univariate analysis found that an increase of >20% during treatment was significantly associated with a worse overall survival for CA 19-9 (HR 2.00, p = 0.018), CEA (HR 2.38, p = 0.004), and CRP (HR 3.06, p < 0.001).
  • These associations remained significant within multivariate analysis for CEA (HR 2.86, p = 0.001) and CRP (HR 3.20, p = 0.001).
  • Serum biomarker kinetics might serve as useful prognostic tools during second-line chemotherapy in advanced pancreatic cancer.
  • [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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12. Kataoka Y, Nio Y, Yano S, Koike M, Hashimoto K, Itakura M, Itagaki T, Nishi T, Endo S, Higami T: [Pancreatic acinar cell carcinoma successfully treated with combination of oral TS-1 and intra-arterial cisplatin]. Gan To Kagaku Ryoho; 2006 Apr;33(4):525-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pancreatic acinar cell carcinoma successfully treated with combination of oral TS-1 and intra-arterial cisplatin].
  • Pancreatic acinar cell carcinomas are rare, and little is reported on their chemotherapy.
  • We report a 49-year old male patient with pancreatic acinar cell carcinoma and multiple liver metastases, which responded to oral TS-1 and hepatic arterial infusion of cisplatin.
  • The patient underwent a partial hepatectomy, MCT abrasions and excision of the pancreatic tumor.
  • Postoperative pathological studies revealed metastases of acinar cell carcinoma to the liver and lymph nodes; the primary lesion was undetermined.
  • Abdominal CT one year after surgery revealed a pancreatic body tumor, which was surgically removed.
  • Pathological studies showed primary pancreatic acinar cell carcinoma, while previous metastases remained under control.
  • To summarize, TS-1 and cisplatin can be effective treatments for pancreatic acinar cell carcinomas.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Cisplatin / administration & dosage. Combined Modality Therapy. Drug Administration Schedule. Drug Combinations. Hepatectomy. Humans. Infusions, Intra-Arterial. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Liver Neoplasms / surgery. Male. Middle Aged. Oxonic Acid / administration & dosage. Pyridines / administration & dosage. Tegafur / administration & dosage

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  • (PMID = 16612167.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Pyridines; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin
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13. Rajpal S, Warren RS, Alexander M, Yeh BM, Grenert JP, Hintzen S, Ljung BM, Bergsland EK: Pancreatoblastoma in an adult: case report and review of the literature. J Gastrointest Surg; 2006 Jun;10(6):829-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatoblastoma in an adult: case report and review of the literature.
  • A 50-year-old man presented with progressive gastrointestinal symptoms.
  • An abdominal computed tomography scan demonstrated a 12 x 12-cm pancreatic mass involving the greater curvature of the stomach and multiple hypervascular hepatic metastases.
  • An initial fine needle aspiration of the pancreatic mass was nondiagnostic, and a subsequent fine needle aspiration of a liver mass was read as metastatic acinar cell carcinoma.
  • The patient underwent a palliative resection for tumor-associated pain and gastrointestinal hemorrhage that revealed a large pancreatic tumor invading through the full thickness of the colon at the splenic flexure and adherent to the posterior gastric wall.
  • The pathology from the distal pancreatectomy, splenectomy, partial gastrectomy, partial colectomy, and cholecystectomy unexpectedly supported a diagnosis of pancreatoblastoma with evidence for squamoid corpuscles as well as areas of acinar formation.
  • Despite multiple chemotherapy regimens, the patient's disease continued to progress in the liver and the lungs.
  • During the course of his therapy, the patient's serum alpha-fetoprotein levels and serum lipase levels rose concurrently, suggesting tumor-associated production of both of these factors.
  • Seventeen months after the diagnosis of metastatic pancreatoblastoma, the patient died from his disease.
  • Our case illustrates the fact that pancreatoblastomas are extremely difficult to diagnosis preoperatively.
  • In addition, our case demonstrates that pancreatoblastomas can be alpha-fetoprotein producing, hormone producing, and enzyme producing when it occurs in adults.
  • [MeSH-major] Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Abdominal Pain / etiology. Biopsy, Fine-Needle. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / secondary. Disease Progression. Humans. Immunohistochemistry. Liver Neoplasms / secondary. Male. Middle Aged. Nausea / etiology. Neoplasm Invasiveness. Satiety Response. Splenic Vein / diagnostic imaging. Splenic Vein / pathology. Stomach / pathology. Tomography, X-Ray Computed. Vomiting / etiology

