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1. Dewald GW, Smyrk TC, Thorland EC, McWilliams RR, Van Dyke DL, Keefe JG, Belongie KJ, Smoley SA, Knutson DL, Fink SR, Wiktor AE, Petersen GM: Fluorescence in situ hybridization to visualize genetic abnormalities in interphase cells of acinar cell carcinoma, ductal adenocarcinoma, and islet cell carcinoma of the pancreas. Mayo Clin Proc; 2009 Sep;84(9):801-10
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  • [Title] Fluorescence in situ hybridization to visualize genetic abnormalities in interphase cells of acinar cell carcinoma, ductal adenocarcinoma, and islet cell carcinoma of the pancreas.
  • OBJECTIVE: To use fluorescence in situ hybridization (FISH) to visualize genetic abnormalities in interphase cell nuclei (interphase FISH) of acinar cell carcinoma, ductal adenocarcinoma, and islet cell carcinoma of the pancreas.
  • PATIENTS AND METHODS: Between April 4, 2007, and December 4, 2008, interphase FISH was used to study paraffin-embedded preparations of tissue obtained from 18 patients listed in the Mayo Clinic Biospecimen Resource for Pancreas Research with a confirmed diagnosis of acinar cell carcinoma, ductal adenocarcinoma, islet cell carcinoma, or pancreas without evidence of neoplasia.
  • RESULTS: FISH abnormalities were observed in 12 (80%) of 15 patients with pancreatic cancer: 5 of 5 patients with acinar cell carcinoma, 5 of 5 patients with ductal adenocarcinoma, and 2 (40%) of 5 patients with islet cell carcinoma.
  • All 3 specimens of pancreatic tissue without neoplasia had normal FISH results.
  • Gains of CTNNB1 due to trisomy 3 occurred in each tumor with acinar cell carcinoma but in none of the other tumors in this study.
  • CONCLUSION: FISH abnormalities of CTNNB1 due to trisomy 3 were observed only in acinar cell carcinoma.
  • FISH abnormalities of genes implicated in familial cancer, tumor progression, and the 5-fluorouracil pathway were common but were not associated with specific types of pancreatic cancer.


2. Radhi J, Tse F, Marcaccio M: Papillocystic variant of acinar cell pancreatic carcinoma. J Oncol; 2010;2010:242016
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  • [Title] Papillocystic variant of acinar cell pancreatic carcinoma.
  • Acinar cell pancreatic carcinoma is a rare solid malignant neoplasm.
  • We report a large 10 cm pancreatic tumor with papillocystic pathology features involving the pancreatic head.
  • The growth pattern of these tumors could be mistaken for intraductal papillary mucinous tumors or other pancreatic cystic neoplasms.

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  • (PMID = 20204128.001).
  • [ISSN] 1687-8469
  • [Journal-full-title] Journal of oncology
  • [ISO-abbreviation] J Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2831459
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3. Hezel AF, Gurumurthy S, Granot Z, Swisa A, Chu GC, Bailey G, Dor Y, Bardeesy N, Depinho RA: Pancreatic LKB1 deletion leads to acinar polarity defects and cystic neoplasms. Mol Cell Biol; 2008 Apr;28(7):2414-25
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  • [Title] Pancreatic LKB1 deletion leads to acinar polarity defects and cystic neoplasms.
  • LKB1 is a key regulator of energy homeostasis through the activation of AMP-activated protein kinase (AMPK) and is functionally linked to vascular development, cell polarity, and tumor suppression.
  • In humans, germ line LKB1 loss-of-function mutations cause Peutz-Jeghers syndrome (PJS), which is characterized by a predisposition to gastrointestinal neoplasms marked by a high risk of pancreatic cancer.
  • The Lkb1-deficient pancreas, although grossly normal at birth, demonstrates a defective acinar cell polarity, an abnormal cytoskeletal organization, a loss of tight junctions, and an inactivation of the AMPK/MARK/SAD family kinases.
  • Rapid and progressive postnatal acinar cell degeneration and acinar-to-ductal metaplasia occur, culminating in marked pancreatic insufficiency and the development of pancreatic serous cystadenomas, a tumor type associated with PJS.
  • These genetic studies provide in vivo evidence of a key role for LKB1 in the establishment of epithelial cell polarity that is vital for pancreatic acinar cell function and viability and for the suppression of neoplasia.

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  • (PMID = 18227155.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084313; United States / NCI NIH HHS / CA / K08CA122835; United States / NCI NIH HHS / CA / P01 CA117969; United States / NCI NIH HHS / CA / P01 CA117969-01; United States / NCI NIH HHS / CA / K01 CA104647; United States / NCI NIH HHS / CA / U01CA084313-09; United States / NCI NIH HHS / CA / K01CA104647; United States / NCI NIH HHS / CA / P01CA117969-03; United States / NCI NIH HHS / CA / K08 CA122835
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.- / Protein Kinases; EC 2.7.1.- / AMP-activated protein kinase kinase; EC 2.7.1.- / Stk11 protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC2268441
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4. 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.
  • 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

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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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5. Sequeira SJ, Ranganathan AC, Adam AP, Iglesias BV, Farias EF, Aguirre-Ghiso JA: Inhibition of proliferation by PERK regulates mammary acinar morphogenesis and tumor formation. PLoS One; 2007 Jul 18;2(7):e615
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  • [Title] Inhibition of proliferation by PERK regulates mammary acinar morphogenesis and tumor formation.
  • This in turn, results in translational repression and the activation of downstream programs that can limit cell growth through cell cycle arrest and/or apoptosis.
  • These responses can also be initiated by perturbations in cell adhesion.
  • Thus, we hypothesized that adhesion-dependent regulation of PERK signaling might determine cell fate.
  • Here we report a novel role for PERK in limiting MCF10A mammary epithelial cell proliferation during acinar morphogenesis in 3D Matrigel culture as well as in preventing mammary tumor formation in vivo.
  • Further, inhibition of endogenous PERK signaling during acinar morphogenesis, using two dominant-negative PERK mutants (PERK-DeltaC or PERK-K618A), does not affect apoptosis but results instead in hyper-proliferative and enlarged lumen-filled acini, devoid of proper architecture.
  • Our results reveal that the PERK pathway is responsive to adhesion-regulated signals and that it is essential for proper acinar morphogenesis and in preventing mammary tumor formation.
  • The possibility that deficiencies in PERK signaling could lead to hyperproliferation of the mammary epithelium and increase the likelihood of tumor formation, is of significance to the understanding of breast cancer.

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  • (PMID = 17637831.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA119018; United States / NCI NIH HHS / CA / R01 CA109182-02; United States / NCI NIH HHS / CA / R01 CA109182-01A1; United States / NCI NIH HHS / CA / CA109182; United States / NCI NIH HHS / CA / R01 CA119018; United States / NCI NIH HHS / CA / R01 CA109182; United States / NCI NIH HHS / CA / R01 CA109182-04; United States / NCI NIH HHS / CA / R01 CA109182-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATF4 protein, human; 0 / DDIT3 protein, human; 0 / Eukaryotic Initiation Factor-2; 0 / RNA, Messenger; 145891-90-3 / Activating Transcription Factor 4; 147336-12-7 / Transcription Factor CHOP; EC 2.7.10.- / PERK kinase; EC 2.7.11.1 / eIF-2 Kinase
  • [Other-IDs] NLM/ PMC1910610
  • [General-notes] NLM/ Original DateCompleted: 20070802
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6. Davis MA, Reynolds AB: Blocked acinar development, E-cadherin reduction, and intraepithelial neoplasia upon ablation of p120-catenin in the mouse salivary gland. Dev Cell; 2006 Jan;10(1):21-31
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  • [Title] Blocked acinar development, E-cadherin reduction, and intraepithelial neoplasia upon ablation of p120-catenin in the mouse salivary gland.
  • Surprisingly, acinar differentiation is completely blocked, resulting in a gland composed entirely of ducts.
  • Moreover, p120 ablation causes E-cadherin deficiency in vivo and severe defects in adhesion, cell polarity, and epithelial morphology.
  • These changes closely phenocopy high-grade intraepithelial neoplasia, a condition that, in humans, typically progresses to invasive cancer.
  • Tumor-like protrusions appear immediately after p120 ablation at e14 and expand into the lumen until shortly after birth, at which time the animals die with completely occluded glands.
  • The data reveal an unexpected role for p120 in salivary acinar development and show that p120 ablation by itself induces effects consistent with a role in tumor progression.
  • [MeSH-major] Cadherins / metabolism. Carcinoma in Situ / metabolism. Cell Adhesion Molecules / deficiency. Epithelial Cells / metabolism. Phosphoproteins / deficiency. Salivary Glands
  • [MeSH-minor] Age Factors. Animals. Animals, Newborn. Apoptosis / genetics. Catenins. Cell Differentiation. Cell Proliferation. Desmoglein 1 / metabolism. Embryo, Mammalian. Gene Expression Regulation, Developmental / genetics. Immunohistochemistry / methods. Membrane Glycoproteins / metabolism. Mice. Mice, Knockout. Molecular Biology / methods. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Skin / metabolism. Sodium-Potassium-Exchanging ATPase / metabolism. Trans-Activators / metabolism. beta Catenin / metabolism


7. Sanati S, Watson MA, Salavaggione AL, Humphrey PA: Gene expression profiles of ductal versus acinar adenocarcinoma of the prostate. Mod Pathol; 2009 Oct;22(10):1273-9
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  • [Title] Gene expression profiles of ductal versus acinar adenocarcinoma of the prostate.
  • Ductal adenocarcinoma is an uncommon variant of prostatic adenocarcinoma with a generally more aggressive clinical course than usual acinar adenocarcinoma.
  • However, the molecular distinction between ductal and acinar adenocarcinomas is not well characterized.
  • The aim of this investigation was to evaluate the relatedness of ductal versus acinar prostatic adenocarcinoma by comparative gene expression profiling.
  • Archived, de-identified, snap frozen tumor tissue from 5 ductal adenocarcinomas, 3 mixed ductal-acinar adenocarcinomas, and 11 acinar adenocarcinomas cases were analyzed.
  • All cases of acinar and ductal adenocarcinomas were matched by Gleason grade.
  • RNA from whole tissue sections of the 5 ductal and 11 acinar adenocarcinomas cases were subjected to gene expression profiling on Affymetrix U133Plus2 microarrays.
  • Independently, laser-capture microdissection was also performed on the three mixed ductal-acinar cases and five pure acinar cases to isolate homogeneous populations of ductal and acinar carcinoma cells from the same tumor.
  • Seven of these laser-capture microdissected samples (three ductal and four acinar cell populations) were similarly analyzed on U133Plus2 arrays.
  • Analysis of data from whole sections of ductal and acinar carcinomas identified only 25 gene transcripts whose expression was significantly and at least two-fold different between ductal and acinar adenocarcinomas.
  • A similar analysis of microdissected cell populations identified 10 transcripts, including the prolactin receptor, with more significant differences in expression of 5- to 27-fold between ductal and acinar adenocarcinomas cells.
  • Overexpression of prolactin receptor protein in ductal versus acinar adenocarcinoma was confirmed by immunohistochemistry in an independent set of tumors.
  • We conclude that ductal and acinar adenocarcinomas of the prostate are strikingly similar at the level of gene expression.
  • However, several of the genes identified in this study, including the prolactin receptor, represent targets for further investigations on the molecular basis for histomorphological and clinical behavioral differences between acinar and ductal adenocarcinomas.
  • [MeSH-major] Biomarkers, Tumor / genetics. Carcinoma, Acinar Cell / genetics. Carcinoma, Ductal / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Cluster Analysis. Humans. Immunohistochemistry. Male. Microdissection. Neoplasm Staging. Oligonucleotide Array Sequence Analysis. Predictive Value of Tests. Prostatectomy. RNA, Messenger / analysis. Receptors, Prolactin / analysis. Receptors, Prolactin / genetics

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  • (PMID = 19633648.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Receptors, Prolactin
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8. Darling MR, Jackson-Boeters L, Daley TD, Diamandis EP: [Human kallikrein 13 expression in salivary gland tumors]. Int J Biol Markers; 2006 Apr-Jun;21(2):106-110
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  • Petraki et al have previously described presence of hK13 in salivary gland tissue, localized to duct epithelia and some acinar cells.
  • The aim of this study was to determine whether hK13 is expressed in salivary gland tissues and salivary gland tumors (both benign and malignant), in order to compare normal with tumor tissues.
  • Pleomorphic adenomas (PA), adenoid cystic carcinomas (ACC), polymorphous low grade adenocarcinomas (PLGA), acinic cell carcinomas (ACI), mucoepidermoid carcinomas (MEC) and adenocarcinomas not otherwise specified (ANOS) of both minor and major salivary glands were examined.

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  • (PMID = 28207129.001).
  • [ISSN] 1724-6008
  • [Journal-full-title] The International journal of biological markers
  • [ISO-abbreviation] Int. J. Biol. Markers
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
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9. Illyés G, Luczay A, Benyó G, Kálmán A, Borka K, Köves K, Rácz K, Tulassay T, Schaff Z: Cushing's syndrome in a child with pancreatic acinar cell carcinoma. Endocr Pathol; 2007;18(2):95-102
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  • [Title] Cushing's syndrome in a child with pancreatic acinar cell carcinoma.
  • A case of pancreatic acinar cell tumor (ACC) is presented in a 10-year-old boy.
  • The tumor manifested clinically with Cushing's syndrome, high serum adrenocorticotropic hormone (ACTH) and cortisol concentrations.
  • Periodic acid Schiff positive cytoplasmic granules, trypsinogen, keratins, alpha-1-antitrypsin, and AFP were identified in the tumor cells.
  • Using immunochemiluminometric assay, a high quantity of ACTH was found in the fresh frozen tumor extract.
  • Combined radiochemotherapy was temporarily effective in reducing the tumor mass and serum AFP.
  • [MeSH-major] Carcinoma, Acinar Cell / complications. Cushing Syndrome / etiology. Pancreatic Neoplasms / complications


10. Stelow EB, Shaco-Levy R, Bao F, Garcia J, Klimstra DS: Pancreatic acinar cell carcinomas with prominent ductal differentiation: Mixed acinar ductal carcinoma and mixed acinar endocrine ductal carcinoma. Am J Surg Pathol; 2010 Apr;34(4):510-8
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  • [Title] Pancreatic acinar cell carcinomas with prominent ductal differentiation: Mixed acinar ductal carcinoma and mixed acinar endocrine ductal carcinoma.
  • BACKGROUND: Pancreatic acinar cell carcinomas (ACCs) are clinically and pathologically distinct from pancreatic ductal adenocarcinomas (PDAs).
  • All cases showed significant evidence of both acinar and ductal differentiation, estimated to be at least 25% of the neoplastic cells, and 3 cases in addition had endocrine differentiation in more than 25% of cells.
  • Five cases were predominately acinar with intracellular and sometimes extracellular mucin ("mucinous acinar cell carcinoma" pattern).
  • Six cases seemed more mixed with areas recapitulating typical PDAs whereas the other portions of the tumors seemed akin to typical acinar cell carcinomas ("combined acinar and ductal" pattern).
  • CONCLUSION: Despite the early embryologic divergence of acinar and ductal cell lineages, rare pancreatic tumors have both acinar and ductal differentiation, usually predominantly the former.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Carcinoma, Islet Cell / pathology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Combined Modality Therapy. DNA Mutational Analysis. DNA, Neoplasm / analysis. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Mucins / metabolism. Mutation. Neoplasms, Multiple Primary. New York / epidemiology. Pancreatectomy. Proto-Oncogene Proteins / genetics. Survival Rate. Virginia / epidemiology. ras Proteins / genetics

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  • (PMID = 20182344.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / Mucins; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
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11. Minakawa K, Oka K, Nihei T, Sando N, Oikawa H, Toda J, Hosokawa Y, Matsumoto T, Yanagisawa A: Pancreatic endocrine tumor with partial acinar cell differentiation. APMIS; 2006 Oct;114(10):720-5
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  • [Title] Pancreatic endocrine tumor with partial acinar cell differentiation.
  • We examined a 70-year-old woman in whom a pancreatic endocrine tumor with partial acinar cell differentiation had been diagnosed.
  • The tumor was located in the pancreatic tail and measured 12.5 x 9.5 x 8 cm.
  • The cells had proliferated in islet-like solid medullary, trabecular, acinar, and papillary patterns.
  • The tumor may be considered an amphicrine tumor.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Islet Cell / diagnosis. Neoplasms, Multiple Primary / diagnosis. Pancreas / pathology. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Biomarkers, Tumor / metabolism. Biopsy, Needle. Cytoplasmic Granules / ultrastructure. Female. Humans. Immunohistochemistry. Secretory Vesicles / ultrastructure. Synaptophysin / analysis. Synaptophysin / metabolism. alpha 1-Antitrypsin / analysis. alpha 1-Antitrypsin / metabolism

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  • (PMID = 17004975.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Synaptophysin; 0 / alpha 1-Antitrypsin
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12. Stelow EB, Bardales RH, Shami VM, Woon C, Presley A, Mallery S, Lai R, Stanley MW: Cytology of pancreatic acinar cell carcinoma. Diagn Cytopathol; 2006 May;34(5):367-72
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  • [Title] Cytology of pancreatic acinar cell carcinoma.
  • Acinar cell carcinoma (ACC) of the pancreas is extremely uncommon and its cytologic features have rarely been described.
  • Original cytologic diagnoses included "acinar cell carcinoma," "pancreatic endocrine tumor," "favor neuroendocrine tumor, low-grade" and "non-diagnostic specimen."
  • The cytologic features included small to moderate-sized loose groups with numerous single cells, prominent acinar formation, little anisonucleosis and prominent nucleoli.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Biopsy, Fine-Needle. Female. Humans. Keratins / analysis. Liver Neoplasms / chemistry. Liver Neoplasms / secondary. Lymph Nodes / pathology. Male. Middle Aged. Pancreas / chemistry. Pancreas / pathology

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  • (PMID = 16604543.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 68238-35-7 / Keratins
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13. Mizuno Y, Sumi Y, Nachi S, Ito Y, Marui T, Saji S, Matsutomo H: Acinar cell carcinoma arising from an ectopic pancreas. Surg Today; 2007;37(8):704-7
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  • [Title] Acinar cell carcinoma arising from an ectopic pancreas.
  • We herein report a rare case of ectopic pancreatic acinar cell carcinoma (ACC) which presented as a submucosal tumor of the pylorus.
  • Esophago-gastroduodenal endoscopy showed no mucosal lesions, but a submucosal tumor was observed around the pylorus.
  • We diagnosed a gastrointestinal stromal tumor or malignant lymphoma preoperatively, and decided to perform an operation in order to confirm the diagnosis and select the optimal treatment.
  • The resected specimen showed the 7.6 x 4.9-cm size tumor to mainly originate from the pylorus.
  • Histopathologically, the tumor was identified as pancreatic ACC with lymph node metastasis.
  • The tumor cells were labeled by immunohistochemical staining for alpha1-antitrypsin.
  • Because of the tumor location, we considered the tumor to have originated from the ectopic pancreatic tissue in the stomach.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology. Pylorus / pathology. Stomach Neoplasms / secondary