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  • (PMID = 16769539.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 21
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14. Fujii M, Sato H, Ogasawara T, Ando T, Tsujii S, Nagahori J, Komatsu Y, Matsuoka A: [A case of liver metastasis of pancreatic acinar cell carcinoma treated with S-1 and intra-arterial CDDP combination therapy]. Gan To Kagaku Ryoho; 2010 Oct;37(10):1987-90
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  • [Title] [A case of liver metastasis of pancreatic acinar cell carcinoma treated with S-1 and intra-arterial CDDP combination therapy].
  • A 55-year-old man underwent a pylorus-preserving pancreatoduodenectomy in August 2006 because of acinar cell carcinoma of the head of the pancreas.
  • Since abdominal CT revealed multiple liver metastases, we started systemic chemotherapy with gemcitabine (1,400 mg/body, day 1, 8, 15/q4w) in October 2006.
  • At the beginning of this treatment, it seemed to be a stable disease, but CT revealed tumor progression in January 2007.
  • Despite the change to oral chemotherapy with S-1 (100 mg/body, day 1-14/q3w), tumors were markedly enlarged in March 2007.
  • Therefore, we selected combination chemotherapy with oral S-1 and hepatic arterial infusion of CDDP (50 mg/body) as third-line.
  • After 6 months of treatment, abdominal CT revealed marked shrinkage of tumors, accompanied by a decrease in AFP level.
  • Though the patient died of hepatic failure in July 2009 (33 months after recurrence), he spent most of his time at home and worked as usual.
  • We suggest that combination chemotherapy with oral S-1 and intra-arterial CDDP can be effective treatments for pancreatic acinar cell carcinoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Cisplatin / therapeutic use. Liver Neoplasms / drug therapy. Oxonic Acid / therapeutic use. Pancreatic Neoplasms / drug therapy. Tegafur / therapeutic use
  • [MeSH-minor] Drug Combinations. Fatal Outcome. Humans. Infusions, Intra-Arterial. Male. Middle Aged. Recurrence. Tomography, X-Ray Computed

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  • (PMID = 20948270.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin
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15. Park CC, Zhang H, Pallavicini M, Gray JW, Baehner F, Park CJ, Bissell MJ: Beta1 integrin inhibitory antibody induces apoptosis of breast cancer cells, inhibits growth, and distinguishes malignant from normal phenotype in three dimensional cultures and in vivo. Cancer Res; 2006 Feb 1;66(3):1526-35
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  • Current therapeutic approaches to cancer are designed to target molecules that contribute to malignant behavior but leave normal tissues intact. beta(1) integrin is a candidate target well known for mediating cell-extracellular matrix (ECM) interactions that influence diverse cellular functions; its aberrant expression has been implicated in breast cancer progression and resistance to cytotoxic therapy.
  • The addition of beta(1) integrin inhibitory agents to breast cancer cells at a single-cell stage in a laminin-rich ECM (three-dimensional lrECM) culture was shown to down-modulate beta(1) integrin signaling, resulting in malignant reversion.
  • To investigate beta(1) integrin as a therapeutic target, we modified the three-dimensional lrECM protocol to approximate the clinical situation: before treatment, we allowed nonmalignant cells to form organized acinar structures and malignant cells to form tumor-like colonies.
  • We then tested the ability of beta(1) integrin inhibitory antibody, AIIB2, to inhibit tumor cell growth in several breast cancer cell lines (T4-2, MDA-MB-231, BT474, SKBR3, and MCF-7) and one nonmalignant cell line (S-1).
  • We show that beta(1) integrin inhibition resulted in a significant loss of cancer cells, associated with a decrease in proliferation and increase in apoptosis, and a global change in the composition of residual colonies.
  • In contrast, nonmalignant cells that formed tissue-like structures remained resistant.
  • Moreover, these cancer cell-specific antiproliferative and proapoptotic effects were confirmed in vivo with no discernible toxicity to animals.
  • Our findings indicate that beta(1) integrin is a promising therapeutic target, and that the three-dimensional lrECM culture assay can be used to effectively distinguish malignant and normal tissue response to therapy.

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  • (PMID = 16452209.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 64786-09; United States / NCI NIH HHS / CA / R37 CA064786; United States / NCI NIH HHS / CA / P50 CA 58207-08; United States / NCI NIH HHS / CA / R01 CA124891; United States / NCI NIH HHS / CA / P50 CA058207; United States / NCI NIH HHS / CA / U54 CA112970; United States / NCI NIH HHS / CA / U54 CA112970-01; United States / NCI NIH HHS / CA / P50 CA 112970-01; United States / NCI NIH HHS / CA / CA064786-09; United States / NCI NIH HHS / CA / CA112970-01; United States / NCI NIH HHS / CA / R01 CA064786; United States / NCI NIH HHS / CA / R01 CA064786-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD29; 0 / Integrins; P188ANX8CK / Trastuzumab
  • [Other-IDs] NLM/ NIHMS225828; NLM/ PMC2933188
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16. Alosi JA, McFadden DW: Peptide YY mediates inhibition of tumor growth and inflammation. Methods Mol Biol; 2009;512:377-94
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  • [Title] Peptide YY mediates inhibition of tumor growth and inflammation.
  • Although the exact mechanism(s) of action are still incompletely understood, PYY interacts at the acinar level with numerous intracellular transcription factors.
  • In addition to ameliorating pancreatic inflammation, novel synthetic analogs of PYY have been developed that are potent inhibitors of pancreatic cancer proliferation, in vitro and in vivo.
  • We, herein, plan to review some of the methods employed in the laboratory while investigating the utility of PYY in the treatment of inflammation and cancer.
  • [MeSH-major] Pancreatic Neoplasms / drug therapy. Pancreatitis / drug therapy. Peptide YY / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. Cell Proliferation / drug effects. Enzyme-Linked Immunosorbent Assay. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Tumor Cells, Cultured