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  • (PMID = 17643220.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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14. Sipos B, Klöppel G: [Acinar cell carcinomas and pancreatoblastomas: related but not the same]. Pathologe; 2005 Feb;26(1):37-40
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  • [Title] [Acinar cell carcinomas and pancreatoblastomas: related but not the same].
  • Acinar cell carcinomas and pancreatoblastomas are malignant tumors of the pancreas, showing predominantly acinar differentiation characterized by the immunohistochemical expression of pancreatic enzymes.
  • Histologically, they usually display acinar and/or solid patterns, but may occasionally also exhibit cystic structures.
  • Acinar cell carcinomas predominantly occur in adults, pancreatoblastomas in children.
  • Both tumor types commonly show allelic losses on chromosome 11p and mutations in the APC/beta-catenin signaling pathway.
  • Pancreatoblastomas, in contrast to acinar cell carcinomas, are potentially curable.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Differentiation. Diagnosis, Differential. Female. Humans. Male. Prognosis. Sex Characteristics

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  • (PMID = 15614488.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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15. Matos JM, Schmidt CM, Turrini O, Agaram NP, Niedergethmann M, Saeger HD, Merchant N, Johnson CS, Lillemoe KD, Grützmann R: Pancreatic acinar cell carcinoma: a multi-institutional study. J Gastrointest Surg; 2009 Aug;13(8):1495-502
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  • [Title] Pancreatic acinar cell carcinoma: a multi-institutional study.
  • INTRODUCTION: The presentation and outcome of patients with acinar cell carcinoma (ACC) of the pancreas compared to the more common ductal cell adenocarcinoma (DCA) may be distinct.
  • Mean tumor size was 5.3 cm.
  • American Joint Commission on Cancer tumor stages were stage I (two), stage II (eight), stage III (four), and stage IV (three).
  • This is in contrast to 1,608 patients with ductal cell adenocarcinoma who underwent resection identified from recent literature reports where the average median survival was only 24 months.
  • CONCLUSION: Acinar cell carcinoma of the pancreas is rare and appears to have a presentation and outcome distinct from the more common pancreatic DCA.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Biopsy. Cholangiopancreatography, Endoscopic Retrograde. Diagnosis, Differential. Follow-Up Studies. Germany / epidemiology. Humans. Incidence. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. Pancreatectomy / methods. Prognosis. Prospective Studies. Survival Rate. United States / epidemiology

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  • (PMID = 19495891.001).
  • [ISSN] 1873-4626
  • [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] Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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16. Bhatia M: Inflammatory response on the pancreatic acinar cell injury. Scand J Surg; 2005;94(2):97-102
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  • [Title] Inflammatory response on the pancreatic acinar cell injury.
  • Acinar cell injury early in acute pancreatitis leads to a local inflammatory reaction; if marked this leads to a systemic inflammatory response syndrome (SIRS).
  • This review intends to present an overview of the inflammatory response that takes place following pancreatic acinar cell injury.
  • [MeSH-minor] Acute Disease. Antigens, CD40 / analysis. Humans. Intercellular Adhesion Molecule-1 / physiology. Interleukin-1 / analysis. Interleukin-10 / analysis. Neprilysin / physiology. Substance P / physiology. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 16111089.001).
  • [ISSN] 1457-4969
  • [Journal-full-title] Scandinavian journal of surgery : SJS : official organ for the Finnish Surgical Society and the Scandinavian Surgical Society
  • [ISO-abbreviation] Scand J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Inflammation Mediators; 0 / Interleukin-1; 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1; 130068-27-8 / Interleukin-10; 33507-63-0 / Substance P; EC 3.4.24.11 / Neprilysin
  • [Number-of-references] 39
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17. Kawakami H, Kuwatani M, Onodera M, Hirano S, Kondo S, Nakanishi Y, Itoh T, Asaka M: Primary acinar cell carcinoma of the ampulla of Vater. J Gastroenterol; 2007 Aug;42(8):694-7
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  • [Title] Primary acinar cell carcinoma of the ampulla of Vater.
  • Acinar cell carcinoma of the pancreatobiliary system is a relatively rare malignant neoplasm arising usually in the pancreatic parenchyma.
  • The patient underwent a curative surgical operation, and histopathological examination revealed that the tumor was confined to the ampulla of Vater with no continuity to the pancreatic parenchyma.
  • The tumor cells showed acinar or tubular arrangement with eosinophilic to basophilic granular cytoplasm, findings identical to those of acinar cell carcinoma of the pancreas.
  • Immunohistochemically, the tumor cells were positive for lipase.
  • From these findings, we concluded that the tumor was primary acinar cell carcinoma arising in the ampulla of Vater, probably originating from heterotopic pancreatic tissue.
  • This is the first reported case of primary acinar cell carcinoma in the ampulla of Vater.
  • [MeSH-major] Ampulla of Vater. Carcinoma, Acinar Cell / diagnosis. Common Bile Duct Neoplasms / diagnosis

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  • (PMID = 17701134.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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18. Xue DB, Zhang WH, Yun XG, Song C, Zheng B, Shi XY, Wang HY: Regulating effects of arsenic trioxide on cell death pathways and inflammatory reactions of pancreatic acinar cells in rats. Chin Med J (Engl); 2007 Apr 20;120(8):690-5
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  • [Title] Regulating effects of arsenic trioxide on cell death pathways and inflammatory reactions of pancreatic acinar cells in rats.
  • We studied the regulatory effect of arsenic trioxide (As(2)O(3)) on apoptosis and oncosis of pancreatic acinar cells in vitro and in vivo and its therapeutic effect on acute pancreatitis.
  • METHODS: Pancreatic acinar cells were isolated by collagenase digestion method.
  • Apoptosis and oncosis of isolated pancreatic acinar cells were detected with Hoechst 33258 + PI or Annexin V + PI double fluorescent staining.
  • Tumor necorsis factor alpha (TNF-alpha) mRNA, myeloperoxidase, nuclear factor-kappaB and histological grading of pancreatic damage were measured.
  • RESULTS: There was an increased apoptosis but a decreased oncosis of pancreatic acinar cell after the treatment with As(2)O(3).
  • CONCLUSIONS: As(2)O(3) can induce apoptosis and reduce oncosis of pancreatic acinar cell, thus resulting in reduced release of endocellular enzyme of acinar cells, reduced inflammatory cell infiltration and decreased the production of inflammatory cytokines, so that the outcome of alleviated pathological changes was finally achieved.
  • [MeSH-minor] Amylases / metabolism. Animals. Flow Cytometry. In Situ Nick-End Labeling. Inflammation / drug therapy. Inflammation / genetics. Inflammation / metabolism. L-Lactate Dehydrogenase / metabolism. Male. NF-kappa B / metabolism. Peroxidase / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Rats, Wistar. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 17517186.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Arsenicals; 0 / NF-kappa B; 0 / Oxides; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 1.11.1.7 / Peroxidase; EC 3.2.1.- / Amylases; S7V92P67HO / arsenic trioxide
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19. Sabbagh C, Fuks D, Chatelain D, Flamant M, Delcenserie R, Yzet T, Regimbeau JM: [Acinar cell carcinoma of the pancreas: a rare tumor with particular clinical and paraclinical presentation]. Rev Med Interne; 2008 Dec;29(12):1046-9
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  • [Title] [Acinar cell carcinoma of the pancreas: a rare tumor with particular clinical and paraclinical presentation].
  • Acinar cell carcinoma of the pancreas is a rare tumour with specific clinical and paraclinical presentation.

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  • (PMID = 18433943.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin
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20. Yamaguchi R, Okabe Y, Jimi A, Shiota K, Kodama T, Naito Y, Yasunaga M, Kinoshita H, Kojiro M: Pancreatic acinar cell carcinoma extending into the common bile and main pancreatic ducts. Pathol Int; 2006 Oct;56(10):633-7
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  • [Title] Pancreatic acinar cell carcinoma extending into the common bile and main pancreatic ducts.
  • Acinar cell carcinoma (ACC) of the pancreas is relatively rare, accounting for only approximately 1% of all exocrine pancreatic tumors.
  • Magnetic resonance cholangiopancreatography showed defect of the lower common bile duct (CBD) due to obstruction by the tumor cast.
  • Histopathologically, the pancreatic head tumor invaded the main pancreatic duct (MPD) and CBD with extension into the CBD in a form of tumor cast.
  • The tumor cells consisted of a solid proliferation with abundant eosinophilic cytoplasm and round nuclei in an acinar and trabecular fashion.
  • Histopathologically, the tumor was encapsulated by fibrous capsule and had extensive central necrosis with solid areas in the tumor periphery, and invaded with extension into the MPD in a form of tumor cast.
  • The tumor cells resembled acinar cells in solid growths.
  • Two resected cases of ACC with unusual tumor extension into the CBD and the MPD, respectively, are reported.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Common Bile Duct / pathology. Common Bile Duct Neoplasms / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Humans. Male. Middle Aged. Neoplasm Invasiveness / pathology

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  • (PMID = 16984622.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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21. Patel M, Fine DR: Fibrogenesis in the pancreas after acinar cell injury. Scand J Surg; 2005;94(2):108-11
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  • [Title] Fibrogenesis in the pancreas after acinar cell injury.
  • It has now been well demonstrated that following injury to acinar cells, pancreatic stellate cell activation, migration and proliferation is the key mediator of this process.
  • The pancreatic stellate cell is likely to play an important role in maintaining the normal extracellular matrix; we speculate that the dysregulation of this process is an important factor in chronic pancreatitis.
  • [MeSH-minor] Apoptosis / physiology. Apoptosis Regulatory Proteins. Chronic Disease. Fibrosis. Humans. Membrane Glycoproteins / metabolism. Metalloproteases / physiology. Pancreatitis / physiopathology. TNF-Related Apoptosis-Inducing Ligand. Transforming Growth Factor beta / physiology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16111091.001).
  • [ISSN] 1457-4969
  • [Journal-full-title] Scandinavian journal of surgery : SJS : official organ for the Finnish Surgical Society and the Scandinavian Surgical Society
  • [ISO-abbreviation] Scand J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; EC 3.4.- / Metalloproteases
  • [Number-of-references] 22
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22. Gamal G, Nagashima T, Kawashima O, Sugano M, Sakurai S, Sano T, Nakajima T: Unique case of pulmonary bronchial gland type tumor with broad spectrum of cell differentiation from the terminal duct-acinar unit to excretory duct. Pathol Int; 2006 Apr;56(4):217-21
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  • [Title] Unique case of pulmonary bronchial gland type tumor with broad spectrum of cell differentiation from the terminal duct-acinar unit to excretory duct.
  • In the lung, acinic cell carcinoma (ACC) is a rare form of tumor.
  • Reported herein is a unique bronchial gland-type tumor diagnosed as well-differentiated ACC that developed in the B9 bronchus of the left lung.
  • Moreover, this tumor contained various sizes of mucous cysts lined by columnar mucous cells, which produced abundant mucin positive for Alcian blue, which is usually present in mucoepidermoid carcinoma.
  • Therefore, the present case is a unique tumor having a broad spectrum of cell differentiation from the terminal duct--acinar unit to the striated duct and excretory duct.
  • This is the first case of unique bronchial gland-type tumor with mixed histological features of ACC and mucoepidermoid carcinoma.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Carcinoma, Bronchogenic / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Cell Differentiation. Humans. Immunohistochemistry. Male. Middle Aged. Thoracoscopy

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  • (PMID = 16634968.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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23. Kolb-van Harten P, Rosien U, Klöppel G, Layer P: Pancreatic acinar cell carcinoma with excessive alpha-fetoprotein expression. Pancreatology; 2007;7(4):370-2
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  • [Title] Pancreatic acinar cell carcinoma with excessive alpha-fetoprotein expression.
  • We report a case of acinar cell carcinoma of the pancreas associated with excessively elevated levels of serum alpha-fetoprotein (>32,000 ng/ml).
  • This regimen was associated with clinical improvement and dramatic decreases in both tumor size and serum alpha-fetoprotein.
  • [MeSH-major] Carcinoma, Acinar Cell / metabolism. Pancreatic Neoplasms / metabolism. alpha-Fetoproteins / metabolism

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  • [Copyright] 2007 S. Karger AG, Basel and IAP
  • (PMID = 17703084.001).
  • [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
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / alpha-Fetoproteins; 0W860991D6 / Deoxycytidine; 50SG953SK6 / Mitomycin; B76N6SBZ8R / gemcitabine
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24. Vona-Davis LC, Frankenberry KA, Waheed U, Peterson E, McFadden DW: Expression of STAT3 and SOCS3 in pancreatic acinar cells. J Surg Res; 2005 Jul 1;127(1):14-20
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  • [Title] Expression of STAT3 and SOCS3 in pancreatic acinar cells.
  • Because activation of STAT3 and SOCS3 is also linked to cytokine stimulation, we tested TNFalpha and LPS, either alone or in combination with IL-1beta or IL-6 in an in vitro model using rat pancreatic acinar cells.
  • METHODS: Rat pancreatic acinar cells (AR42J) were treated with combinations of LPS (10 microg/ml) or TNFalpha (10, 100, or 200 ng/ml) in the presence or absence of IL-1beta or IL-6 for 15, 30, 45, 60, 180, or 360 min.
  • RESULTS: LPS and TNFalpha activated STAT3 and SOCS3 in pancreatic acinar cells.
  • [MeSH-major] DNA-Binding Proteins / genetics. Pancreas / physiology. Repressor Proteins / genetics. Trans-Activators / genetics. Transcription Factors / genetics. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Acute-Phase Proteins / genetics. Animals. Cell Line. Gene Expression Regulation / drug effects. Lipopolysaccharides / pharmacology. RNA / genetics. RNA / isolation & purification. Rats. Reverse Transcriptase Polymerase Chain Reaction. STAT3 Transcription Factor. Suppressor of Cytokine Signaling Proteins

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  • (PMID = 15893771.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acute-Phase Proteins; 0 / DNA-Binding Proteins; 0 / Lipopolysaccharides; 0 / Repressor Proteins; 0 / STAT3 Transcription Factor; 0 / Socs3 protein, rat; 0 / Stat3 protein, rat; 0 / Suppressor of Cytokine Signaling Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 63231-63-0 / RNA
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25. Ban D, Shimada K, Sekine S, Sakamoto Y, Kosuge T, Kanai Y, Hiraoka N: Pancreatic ducts as an important route of tumor extension for acinar cell carcinoma of the pancreas. Am J Surg Pathol; 2010 Jul;34(7):1025-36
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  • [Title] Pancreatic ducts as an important route of tumor extension for acinar cell carcinoma of the pancreas.
  • Acinar cell carcinoma (ACC) of the pancreas is very rare, which usually grows expansively.
  • We reviewed the detailed gross and histologic features of 13 cases of ACC, of which 7 (54%) showed intraductal polypoid growth (IPG) of the tumor in the large pancreatic ducts with a mean IPG length of 24.8 mm.
  • Comparison of the clinicopathologic characteristics showed that ACC with IPG had less infiltrative features including lymphatic, venous, and neural invasion, formation of tumor thrombus in the portal vein, nodal metastasis, and invasion beyond the pancreas to the surrounding organs; death in only 1 case (14%) of ACC with IPG was the result of ACC itself.
  • In contrast, ACC without IPG frequently showed more infiltrative growth, and was the cause of death in 50% of patients with this type of tumor.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Female. Humans. Japan / epidemiology. Male. Middle Aged. Neoplasm Invasiveness. Survival Rate

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  • (PMID = 20534994.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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26. Liang T, Liu TF, Xue DB, Sun B, Shi LJ: Different cell death modes of pancreatic acinar cells on macrophage activation in rats. Chin Med J (Engl); 2008 Oct 5;121(19):1920-4
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  • [Title] Different cell death modes of pancreatic acinar cells on macrophage activation in rats.
  • The aim of this study was to explore the relationship between modes of cell death in pancreatic acinar cells, the release of cell contents and the inflammatory response of macrophages.
  • CONCLUSION: There is a close relationship between modes of pancreatic acinar cell death, the release of cell contents and the inflammatory reaction of macrophages.
  • [MeSH-minor] Amylases / secretion. Animals. Interleukin-1beta / secretion. L-Lactate Dehydrogenase / secretion. Male. NF-kappa B / metabolism. Rats. Rats, Wistar. Tumor Necrosis Factor-alpha / secretion

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  • (PMID = 19080125.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Interleukin-1beta; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 3.2.1.- / Amylases
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27. Chiaravalli AM, Finzi G, Bertolini V, La Rosa S, Capella C: Colonic carcinoma with a pancreatic acinar cell differentiation. A case report. Virchows Arch; 2009 Dec;455(6):527-31
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  • [Title] Colonic carcinoma with a pancreatic acinar cell differentiation. A case report.
  • A case of a colonic carcinoma showing a pancreatic acinar cell differentiation is described for the first time.
  • A 65-year-old woman underwent surgical resection for an ulcerated protruding tumour of 4 x 2.5 cm in size on the anterior wall of the sigmoid colon.
  • Histologically, tumour cells were organized in acinar structures resembling pancreatic acini and in solid nests and ribbons or diffusely infiltrated as poorly cohesive cells.
  • The ultrastructural analysis of the primary tumour indicated the presence of zymogen-like granules in the cytoplasm of tumour cells.
  • Immunohistochemically, both acinar and diffuse patterns of growth showed an intense staining for trypsin, chymotrypsin and BCL10 and a weaker immunoreactivity for lipase and carboxyl ester hydrolase.
  • Most tumour cells were cytokeratin 20, CDX2 and p53 positive; whereas, mucin (MUC)2 immunoreactivity was observed only in the signet ring cells present in the diffuse pattern and chromogranin A in rare isolated tumour cells.
  • There was no evidence of a pancreatic acinar cell carcinoma or of heterotopic pancreatic tissue.
  • A colonic origin ought to be suspected when a metastatic carcinoma of unknown primary shows an acinar differentiation.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Colonic Neoplasms / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Cell Differentiation. Fatal Outcome. Female. Homeodomain Proteins / metabolism. Humans. Immunohistochemistry. Keratin-20 / metabolism. Lymphatic Metastasis. Tumor Suppressor Protein p53 / metabolism