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  • (PMID = 19347290.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 106388-42-5 / Peptide YY
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17. Erkan M, Kleeff J, Esposito I, Giese T, Ketterer K, Büchler MW, Giese NA, Friess H: Loss of BNIP3 expression is a late event in pancreatic cancer contributing to chemoresistance and worsened prognosis. Oncogene; 2005 Jun 23;24(27):4421-32
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  • In the present study, the hypoxia-inducible proapoptotic gene, BNIP3, was analysed in terms of expression, effect on patient survival, and chemo-responsiveness in pancreatic cancer cell lines. cDNA microarray, real-time light cycler quantitative polymerase chain reaction, laser-capture microdissection, and immunohistochemistry analyses were used to evaluate BNIP3 expression in normal and diseased pancreatic specimens.
  • BNIP3 mRNA levels were 3.0- and 6.3-fold lower in chronic pancreatitis and pancreatic cancer compared to the normal pancreas, respectively.
  • Microdissection analysis confirmed the reduction of BNIP3 expression in pancreatic cancer cells compared to normal duct cells.
  • By immunohistochemistry, BNIP3 was predominantly expressed in the acinar cells of the normal and diseased pancreas.
  • Hypoxia induced BNIP3 expression in four out of eight pancreatic cancer cell lines, while it was absent under normoxic and hypoxic conditions in the remaining four.
  • In conclusion, loss of BNIP3 expression occurs late in pancreatic cancer, contributes to resistance to chemotherapy, and correlates with a worsened prognosis.
  • [MeSH-major] Deoxycytidine / analogs & derivatives. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Membrane Proteins / deficiency. Membrane Proteins / genetics. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology. Proto-Oncogene Proteins / deficiency. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Cell Line, Tumor. Fluorouracil / pharmacology. Humans. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Survival Rate

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  • (PMID = 15856026.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BNIP3 protein, human; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; U3P01618RT / Fluorouracil
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18. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • At early BPDO times, L364,718 treatment partially inhibited leukocytosis and increase in peripheral blood neutrophils and monocytes as well as TNF-alpha expression by monocytes.
  • However, from 6 h onwards after BPDO, L364,718 treatment was unable to prevent either pancreatic and lung neutrophil infiltration or the release of TNF-alpha from activated monocytes.
  • By its action on circulating lymphocytes, L364,718 treatment enhanced the severity of the inflammatory response induced by BPDO.
  • Peripheral blood lymphocytes were recruited from earlier BPDO times, and 12 h after BPDO, T cells displayed a significantly higher reserve of TNF-alpha able to be released under stimulation but lower functional reserve of interleukin-10 (IL-10) than observed in untreated rats.
  • It is concluded that lowering the acinar enzyme content through L364,718 treatment prevents earlier systemic immune events in BPDO-induced AP.
  • However, at the point of maximal injury, the inflammatory response became pronounced, largely due to the role played by activated T lymphocytes.
  • [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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19. Paszkowski AS, Rau B, Mayer JM, Möller P, Beger HG: Therapeutic application of caspase 1/interleukin-1beta-converting enzyme inhibitor decreases the death rate in severe acute experimental pancreatitis. Ann Surg; 2002 Jan;235(1):68-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic application of caspase 1/interleukin-1beta-converting enzyme inhibitor decreases the death rate in severe acute experimental pancreatitis.
  • OBJECTIVE: To assess the effect of therapeutic inhibition of interleukin 1beta-converting enzyme (ICE) in an experimental model of severe acute pancreatitis (SAP).
  • SUMMARY BACKGROUND DATA: Several lines of evidence suggest that cytokines activated by ICE play an instrumental role in the course of acute pancreatitis.
  • Recent studies have shown that pharmacologic or genetic blockade of ICE significantly ameliorates the overall severity of and the death rate in SAP.
  • Control animals in group 1 received treatment with saline; in group 2 rats, ICE inhibition was started 6 hours after the onset of pancreatitis; and in group 3 rats, ICE inhibition was started 12 hours after the onset of pancreatitis.
  • After a 7-day observation period, surviving rats were killed and blood, plasma, pancreas, lung, and liver were used for subsequent analysis.
  • RESULTS: Inhibition of ICE decreased the 7-day death rate from 87.5% to 38.9% irrespective whether treatment was started 6 hours or 12 hours after induction of SAP.
  • Morphometric analysis revealed a significant reduction of acinar cell necrosis in both treated groups, whereas pancreatitis-associated pulmonary and hepatic damage was uniformly low and not influenced by ICE inhibition.
  • Tissue myeloperoxidase concentrations were dramatically decreased in the pancreas and the lung after either regimen of ICE inhibitor treatment.
  • In contrast to lung and liver, marked upregulation of interleukin 1beta, tumor necrosis factor alpha, and ICE mRNA was observed in the pancreas, with levels of interleukin 1beta and tumor necrosis factor alpha being reduced in ICE-inhibited animals.
  • Compared with nontreated rats, plasma amylase levels were higher in both treatment groups, whereas lipase and hematocrit showed no difference.
  • Changes of the differential white blood count including neutrophils, lymphocytes, and monocytes were attenuated in both groups after ICE inhibitor treatment.
  • CONCLUSIONS: Pharmacologic inhibition of ICE significantly improves the overall severity of and the death rate in SAP.
  • A substantial reduction of neutrophil-mediated tissue injury in pancreas and lung seems to contribute to the beneficial effects of this approach.
  • Moreover, ICE inhibition is still effective after a therapeutic window of 12 hours.
  • [MeSH-major] Caspase Inhibitors. Enzyme Inhibitors / therapeutic use. Pancreatitis / drug therapy
  • [MeSH-minor] Acute Disease. Amylases / blood. Animals. Caspase 1 / genetics. Data Interpretation, Statistical. Hematocrit. Interleukin-1 / genetics. Lipase / blood. Male. Necrosis. Pancreas / pathology. Pancreatitis, Acute Necrotizing / pathology. Peroxidase / metabolism. RNA, Messenger / analysis. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 11753044.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caspase Inhibitors; 0 / Enzyme Inhibitors; 0 / Interleukin-1; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 1.11.1.7 / Peroxidase; EC 3.1.1.3 / Lipase; EC 3.2.1.- / Amylases; EC 3.4.22.36 / Caspase 1
  • [Other-IDs] NLM/ PMC1422397
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20. Cavallini A, Falconi M, Bortesi L, Crippa S, Barugola G, Butturini G: Pancreatoblastoma in adults: a review of the literature. Pancreatology; 2009;9(1-2):73-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Pancreatoblastoma is a very uncommon neoplasm in adults and its management represents a great challenge with regards to different treatment options.
  • Given the rarity of the disease, the aim of this study was to review our personal experience with adult pancreatoblastoma as well as the cases reported in the literature in order to support clinicians observing this entity.
  • After a search on the Medline database, a review of all cases was performed as well, focusing on clinical, radiological and hystopathological features and treatment options.
  • RESULTS: At our Institution, 2 adult males, 26 and 69 years old, underwent successful pancreatic resection for pancreatoblastoma.
  • In general, despite aggressive treatment, pancreatoblastoma in adults is associated with poorer outcome than in children, with a median survival time of 18.5 months.
  • Both our patients are disease free after 15 months (case 2) and 51 months (case 1).
  • The latter represents the most successful result in long-term disease-free survival.
  • CONCLUSION: Pancreatoblastoma is a rare neoplasm in adults.
  • The differential diagnosis includes nonfunctional pancreatic endocrine tumor, acinar cell carcinoma, solid pseudopapillary tumor and adenocarcinoma.
  • Surgical resection is the only treatment associated with long-term survival.
  • Chemotherapy may play a role as palliative treatment in advanced disease.
  • [MeSH-major] Carcinoma, Neuroendocrine. Pancreatic Neoplasms
  • [MeSH-minor] Adult. Aged. Child. Child, Preschool. Diagnosis, Differential. Humans. Male. Pancreaticoduodenectomy