28. 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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  • [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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29. Ramudo L, Manso MA, De Dios I: Biliary pancreatitis-associated ascitic fluid activates the production of tumor necrosis factor-alpha in acinar cells. Crit Care Med; 2005 Jan;33(1):143-8; discussion 248
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  • [Title] Biliary pancreatitis-associated ascitic fluid activates the production of tumor necrosis factor-alpha in acinar cells.
  • OBJECTIVE: Acute pancreatitis is associated with increased cytokine release from different cell sources.
  • We have investigated the ability of acinar cells, in comparison with inflammatory peripheral blood cells, to produce tumor necrosis factor (TNF)-alpha in response to pancreatitis-associated ascitic fluid (PAAF).
  • MEASUREMENTS AND MAIN RESULTS: PAAF (20%, v:v) obtained from rats with acute pancreatitis induced by bile-pancreatic duct obstruction significantly increased TNF-alpha production in acinar cells, as measured by flow cytometry using phycoerythrin-labeled monoclonal anti-TNF-alpha antiserum.
  • Neither heating of PAAF nor the addition of soybean trypsin inhibitor or neutralizing amounts of anti-TNF-alpha monoclonal antiserum reduced the acinar cell TNF-alpha production.
  • Likewise, the typical monocyte and lymphocyte stimulating factors-lipopolysaccharide (10 microg/microL) and phorbol 12-myristate 13-acetate (250 ng/mL) plus ionomycin (1 microg/mL), respectively-were not able to produce TNF-alpha in acinar cells.
  • By comparison of the two acinar cell populations differentiated by flow cytometry, R2 cells (with higher forward scatter values) showed a greater ability to produce TNF-alpha in response to PAAF than R1 cells.
  • Acinar cell nuclear factor-kappaB was activated, but TNF-alpha production was not totally inhibited in presence of N-acetyl cysteine (30, 100 mM).
  • CONCLUSIONS: The production of TNF-alpha from different cell sources is selectively activated.
  • PAAF may be involved in the pathophysiology of acute pancreatitis by TNF-alpha production in acinar cells through mechanisms partially mediated by nuclear factor-kappaB activation.
  • PAAF components, such as TNF-alpha or trypsin, are not responsible for acinar cell activation.
  • TNF-alpha was induced by heat-resistant PAAF factors, displaying acinar cells with higher forward scatter (R2) a greater ability to increase the TNF-alpha production than R1 cells.
  • [MeSH-major] Ascitic Fluid / immunology. Cholestasis, Extrahepatic / immunology. Pancreas, Exocrine / immunology. Tumor Necrosis Factor-alpha / metabolism

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  • [CommentIn] Crit Care Med. 2005 Jan;33(1):248 [15644687.001]
  • (PMID = 15644661.001).
  • [ISSN] 0090-3493
  • [Journal-full-title] Critical care medicine
  • [ISO-abbreviation] Crit. Care Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha
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30. Kuroda N, Katto K, Tamura M, Shiotsu T, Nakamura S, Ohtsuki Y, Hes O, Michal M, Inoue K, Ohara M, Mizuno K, Lee GH: Immunohistochemical application of D2-40 as basal cell marker in evaluating atypical small acinar proliferation of initial routine prostatic needle biopsy materials. Med Mol Morphol; 2010 Sep;43(3):165-9
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  • [Title] Immunohistochemical application of D2-40 as basal cell marker in evaluating atypical small acinar proliferation of initial routine prostatic needle biopsy materials.
  • D2-40 has been recently discovered as a lymphatic endothelial cell marker, and some investigators have found that D2-40 is also expressed in myoepithelial cells of salivary gland or breast.
  • In this study, we evaluated D2-40 expression of basal cells and applied D2-40 immunohistochemistry in the combination of P504S, cytokeratin 5, and p63 for ten lesions with atypical small acinar proliferation (ASAP) in initial prostatic needle biopsy.
  • D2-40 was comparable to cytokeratin 5 and p63 as a basal cell marker, and there were no lesions that failed to provide an accurate final diagnosis using only D2-40 immunohistochemistry without cytokeratin 5 or p63.
  • [MeSH-major] Antibodies, Monoclonal / analysis. Biomarkers, Tumor / analysis. Carcinoma, Acinar Cell / diagnosis. Prostatic Neoplasms / diagnosis

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  • (PMID = 20857265.001).
  • [ISSN] 1860-1499
  • [Journal-full-title] Medical molecular morphology
  • [ISO-abbreviation] Med Mol Morphol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Keratin-5; 0 / Membrane Proteins; 0 / monoclonal antibody D2-40; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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31. de Dios I, Ramudo L, García-Montero AC, Manso MA: Redox-sensitive modulation of CD45 expression in pancreatic acinar cells during acute pancreatitis. J Pathol; 2006 Oct;210(2):234-9
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  • [Title] Redox-sensitive modulation of CD45 expression in pancreatic acinar cells during acute pancreatitis.
  • CD45, a transmembrane protein tyrosine phosphatase required for signal transduction in leukocytes, has recently been found in pancreatic acinar cells.
  • We have investigated the relationship between kinetic expression of CD45 on acinar cells during acute pancreatitis (AP) and the ability of these cells to produce tumour necrosis factor-alpha (TNF-alpha) through mechanisms sensitive to the cellular redox state.
  • Flow cytometric analysis showed a significant decrease in the constitutive expression of CD45 in acinar cells from six hours onwards after inducing AP by bile-pancreatic duct obstruction (BPDO) in parallel with a significant increase in acinar TNF-alpha production.
  • Changes in protein expression on the acinar cell surface preceded CD45 mRNA down-regulation, which was not found until 12 hours after BPDO.
  • N-Acetylcysteine treatment delayed and reduced the down-regulation of CD45 expression induced by AP and prevented acinar cells from producing TNF-alpha.
  • Our results show that CD45 expression is down-regulated in acinar cells during acute pancreatitis by redox-sensitive mechanisms, and they support the notion that CD45 negatively controls the production of cytokines in pancreatic acinar cells.
  • [MeSH-minor] Acute Disease. Animals. Cells, Cultured. Down-Regulation. Flow Cytometry / methods. Gene Expression. Humans. Male. Oxidation-Reduction. RNA, Messenger / genetics. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 16886168.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 3.1.3.48 / Antigens, CD45
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32. 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.
  • 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.
  • [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

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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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33. Azuma M, Ashida Y, Tamatani T, Motegi K, Takamaru N, Ishimaru N, Hayashi Y, Sato M: Cepharanthin, a biscoclaurine alkaloid, prevents destruction of acinar tissues in murine Sjögren's syndrome. J Rheumatol; 2006 May;33(5):912-20
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  • [Title] Cepharanthin, a biscoclaurine alkaloid, prevents destruction of acinar tissues in murine Sjögren's syndrome.
  • OBJECTIVE: Our previous study suggested that suppression by cepharanthin of tumor necrosis factor-a (TNF-a)-induced matrix metalloproteinase-9 (MMP-9) could prevent destruction of the acinar structure in the salivary glands of patients with Sjögren's syndrome (SS).
  • In this study, we observed that in vivo administration of cepharanthin prevented severe damage to acinar tissues in the murine model of human SS.
  • The apoptotic cell death of acinar cells was determined.
  • RESULTS: Although extensive mononuclear cell infiltration and destruction of acinar tissue in salivary and lacrimal glands were observed in control mice, significant improvement of these lesions was evident in mice treated with cepharanthin.
  • Immunohistochemical analysis revealed that p65, phosphorylated IkB-a, and MMP-9 were more strongly stained in the acinar cells of control mice than in cepharanthin-treated mice.
  • Although no staining for type IV collagen was observed in the acinar tissues of control mice, continuity of staining for type IV collagen was observed in acinar tissues of cepharanthin-treated mice.
  • Destruction of acinar tissues was attributed to the induction of apoptosis, suggesting that cepharanthin inhibits apoptosis by suppressing phosphorylation of IkB-a, followed by prevention of MMP-9 activation.
  • CONCLUSION: Our findings suggest that cepharanthin may be a promising agent for use in preventing destruction of acinar tissues in murine SS.
  • [MeSH-minor] Animals. Apoptosis. Benzylisoquinolines. Carrier Proteins / analysis. Collagen Type IV / analysis. Female. I-kappa B Proteins / analysis. Immunohistochemistry. Matrix Metalloproteinase 9 / analysis. Mice. Mice, Mutant Strains. Neoplasm Proteins / analysis. Transcription Factor RelA

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  • (PMID = 16652422.001).
  • [ISSN] 0315-162X
  • [Journal-full-title] The Journal of rheumatology
  • [ISO-abbreviation] J. Rheumatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Benzylisoquinolines; 0 / Carrier Proteins; 0 / Collagen Type IV; 0 / I-kappa B Proteins; 0 / Neoplasm Proteins; 0 / Rela protein, mouse; 0 / Transcription Factor RelA; 139874-52-5 / NF-kappaB inhibitor alpha; 7592YJ0J6T / cepharanthine; EC 3.4.24.35 / Matrix Metalloproteinase 9
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34. Sanchez D, Mueller CM, Zenilman ME: Pancreatic regenerating gene I and acinar cell differentiation: influence on cellular lineage. Pancreas; 2009 Jul;38(5):572-7
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  • [Title] Pancreatic regenerating gene I and acinar cell differentiation: influence on cellular lineage.
  • Acinar cells can transdifferentiate into other pancreatic-derived cells, and we postulated that changes in intracellular levels of reg I would affect the state of differentiation.
  • CONCLUSIONS: These data demonstrate that in acinar cells, reg I overexpression is linked to acinar cell differentiation, whereas inhibition of reg I leads to beta cell and possibly ductal phenotype.
  • Reg I expression in acinar cells is important in maintaining pancreatic cell lineage, and when decreased, cells can dedifferentiate and move toward becoming other pancreatic cells.