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  • [Copyright] Copyright 2008 S. Karger AG, Basel and IAP.
  • (PMID = 19077457.001).
  • [ISSN] 1424-3911
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 36
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21. Nishii T, Amano R, Nakao S, Doi Y, Yamada N, Ohira M, Hirakawa K: [A case of liver metastasis of mixed acinar-endocrine carcinoma treated with various loco-regional cancer therapies]. Gan To Kagaku Ryoho; 2008 Nov;35(12):2126-8
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  • [Title] [A case of liver metastasis of mixed acinar-endocrine carcinoma treated with various loco-regional cancer therapies].
  • Mixed acinar-endocrine carcinoma of pancreas is a very rare tumor.
  • We report a 60s female patient with pancreatic mixed acinar-endocrine carcinoma and liver metastasis.
  • Computed tomography scan of abdomen showed a large tumor in pancreatic head and liver tumor.
  • We conducted a pylorus-preserved pancreatoduodenectomy with resection of the portal vein on the diagnosis of acinar cell carcinoma by fine needle aspiration biopsy.
  • Pathological examination showed a mixed acinar-endocrine carcinoma.
  • Following the operation, the liver metastasis was controlled with various loco-regional cancer therapies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Carcinoma, Acinar Cell / pathology. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Angiography. Biopsy. Female. Humans. Infusions, Intra-Arterial. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 19106545.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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22. Kebir FZ, Lahmar A, Arfa N, Manai S, El Ouaer MA, Bouraoui S, Gouttalier C, Mezabi-Regaya S: Acinar cell carcinoma of the pancreas in a young patient with chronic pancreatitis. Hepatobiliary Pancreat Dis Int; 2010 Feb;9(1):103-6
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  • [Title] Acinar cell carcinoma of the pancreas in a young patient with chronic pancreatitis.
  • BACKGROUND: Acinar cell carcinoma (ACC) is a rare malignancy of the pancreas arising from acinar cells.
  • Unlike ductal adenocarcinoma, this tumor rarely presents with pancreatitis.
  • METHODS: We present a case of ACC associated with chronic calcifying pancreatitis, and a review of the literature focusing on diagnosis and management.
  • RESULTS: A 43-year-old man was proposed for Wirsungojejunal derivation for chronic pancreatitis.
  • Histopathological examination of the tissue extracted revealed an ACC.
  • Six months post-operatively, the patient developed hepatic metastasis and was treated with gemcitabine as palliative chemotherapy.
  • CONCLUSIONS: The clinical presentation of ACC of the pancreas is not specific and the tumor can be under-diagnosed when associated with chronic pancreatitis.
  • Data regarding course, treatment, and prognosis of this tumor are generally lacking.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Neoplasms / diagnosis. Pancreatitis, Chronic / complications
  • [MeSH-minor] Adult. Humans. Male. Prognosis

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  • (PMID = 20133240.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
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23. Seki Y, Okusaka T, Ikeda M, Morizane C, Ueno H: Four cases of pancreatic acinar cell carcinoma treated with gemcitabine or S-1 as a single agent. Jpn J Clin Oncol; 2009 Nov;39(11):751-5
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  • [Title] Four cases of pancreatic acinar cell carcinoma treated with gemcitabine or S-1 as a single agent.
  • Pancreatic acinar cell carcinoma (ACC) is a comparatively rare tumor and account for approximately 1% of all cases of pancreatic cancer.
  • Clinical presentation is usually related to either local spread or metastasis.
  • The clinical features, especially those related to the prognosis and treatment outcomes, have not yet been fully clarified.
  • There are no established treatments for unresectable pancreatic ACC.
  • We administered gemcitabine monotherapy to four patients with ACC; however, the results were not satisfactory.
  • Disease control without obvious tumor shrinkage was observed in one patient.
  • On the other hand, fluoropyrimidine-based chemotherapy may have some activity against this tumor, because one of the three patients who received S-1 as second-line chemotherapy showed a partial response.
  • Prospective clinical trials are necessary to confirm the effectiveness of fluoropyrimidine for the treatment of pancreatic ACC.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Deoxycytidine / analogs & derivatives. Oxonic Acid / therapeutic use. Pancreatic Neoplasms / drug therapy. Tegafur / therapeutic use
  • [MeSH-minor] Aged. Disease-Free Survival. Drug Combinations. Female. Humans. Male. Middle Aged. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 19666905.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 0W860991D6 / Deoxycytidine; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; B76N6SBZ8R / gemcitabine
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24. Zhang K, Watanabe M, Kashiwakura Y, Li SA, Edamura K, Huang P, Yamaguchi K, Nasu Y, Kobayashi Y, Sakaguchi M, Ochiai K, Yamada H, Takei K, Ueki H, Huh NH, Li M, Kaku H, Na Y, Kumon H: Expression pattern of REIC/Dkk-3 in various cell types and the implications of the soluble form in prostatic acinar development. Int J Oncol; 2010 Dec;37(6):1495-501

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression pattern of REIC/Dkk-3 in various cell types and the implications of the soluble form in prostatic acinar development.
  • The tumor suppressor REIC/Dkk-3 is a secretory protein which was originally identified to be downregulated in human immortalized cells.
  • In the present study, we investigated the expression pattern of REIC/Dkk-3 in various cell types to characterize its physiological functions.
  • We first examined the expression level of REIC/Dkk-3 in a broad range of cancer cell types and confirmed that it was significantly downregulated in all of the cell types.
  • We also examined the tissue distribution pattern in a variety of normal mouse organs.
  • The expression was abundant in the liver, heart and brain tissue, but was absent in the spleen and peripheral blood mononuclear cells.
  • The immunohistochemical analyses revealed that the subcellular localization of REIC/Dkk-3 had a punctate pattern around the nucleus, indicating its association with secretory vesicles.
  • Because REIC/Dkk-3 was found to be abundantly expressed in the acinar epithelial cells of the mouse prostate, we analyzed the effects of recombinant REIC/Dkk-3 protein on the acinar morphogenesis of RWPE-1 cells, which are derived from human normal prostate epithelium.
  • Statistically significant acinar growth was observed in the culture condition with 10 µg/ml REIC/Dkk-3 protein, implicating the soluble form in prostatic acinar development.
  • Current results suggest that REIC/Dkk-3 may play a role in regulating the morphological process of normal tissue architecture through an autocrine and/or paracrine manner.
  • [MeSH-major] Cells / metabolism. Intercellular Signaling Peptides and Proteins / genetics. Prostate / growth & development
  • [MeSH-minor] Animals. Autocrine Communication / drug effects. Cells, Cultured. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. HeLa Cells. Hep G2 Cells. Humans. Male. Mice. Mice, Inbred C57BL. Morphogenesis / drug effects. Morphogenesis / genetics. Organ Specificity / genetics. Solubility

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  • (PMID = 21042718.001).
  • [ISSN] 1791-2423
  • [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
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DKK3 protein, human; 0 / Intercellular Signaling Peptides and Proteins
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25. Morishima K, Hyodo M, Nihei Y, Sata N, Yasuda Y: [A case of acinar cell carcinoma of pancreas with liver metastases treated effectively by S-1]. Gan To Kagaku Ryoho; 2010 Jan;37(1):127-9
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  • [Title] [A case of acinar cell carcinoma of pancreas with liver metastases treated effectively by S-1].
  • A 65-year-old man underwent a total gastrectomy and distal pancreatectomy for acinar cell carcinoma of the pancreas.
  • Multiple metastatic liver lesions were found one year postoperatively.
  • He was treated with S-1 chemotherapy over 34 months, and the tumors significantly reduced in size without severe side effects.
  • Four years after surgery, the liver metastases increased in size, associated with pain especially in the right upper quadrant.
  • Acinar cell carcinoma of the pancreas is a rare and highly malignant tumor, and there are few reports regarding treatment with chemotherapy.
  • Herein, we report a case with multiple liver metastases which were controlled by systemic chemotherapy using S-1.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / therapy. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Oxonic Acid / therapeutic use. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / therapy. Tegafur / therapeutic use
  • [MeSH-minor] Aged. Drug Combinations. Gastrectomy. Hepatectomy. Humans. Male. Pancreatectomy