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  • (PMID = 19557902.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK054511; United States / NIDDK NIH HHS / DK / DK054511-03; United States / NIDDK NIH HHS / DK / R01 DK054511-04; United States / NIDDK NIH HHS / DK / DK054511-04; United States / NIDDK NIH HHS / DK / R01 DK054511-03; United States / NIDDK NIH HHS / DK / Z01 DK054511
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Homeodomain Proteins; 0 / Insulin; 0 / Lithostathine; 0 / RNA, Messenger; 0 / Reg1 protein, rat; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein; EC 3.2.1.- / Amylases
  • [Other-IDs] NLM/ NIHMS100566; NLM/ PMC2702698
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35. Khalili M, Wax BN, Reed WP, Schuss A, Drexler S, Weston SR, Katz DS: Radiology-pathology conference. Acinar cell carcinoma of the pancreas. Clin Imaging; 2006 Sep-Oct;30(5):343-6
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  • [Title] Radiology-pathology conference. Acinar cell carcinoma of the pancreas.
  • Acinar cell carcinoma (ACC) is a rare tumor that constitutes 1% of pancreatic neoplasms.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Intestinal Obstruction / diagnosis. Pancreatic Neoplasms / diagnosis. Retroperitoneal Neoplasms / diagnosis

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  • (PMID = 16919557.001).
  • [ISSN] 0899-7071
  • [Journal-full-title] Clinical imaging
  • [ISO-abbreviation] Clin Imaging
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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36. Tapia B, Ahrens W, Kenney B, Touloukian R, Reyes-Múgica M: Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature. Pediatr Dev Pathol; 2008 Sep-Oct;11(5):384-90
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  • [Title] Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature.
  • Primary epithelial tumors of the pancreas are extremely uncommon in children, and among these, acinar cell carcinoma (ACC) is the most rare.
  • We also provide a comparison with an example of solid pseudopapillary tumor, another relatively infrequent epithelial tumor of the pancreas in the young.
  • We review the relevant literature addressing the clinical and pathologic features of ACC and its distinction from other pancreatic neoplasms.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / pathology. Pancreatic Cyst / pathology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / pathology

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  • (PMID = 19006424.001).
  • [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] Case Reports; Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SERPINA1 protein, human; 0 / alpha 1-Antitrypsin
  • [Number-of-references] 37
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37. Roldo C, Missiaglia E, Hagan JP, Falconi M, Capelli P, Bersani S, Calin GA, Volinia S, Liu CG, Scarpa A, Croce CM: MicroRNA expression abnormalities in pancreatic endocrine and acinar tumors are associated with distinctive pathologic features and clinical behavior. J Clin Oncol; 2006 Oct 10;24(29):4677-84
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  • [Title] MicroRNA expression abnormalities in pancreatic endocrine and acinar tumors are associated with distinctive pathologic features and clinical behavior.
  • PURPOSE: We investigated the global microRNA expression patterns in normal pancreas, pancreatic endocrine tumors and acinar carcinomas to evaluate their involvement in transformation and malignant progression of these tumor types.
  • Recent evidence indicates that microRNAs can contribute to tumor development and progression and may have diagnostic and prognostic value in several human malignancies.
  • MATERIALS AND METHODS: Using a custom microarray, we studied the global microRNA expression in 12 nontumor pancreas and 44 pancreatic primary tumors, including 12 insulinomas, 28 nonfunctioning endocrine tumors, and four acinar carcinomas.
  • RESULTS: Our data showed that a common pattern of microRNA expression distinguishes any tumor type from normal pancreas, suggesting that this set of microRNAs might be involved in pancreatic tumorigenesis; the expression of miR-103 and miR-107, associated with lack of expression of miR-155, discriminates tumors from normal; a set of 10 microRNAs distinguishes endocrine from acinar tumors and is possibly associated with either normal endocrine differentiation or endocrine tumorigenesis; miR-204 is primarily expressed in insulinomas and correlates with immunohistochemical expression of insulin; and the overexpression of miR-21 is strongly associated with both a high Ki67 proliferation index and presence of liver metastasis.
  • CONCLUSION: These results suggest that alteration in microRNA expression is related to endocrine and acinar neoplastic transformation and progression of malignancy, and might prove useful in distinguishing tumors with different clinical behavior.
  • [MeSH-major] Carcinoma, Acinar Cell / genetics. Carcinoma, Acinar Cell / pathology. Insulinoma / genetics. Insulinoma / pathology. MicroRNAs / metabolism. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Transformation, Neoplastic. Gene Expression Profiling. Humans. Liver Neoplasms / secondary. Pancreas / metabolism. Prognosis. Survival

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  • (PMID = 16966691.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA76259; United States / NCI NIH HHS / CA / P01CA81534
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
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38. Suzuki A, Sakaguchi T, Morita Y, Oishi K, Fukumoto K, Inaba K, Takehara Y, Baba S, Suzuki S, Konno H: Long-term survival after a repetitive surgical approach in a patient with acinar cell carcinoma of the pancreas and recurrent liver metastases: report of a case. Surg Today; 2010 Jul;40(7):679-83
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  • [Title] Long-term survival after a repetitive surgical approach in a patient with acinar cell carcinoma of the pancreas and recurrent liver metastases: report of a case.
  • Acinar cell carcinoma is a relatively rare malignant neoplasm, which represents 1%-2% of all pancreatic exocrine tumors.
  • This report concerns a case of a long-term survivor of metastatic acinar cell carcinoma who was successfully treated with repetitive surgery.
  • A 62-year-old man underwent a distal pancreatectomy for a pancreatic tumor, which was histologically diagnosed as an acinar cell carcinoma.
  • The tumor recurred in the liver three times within 41 months.
  • Although no consensus has been reached on surgery for metastatic acinar cell carcinoma, the current case has important implications for establishing an appropriate treatment strategy.
  • [MeSH-major] Carcinoma, Acinar Cell / surgery. Hepatectomy. Liver Neoplasms / surgery. Neoplasm Recurrence, Local / surgery. Pancreatectomy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Humans. Male. Middle Aged. Neoplasm Metastasis. Reoperation. Survivors

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  • (PMID = 20582524.001).
  • [ISSN] 1436-2813
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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39. Kereszturi E, Sahin-Tóth M: Intracellular autoactivation of human cationic trypsinogen mutants causes reduced trypsinogen secretion and acinar cell death. J Biol Chem; 2009 Nov 27;284(48):33392-9
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  • [Title] Intracellular autoactivation of human cationic trypsinogen mutants causes reduced trypsinogen secretion and acinar cell death.
  • In the present study, we characterized the cell biological effects of these mutants using human embryonic kidney 293T and AR42J rat acinar cells.
  • Acinar cells expressing the p.D22G mutant detached from the culture plate over time, became terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive, and exhibited elevated levels of the proapoptotic transcription factor CHOP.
  • The observations indicate that activation peptide mutants of human cationic trypsinogen undergo autoactivation intracellularly, which leads to decreased trypsinogen secretion and eventual acinar cell death.

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  • (PMID = 19801634.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK058088; United States / NIDDK NIH HHS / DK / DK058088; United States / NIDDK NIH HHS / DK / R01 DK058088-08; United States / NIDDK NIH HHS / DK / R01 DK058088-07; United States / NIDDK NIH HHS / DK / R01 DK058088-09; United States / NIDDK NIH HHS / DK / DK058088-07; United States / NIDDK NIH HHS / DK / DK058088-04; United States / NIDDK NIH HHS / DK / R01 DK058088-03; United States / NIDDK NIH HHS / DK / DK058088-08; United States / NIDDK NIH HHS / DK / R01 DK058088-04; United States / NIDDK NIH HHS / DK / DK058088-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DDIT3 protein, human; 147336-12-7 / Transcription Factor CHOP; EC 3.4.21.4 / PRSS1 protein, human; EC 3.4.21.4 / Trypsin; EC 3.4.22.1 / Cathepsin B
  • [Other-IDs] NLM/ PMC2785183
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40. Robinson K, Vona-Davis L, Riggs D, Jackson B, McFadden D: Peptide YY attenuates STAT1 and STAT3 activation induced by TNF-alpha in acinar cell line AR42J. J Am Coll Surg; 2006 May;202(5):788-96
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  • [Title] Peptide YY attenuates STAT1 and STAT3 activation induced by TNF-alpha in acinar cell line AR42J.
  • We hypothesized that tumor necrosis factor (TNF)-alpha would induce STAT1 and STAT3, and PYY would attenuate their transcription factor binding.
  • STUDY DESIGN: Rat pancreatic acinar cells were treated with recombinant TNF-alpha (200 ng/mL); PYY (3-36; 500 pM) was added 30 minutes post-TNF-alpha treatment.
  • CONCLUSIONS: In pancreatic acinar cells, TNF-alpha activated STAT1 and STAT3, known mediators of inflammatory cytokines.
  • [MeSH-major] Pancreas / cytology. Peptide YY / pharmacology. STAT1 Transcription Factor / drug effects. STAT3 Transcription Factor / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Amylases / metabolism. Animals. Cell Line. Cytokines / metabolism. Enzyme-Linked Immunosorbent Assay. In Vitro Techniques. Rats. STAT4 Transcription Factor / drug effects. STAT4 Transcription Factor / metabolism. STAT5 Transcription Factor / drug effects. STAT5 Transcription Factor / metabolism. STAT6 Transcription Factor / drug effects. STAT6 Transcription Factor / metabolism. Signal Transduction