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  • (PMID = 20087046.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid
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26. Joo KR, Shin HP, Cha JM, Nam S, Huh Y: Effect of Korean red ginseng on superoxide dismutase inhibitor-induced pancreatitis in rats: a histopathologic and immunohistochemical study. Pancreas; 2009 Aug;38(6):661-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We examined the effects of KRG treatment on superoxide dismutase inhibitor-induced experimental pancreatitis.
  • METHODS: Sprague-Dawley rats and KRG from the roots of a 6-year-old fresh Panax ginseng C. A.
  • At week 7, all rats were killed, and pancreatic tissues were analyzed.
  • Tissues from the non-KRG-treated pancreatitis group exhibited marked pancreatic damage including changes in histological architecture, acinar cell necrosis and degeneration, and cytoplasmic vacuolization.
  • However, tissues from the KRG-treated pancreatitis group exhibited no cellular damage and had normal histological pancreatic architecture.
  • Immunohistochemical examination revealed that the expressions of nuclear factor kappaB, tumor necrosis factor alpha, inducible nitric oxide synthase, and the oxidant stress markers, malondialdehyde and 4-hydroxynonenal, were significantly decreased in the KRG-treated pancreatitis group as compared with the non-KRG-treated pancreatitis group.
  • CONCLUSIONS: Our results suggest that KRG has antioxidant therapeutic effects on superoxide dismutase inhibitor-induced pancreatitis by inhibition of nuclear factor kappaB.
  • [MeSH-major] Drugs, Chinese Herbal / pharmacology. Panax. Pancreatitis / drug therapy. Phytotherapy. Superoxide Dismutase / antagonists & inhibitors
  • [MeSH-minor] Animals. Antioxidants / pharmacology. Ditiocarb / toxicity. Enzyme Inhibitors / toxicity. Korea. Male. NF-kappa B / metabolism. Nitric Oxide Synthase Type II / metabolism. Oxidative Stress / drug effects. Peroxidase / metabolism. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19531970.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Drugs, Chinese Herbal; 0 / Enzyme Inhibitors; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 99Z2744345 / Ditiocarb; EC 1.11.1.7 / Peroxidase; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, rat; EC 1.15.1.1 / Superoxide Dismutase
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27. Dobashi Y, Suzuki S, Matsubara H, Kimura M, Endo S, Ooi A: Critical and diverse involvement of Akt/mammalian target of rapamycin signaling in human lung carcinomas. Cancer; 2009 Jan 1;115(1):107-18
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Critical and diverse involvement of Akt/mammalian target of rapamycin signaling in human lung carcinomas.
  • One representative cascade is the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin (mTOR) pathway.
  • METHODS: The authors investigated the involvement of mTOR in the pathobiologic profiles of 150 specimens of lung carcinoma by immunohistochemistry and immunoblotting in correlation with the upstream and downstream proteins Akt and p70S6-kinase (S6K), respectively.
  • In AC, the frequency of p-mTOR staining was higher in the well differentiated subtype, in particular, in the acinar structure.
  • Conversely, in squamous cell carcinomas, mTOR activation was associated with a significantly higher frequency of lymph node metastasis.
  • First, mTOR may function not only in the proliferation of tumor cells as an effector molecule downstream of EGFR but also possibly in the morphogenesis of AC.
  • Second, the activation of mTOR may play a key role in metastasis in squamous cell carcinoma.
  • Overall, the current results demonstrated the potential for the application of rapamycin, an mTOR inhibitor, as an additional novel component of chemotherapy for a defined subset of patients with lung carcinoma.
  • [MeSH-major] Lung Neoplasms / metabolism. Protein Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Humans. Neoplasm Metastasis. Neoplasms, Squamous Cell / metabolism. Neoplasms, Squamous Cell / pathology. Phosphorylation. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction. TOR Serine-Threonine Kinases