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  • (PMID = 16648019.001).
  • [ISSN] 1072-7515
  • [Journal-full-title] Journal of the American College of Surgeons
  • [ISO-abbreviation] J. Am. Coll. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / STAT1 Transcription Factor; 0 / STAT3 Transcription Factor; 0 / STAT4 Transcription Factor; 0 / STAT5 Transcription Factor; 0 / STAT6 Transcription Factor; 0 / Stat1 protein, rat; 0 / Stat3 protein, rat; 0 / Tumor Necrosis Factor-alpha; 106388-42-5 / Peptide YY; EC 3.2.1.- / Amylases
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41. 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.
  • MRI-imaging showed a tumor within the head of the pancreas concomitant with Serum-Lipase and CA19-9.
  • Endosonographic fine needle biopsy confirmed an acinar cell carcinoma.
  • Laparotomy presented an locally advanced tumor with venous infiltration that was consequently deemed unresectable.
  • 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.
  • [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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42. Igarashi H, Shinozaki S, Mukada T: A case of acinar cell carcinoma of the pancreas that formed extensive tumor thrombus of the portal vein. Clin J Gastroenterol; 2009 Apr;2(2):96-102
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  • [Title] A case of acinar cell carcinoma of the pancreas that formed extensive tumor thrombus of the portal vein.
  • Furthermore, tumor thrombus continuously involved the splenic and proximal superior mesenteric vein, main portal vein, and its right intrahepatic branch.
  • The specimens obtained from portal tumor thrombus were histologically compatible with acinar cell carcinoma.
  • Portal tumor thrombus is a rare condition in pancreatic tumors; however, it seems to be important to differentiate tumor thrombus from blood thrombus of the portal vein in order to know the true clinical stage and provide a suitable treatment.

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  • (PMID = 26192173.001).
  • [ISSN] 1865-7257
  • [Journal-full-title] Clinical journal of gastroenterology
  • [ISO-abbreviation] Clin J Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Keywords] NOTNLM ; Acinar cell carcinoma / Pancreas / Portal vein / Tumor thrombus
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43. Yu JH, Seo JY, Kim KH, Kim H: Differentially expressed proteins in cerulein-stimulated pancreatic acinar cells: implication for acute pancreatitis. Int J Biochem Cell Biol; 2008;40(3):503-16
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  • [Title] Differentially expressed proteins in cerulein-stimulated pancreatic acinar cells: implication for acute pancreatitis.
  • The proteins expressed in pancreatic acinar cells during the initiation of acute pancreatitis may determine the severity of the disease.
  • Present study aims to determine the differentially expressed proteins in cerulein-stimulated pancreatic acinar cells as an in vitro model for acute pancreatitis.
  • Rat pancreatic acinar AR42J cells were treated with 10(-8)M cerulein for 12h.
  • As a result, 10 proteins (Orp150 protein, protein disulfide isomerase related protein, dnaK-type molecular chaperone hsp72-ps1, mitochondrial glutamate dehydrogenase, similar to chaperonin containing TCP-1 beta subunit, RuvB-like protein 1, heterogeneous nuclear ribonucleoprotein H1, aldehyde reductase 1, triosephosphate isomerase 1, peroxiredoxin 2) were up-regulated while four proteins (vasolin-containing protein, 78 kDa glucose-regulated protein precursor, heat shock protein 8, adenosylhomocysteinase) were down-regulated by cerulein in pancreatic acinar AR42J cells.
  • These proteins are related to chaperone, cell defense mechanism against oxidative stress or DNA damage, anti-apoptosis and energy generation.
  • The differentially expressed proteins by ceruein share their functional roles in pancreatic acinar cells, suggesting the possible involvement of oxidative stress, DNA damage, and anti-apoptosis in pathogenesis of acute pancreatitis.
  • Proteins involved in cellular defense mechanism and energy production may protect pancreatic acinar cells during the development of pancreatitis.
  • [MeSH-minor] Acute Disease. Animals. Cell Line, Tumor. Ceruletide. Disease Models, Animal. Down-Regulation. Electrophoresis, Gel, Two-Dimensional. Protein Array Analysis. Rats. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Up-Regulation


44. De La O JP, Emerson LL, Goodman JL, Froebe SC, Illum BE, Curtis AB, Murtaugh LC: Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia. Proc Natl Acad Sci U S A; 2008 Dec 2;105(48):18907-12
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  • [Title] Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia.
  • Efforts to model pancreatic cancer in mice have focused on mimicking genetic changes found in the human disease, particularly the activating KRAS mutations that occur in pancreatic tumors and their putative precursors, pancreatic intraepithelial neoplasia (PanIN).
  • The basis for this selective response is unknown, and it is similarly unknown what cell types in the mature pancreas actually contribute to PanINs.
  • We hypothesize that Notch, which inhibits differentiation in the embryonic pancreas, contributes to PanIN formation by abrogating the normal differentiation program of tumor-initiating cells.
  • Furthermore, we find that Kras activation in mature acinar cells induces PanIN lesions identical to those seen upon ubiquitous Kras activation, and that Notch promotes both initiation and dysplastic progression of these acinar-derived PanINs, albeit short of invasive adenocarcinoma.
  • At the cellular level, Notch/Kras coactivation promotes rapid reprogramming of acinar cells to a duct-like phenotype, providing an explanation for how a characteristically ductal tumor can arise from nonductal acinar cells.

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  • (PMID = 19028876.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21-CA123066; United States / NCI NIH HHS / CA / P30-CA042014; United States / NICHD NIH HHS / HD / 5T32-HD07491; United States / NCI NIH HHS / CA / CA123066-02; United States / NCI NIH HHS / CA / R21 CA123066; United States / NCI NIH HHS / CA / R21 CA123066-02; United States / NICHD NIH HHS / HD / T32 HD007491; United States / NCI NIH HHS / CA / P30 CA042014
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Notch; 094ZI81Y45 / Tamoxifen; EC 3.6.5.2 / ras Proteins
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45. 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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  • [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.
  • 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%.
  • [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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46. Sphyris N, Harrison DJ: p53 deficiency exacerbates pleiotropic mitotic defects, changes in nuclearity and polyploidy in transdifferentiating pancreatic acinar cells. Oncogene; 2005 Mar 24;24(13):2184-94
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  • [Title] p53 deficiency exacerbates pleiotropic mitotic defects, changes in nuclearity and polyploidy in transdifferentiating pancreatic acinar cells.
  • In a primary culture model for pancreatic acinar-ductal transdifferentiation, cells exhibited increased proliferation, changes in nuclearity and polyploidy.
  • We identify the 'nucleus to centrosome' ratio of the progenitor cell, the dissemination of centrosomes at spindle poles and cytokinesis failure as critical determinants of mitosis outcome and centrosome inheritance.
  • Abortive cytokinesis of mononuclear cells contributes to the binuclear cell pool, whereas enclosure of entire mitotic formations, within a single nuclear envelope, perpetuates polyploidization.
  • Binuclear cell nuclei combine their genomes on a single metaphase plate, doubling descendant ploidy.
  • We detected constitutively nuclear mdm2, which may circumvent endogenous cell-cycle checkpoints, and pronounced accumulation of p21 and p27 in multinuclear cells and giant nuclei, consistent with roles in polyploidization.
  • [MeSH-major] Pancreas / cytology. Tumor Suppressor Protein p53 / deficiency. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Animals. Cell Differentiation. Cell Nucleus / physiology. Cell Nucleus / ultrastructure. Centrosome / physiology. Gene Amplification. Genome. Mice. Mice, Knockout. Ploidies. Polyploidy

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  • (PMID = 15735758.001).
  • [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 / Tumor Suppressor Protein p53
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47. Zhang N, Lyons S, Lim E, Lassota P: A spontaneous acinar cell carcinoma model for monitoring progression of pancreatic lesions and response to treatment through noninvasive bioluminescence imaging. Clin Cancer Res; 2009 Aug 1;15(15):4915-24
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  • [Title] A spontaneous acinar cell carcinoma model for monitoring progression of pancreatic lesions and response to treatment through noninvasive bioluminescence imaging.
  • PURPOSE: We have generated an EL1-luc/TAg transgenic mouse model that develops spontaneous and bioluminescent acinar cell carcinomas.
  • We applied this model to noninvasively monitor tumor development and drug response.
  • Tumor development was monitored through bioluminescence imaging and necropsy at the study end point.
  • RESULTS: EL1-luc/TAg transgenic mice showed pancreas-specific bioluminescence signal before tumor progression and produced increasing light emission from the onset of the pancreatic acinar cell carcinomas.
  • The latency of tumor development ranged from 10 to >20 weeks of age in these mice.
  • Progression of the primary acinar cell carcinoma was accompanied by emergence of metastatic lesions in the abdominal organs, including liver and gastrointestinal fat tissues.
  • Rapamycin treatment suppressed tumor development.
  • CONCLUSIONS: The EL1-luc/TAg mouse provides a noninvasive approach for monitoring spontaneous acinar cell carcinoma development and comprises a convenient tool for the evaluation of novel therapeutics against pancreatic cancers.
  • Tumor growth suppression through inhibition of the mammalian target of rapamycin pathway further validates this model as clinically relevant.
  • [MeSH-major] Antibiotics, Antineoplastic / metabolism. Carcinoma, Acinar Cell / metabolism. Drug Monitoring. Pancreas / pathology. Pancreatic Neoplasms / pathology