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  • [Copyright] Copyright (c) 2008 American Cancer Society.
  • (PMID = 19090006.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa
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28. Chilosi M, Murer B: Mixed adenocarcinomas of the lung: place in new proposals in classification, mandatory for target therapy. Arch Pathol Lab Med; 2010 Jan;134(1):55-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mixed adenocarcinomas of the lung: place in new proposals in classification, mandatory for target therapy.
  • CONTEXT: Lung cancer is one of the most frequent and lethal malignant neoplasms, but knowledge regarding the molecular basis of its pathogenesis is far from complete due to the striking diversity of different forms.
  • The current lung cancer classification (World Health Organization 2004) can efficiently distinguish clinically relevant major subtypes (small cell and non-small cell carcinomas), but its results are partly inadequate when facing prognostic and therapeutic decisions for non-small cell carcinomas, especially for the group of tumors classified as adenocarcinoma.
  • Lung adenocarcinoma comprises a heterogeneous group of tumors characterized by diverse morphologic features and molecular pathogenesis.
  • The category of mixed adenocarcinomas includes most adenocarcinomas (approximately 80%) and, according to World Health Organization criteria, is defined by the occurrence of a mixed array of different patterns (acinar, papillary, bronchioloalveolar, solid with mucin).
  • The histologic recognition of mixed adenocarcinoma is subjective and cannot consistently discriminate between responders and nonresponders to new targeted therapies (eg, tyrosine kinase inhibitors).
  • Diagnostic problems are mainly related to the poor reproducibility of histologic criteria, especially when applied in small biopsies and cytology, and to the difficulty in assigning each form to a precisely defined entity, as needed by updated therapeutic approaches.
  • In this evolving scenario, pathologists face new challenging diagnostic roles that include not only the precise morphologic definition of carcinoma subtypes but also their molecular characterization.
  • OBJECTIVE: To use a comprehensive critical analysis reconciling the overwhelming variety of biologic, morphologic, molecular, and clinical data to define new classification schemes for lung adenocarcinoma.
  • CONCLUSIONS: A new classification approach should redefine lung adenocarcinoma heterogeneity reconciling classic morphology, immunophenotypic and molecular features of neoplastic cells, and also relevant information provided by stem cell biology.
  • This approach, which has been already successfully applied in World Health Organization classification of other tumors, could improve the recognition of new reproducible profiles for adenocarcinomas, more closely and reproducibly related to clinical features and response to specific therapies, limiting the use of "wastebasket" categories such as mixed adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / classification. Adenocarcinoma / pathology. Lung Neoplasms / classification. Lung Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor. Cell Differentiation. Drug Therapy. Humans. Stem Cells / pathology. World Health Organization

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  • (PMID = 20073606.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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29. Dall'igna P, Cecchetto G, Bisogno G, Conte M, Chiesa PL, D'Angelo P, De Leonardis F, De Salvo G, Favini F, Ferrari A, TREP Group: Pancreatic tumors in children and adolescents: the Italian TREP project experience. Pediatr Blood Cancer; 2010 May;54(5):675-80
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  • INTRODUCTION: Malignant pancreatic tumors are exceedingly rare in pediatric age and their clinical features and treatment usually go unappreciated by most pediatric oncologists and surgeons.
  • RESULTS: Tumor types were 4 pancreatoblastomas, 2 pancreatic carcinomas, 3 neoplasms of the endocrine pancreas, and 12 solid pseudopapillary tumors.
  • Three of the four patients with pancreatoblastoma had advanced disease at diagnosis and were given chemotherapy; at the time of this report, three patients were alive in first remission, while one died due to treatment toxicity.
  • Both the cases of pancreatic carcinoma had the acinar cell subtype and successfully underwent pancreaticoduodenectomy with complete tumor resection, remaining without evidence of disease at the time of this analysis.
  • The histological diagnoses of the three endocrine tumors were a malignant islet cell tumor, a gastrinoma, and a well-differentiated tumor.
  • All 12 patients with solid pseudopapillary tumors underwent complete tumor resection and were given no adjuvant treatment; 11 were alive in first remission, while one experienced a local and distant relapse 5 years after diagnosis.
  • CONCLUSIONS: Surgery remains the keystone of treatment for pancreatic tumors in pediatric age as in adults.
  • [MeSH-major] Pancreatic Neoplasms / epidemiology. Rare Diseases / epidemiology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Italy / epidemiology. Male. Prospective Studies. Treatment Outcome

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  • [CommentIn] Pediatr Blood Cancer. 2010 May;54(5):659-60 [20063425.001]
  • (PMID = 19998473.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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30. Kitagami H, Kondo S, Hirano S, Kawakami H, Egawa S, Tanaka M: Acinar cell carcinoma of the pancreas: clinical analysis of 115 patients from Pancreatic Cancer Registry of Japan Pancreas Society. Pancreas; 2007 Jul;35(1):42-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinar cell carcinoma of the pancreas: clinical analysis of 115 patients from Pancreatic Cancer Registry of Japan Pancreas Society.
  • OBJECTIVES: Acinar cell carcinoma (ACC) of the pancreas is a rare tumor, and many aspects remain unclear because no large-scale clinical studies have been conducted.
  • METHODS: The present study investigated the clinical characteristics, treatment, and therapeutic outcomes of 115 patients registered in the Pancreatic Cancer Registry of the Japan Pancreas Society, and therapeutic plans were reviewed.
  • RESULTS: Although ACC has been associated with advanced stage and poor prognosis, this tumor was resectable in 76.5% of the patients, and the 5-year survival rate after resection was favorable, being 43.9%.
  • If ACC is unresectable or recurrent, chemotherapy is likely to prove useful.
  • Multidisciplinary therapy centering on the role of surgery will need to be established.
  • [MeSH-major] Carcinoma, Acinar Cell / mortality. Pancreatic Neoplasms / mortality. Registries / statistics & numerical data
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor. Female. Humans. Japan / epidemiology. Male. Middle Aged. Neoplasm Staging / statistics & numerical data. Prognosis. Survival Rate. Treatment Outcome

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  • (PMID = 17575544.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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31. Schindler G, Kincius M, Liang R, Backhaus J, Zorn M, Flechtenmacher C, Gebhard MM, Büchler MW, Schemmer P: Fundamental efforts toward the development of a therapeutic cocktail with a manifold ameliorative effect on hepatic ischemia/reperfusion injury. Microcirculation; 2009 Oct;16(7):593-602
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fundamental efforts toward the development of a therapeutic cocktail with a manifold ameliorative effect on hepatic ischemia/reperfusion injury.
  • The present study was designed to evaluate the effect of a multiple pharmacological approach toward ischemia/reperfusion injury reduction.
  • METHODS: The left liver lobe of Sprague-Dawley rats underwent normothermic ischemia for 90 minutes after a cocktail (glycine, taurine, alanine, arginine, and prednisolon) intravenous administration.
  • Liver injury (transaminases, histology) and cellular activation [Kupffer cell phagocytosis, production of tumor necrosis factor-alpha (TNFalpha), and prostaglandin E-2 (PGE(2))], as well as microcirculation and leukocyte-endothelial interaction (in vivo microscopy), were assessed.
  • RESULTS: Whereas in controls a substantial increase of aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase to 2,341+/-477, 1,442+/-262, and 1,973+/-73 U/L, respectively, was measured eight hours after reperfusion, the cocktail significantly reduced the increase of enzymes by 33-80% (P<0.05).
  • Moreover, the cocktail improved acinar and sinusoidal perfusion, while the sinusoidal diameters, leukocyte-endothelial interaction, Kupffer cell phagocytic activity, and TNFalpha/PGE(2) serum levels were significantly reduced, the latter by 86% and to 1.64-fold, respectively.
  • CONCLUSIONS: This study depicts that multifaceted pharmacological tackling of ischemia/reperfusion injury is feasible and protects rat liver tissue from warm ischemia/reperfusion injury.
  • [MeSH-major] Reperfusion Injury / drug therapy
  • [MeSH-minor] Alanine / therapeutic use. Animals. Arginine / therapeutic use. Chemotaxis, Leukocyte. Clinical Enzyme Tests. Drug Therapy, Combination. Glycine / therapeutic use. Liver Circulation. Liver Diseases / drug therapy. Liver Diseases / enzymology. Liver Diseases / pathology. Necrosis. Phagocytosis. Prednisolone / therapeutic use. Rats. Rats, Sprague-Dawley. Taurine / therapeutic use. Treatment Outcome

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  • (PMID = 19626553.001).
  • [ISSN] 1549-8719
  • [Journal-full-title] Microcirculation (New York, N.Y. : 1994)
  • [ISO-abbreviation] Microcirculation
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 1EQV5MLY3D / Taurine; 94ZLA3W45F / Arginine; 9PHQ9Y1OLM / Prednisolone; OF5P57N2ZX / Alanine; TE7660XO1C / Glycine
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32. Petropavlovskaia M, Makhlin J, Sampalis J, Rosenberg L: Development of an in vitro pancreatic tissue model to study regulation of islet neogenesis associated protein expression. J Endocrinol; 2006 Oct;191(1):65-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of an in vitro pancreatic tissue model to study regulation of islet neogenesis associated protein expression.
  • Restoration of a functional beta-cell mass in a patient with diabetes may hold the key for curing the disease.
  • In recent years, there has been increasing interest in the development of new strategies to induce beta-cell regeneration and new islet formation in situ and a role for Reg proteins has been suggested.
  • One such protein, islet neogenesis associated protein (INGAP), is a member of the Reg3 family of proteins and has been shown to induce islet neogenesis.
  • Here, we report the establishment of the first in vitro tissue model of INGAP expression that consists of epithelial cystic structures derived from hamster pancreatic acinar tissue cultured in collagen matrix.
  • Using quantitative reverse transcriptase PCR, we show that INGAP expression correlates with cyst formation and size suggesting the involvement of intra-luminal pressure associated with cyst growth.
  • We also demonstrate for the first time that INGAP gene expression was significantly induced by treatment with interleukin (IL)-6 and further enhanced by a combination of IL-6 with dexamethazone and nicotinamide.
  • Additionally, our data suggest that the effect of IL-6 on INGAP expression is mediated via the JAK/STAT3 signaling pathway.
  • In summary, the in vitro model of INGAP expression described here represents an important step in the development of strategies for the use of INGAP and related proteins as islet neogenic agents in the pharmacotherapy of both type-1 and type-2 diabetes.
  • [MeSH-major] Cytokines / pharmacology. Gene Expression Regulation. Lectins, C-Type / genetics. Models, Animal. Pancreas, Exocrine / metabolism. Pancreas, Exocrine / pathology. Regeneration
  • [MeSH-minor] Animals. Blotting, Western / methods. Cell Differentiation. Collagen. Cricetinae. DNA Primers. Dactinomycin / pharmacology. Genetic Engineering. Interferon-gamma / pharmacology. Interleukin-1beta / pharmacology. Interleukin-6 / pharmacology. Male. Mesocricetus. Microscopy, Confocal. Pancreatic Ducts / physiology. Pancreatic Ducts / ultrastructure. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Tissue Culture Techniques. Transcription, Genetic / drug effects. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 17065390.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / DNA Primers; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Lectins, C-Type; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 1CC1JFE158 / Dactinomycin; 82115-62-6 / Interferon-gamma; 9007-34-5 / Collagen
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