48. Takanami K, Abe K, Mitamura A, Miyazaki S, Abe K, Ishida K, Yamada S, Takahashi S: Two cases of 18 F-FDG PET/CT findings in acinar cell carcinoma of the pancreas. Clin Nucl Med; 2009 Apr;34(4):209-12
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  • [Title] Two cases of 18 F-FDG PET/CT findings in acinar cell carcinoma of the pancreas.
  • They underwent F-18 FDG PET/CT and subsequently a pancreaticoduodenectomy and acinar cell carcinoma in the pancreas was proven histopathologically.
  • In one case, the tumor consisted of a solid component presenting intense FDG uptake and necrotic tissue.
  • In another case, the tumor consisted of cystic and papillary components presenting with weak FDG uptake.
  • This report thus documents 2 cases of acinar cell carcinoma that showed contrasting histopathologic and F-18 FDG PET/CT findings.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / radionuclide imaging. Fluorodeoxyglucose F18 / pharmacology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / radionuclide imaging. Positron-Emission Tomography / methods. Tomography, X-Ray Computed / methods

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  • (PMID = 19300048.001).
  • [ISSN] 1536-0229
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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49. Basturk O, Zamboni G, Klimstra DS, Capelli P, Andea A, Kamel NS, Adsay NV: Intraductal and papillary variants of acinar cell carcinomas: a new addition to the challenging differential diagnosis of intraductal neoplasms. Am J Surg Pathol; 2007 Mar;31(3):363-70
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  • [Title] Intraductal and papillary variants of acinar cell carcinomas: a new addition to the challenging differential diagnosis of intraductal neoplasms.
  • The recognition and differential diagnosis of pancreatic intraductal neoplasms (IN) have gained importance in the past few years, as the incidence of these tumors (especially intraductal papillary mucinous neoplasms-IPMNs) have risen to >10% of pancreatic resections, and their significance as precursors of invasive cancer is better appreciated.
  • Acinar cell carcinomas (ACCs) are typically solid tumors; however, we have recently encountered 7 ACCs with either intraductal growth and/or a papillary/papillocystic pattern that could be mistaken for IN.
  • Four patients were male and 3 female, with a mean age of 59 and mean tumor size of 4.9 cm (as compared with 10 cm in conventional ACCs).
  • In 5 cases, the tumors had nodular growth of sheet-forming acinar cells, some of which were within ducts, as evidenced by the polypoid nature of the process, partial ductal lining, and presence of small tributary ducts in the walls.
  • In 3 cases, the tumor had papillary and/or papillocystic growth, at least focally.
  • In such cases, attention to morphologic details described above, and immunohistochemistry are helpful.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Papillary / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Periodic Acid-Schiff Reaction. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 17325477.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50-CA62924
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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50. 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.
  • Acinar cell carcinoma of the pancreas is a rare and highly malignant tumor, and there are few reports regarding treatment with chemotherapy.
  • [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

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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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51. Comper F, Antonello D, Beghelli S, Gobbo S, Montagna L, Pederzoli P, Chilosi M, Scarpa A: Expression pattern of claudins 5 and 7 distinguishes solid-pseudopapillary from pancreatoblastoma, acinar cell and endocrine tumors of the pancreas. Am J Surg Pathol; 2009 May;33(5):768-74
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  • [Title] Expression pattern of claudins 5 and 7 distinguishes solid-pseudopapillary from pancreatoblastoma, acinar cell and endocrine tumors of the pancreas.
  • Solid-pseudopapillary tumor (SPT) of the pancreas is characterized by a discohesive appearance of the neoplastic cells.
  • This latter includes pancreatic endocrine tumor (PET) as SPT may show neuroendocrine differentiation, and pancreatic acinar cell carcinoma (ACC) and pancreatoblastoma (PB) that may often show nuclear beta-catenin staining.
  • However, the role of additional cell-cell adhesion systems remains to be elucidated in SPT, particularly that of claudins that are essential components of tight junctions showing modulated expression in diverse tumor types.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Acinar Cell / chemistry. Membrane Proteins / analysis. Pancreas / chemistry. Pancreatic Neoplasms / chemistry. Tight Junctions / chemistry

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  • (PMID = 19194274.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDH1 protein, human; 0 / CLDN5 protein, human; 0 / CLDN7 protein, human; 0 / CTNNB1 protein, human; 0 / Cadherins; 0 / Claudin-5; 0 / Claudins; 0 / Membrane Proteins; 0 / beta Catenin
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52. Yuan J, Lugea A, Zheng L, Gukovsky I, Edderkaoui M, Rozengurt E, Pandol SJ: Protein kinase D1 mediates NF-kappaB activation induced by cholecystokinin and cholinergic signaling in pancreatic acinar cells. Am J Physiol Gastrointest Liver Physiol; 2008 Dec;295(6):G1190-201
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  • [Title] Protein kinase D1 mediates NF-kappaB activation induced by cholecystokinin and cholinergic signaling in pancreatic acinar cells.
  • The transcription factor NF-kappaB plays a critical role in inflammatory and cell death responses during acute pancreatitis.
  • Previous studies in our laboratory demonstrated that protein kinase C (PKC) isoforms PKCdelta and epsilon are key regulators of NF-kappaB activation induced by cholecystokinin-8 (CCK-8), tumor necrosis factor-alpha, and ethanol.
  • Here, we demonstrate that protein kinase D1 (PKD1) is a key downstream target of PKCdelta and PKCepsilon in pancreatic acinar cells stimulated by two major secretagogues, CCK-8 and the cholinergic agonist carbachol (CCh), and that PKD1 is necessary for NF-kappaB activation induced by CCK-8 and CCh.
  • Both CCK-8 and CCh dose dependently induced a rapid and striking activation of PKD1 in rat pancreatic acinar cells, as measured by in vitro kinase assay and by phosphorylation at PKD1 activation loop (Ser744/748) or autophosphorylation site (Ser916).
  • Either inhibition of PKCdelta or epsilon by isoform-specific inhibitory peptides, genetic deletion of PKCdelta and epsilon in pancreatic acinar cells, or knockdown of PKD1 by using small interfering RNAs in AR42J cells resulted in a marked decrease in PKD1 and NF-kappaB activation stimulated by CCK-8 or CCh.

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  • (PMID = 18845574.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK 55003; United States / NIAAA NIH HHS / AA / P50 AA11999
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cholinergic Agonists; 0 / NF-kappa B; 888Y08971B / Ceruletide; 8Y164V895Y / Carbachol; 9011-97-6 / Cholecystokinin; EC 2.7.- / Protein Kinases; EC 2.7.10.- / protein kinase D; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C-delta; EC 2.7.11.13 / Protein Kinase C-epsilon
  • [Other-IDs] NLM/ PMC2604803
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53. Bennett HL, Brummer T, Jeanes A, Yap AS, Daly RJ: Gab2 and Src co-operate in human mammary epithelial cells to promote growth factor independence and disruption of acinar morphogenesis. Oncogene; 2008 Apr 24;27(19):2693-704
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  • [Title] Gab2 and Src co-operate in human mammary epithelial cells to promote growth factor independence and disruption of acinar morphogenesis.
  • Since Gab2 is phosphorylated by c-Src, and both proteins are overexpressed in breast cancers, we have determined the biological consequences of their co-expression in the immortalized human mammary epithelial cell line MCF-10A.
  • While overexpression of c-Src did not affect acinar morphogenesis or growth factor dependence in three-dimensional culture, c-Src co-operated with Gab2 to promote epidermal growth factor (EGF)-independent acinar growth.
  • Gab2 associated with E-cadherin in the presence and absence of v-Src, indicating that the ability of Gab2 to weaken the strength of cell-cell contacts may reflect enhanced activation of PI3-kinase at adherens junctions.
  • [MeSH-minor] Cell Line, Transformed. Cell Line, Tumor. Cell Polarity / genetics. Cell Polarity / physiology. Humans. src-Family Kinases

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  • (PMID = 17998934.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [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] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / GAB2 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / src-Family Kinases
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54. Du YC, Klimstra DS, Varmus H: Activation of PyMT in beta cells induces irreversible hyperplasia, but oncogene-dependent acinar cell carcinomas when activated in pancreatic progenitors. PLoS One; 2009 Sep 07;4(9):e6932
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  • [Title] Activation of PyMT in beta cells induces irreversible hyperplasia, but oncogene-dependent acinar cell carcinomas when activated in pancreatic progenitors.
  • It is unclear whether the cellular origin of various forms of pancreatic cancer involves transformation or transdifferentiation of different target cells or whether tumors arise from common precursors, with tumor types determined by the specific genetic alterations.
  • To ask whether PyMT transforms and transdifferentiates endocrine cells toward exocrine tumor phenotypes, we generated transgenic mice that carry tetracycline-inducible PyMT and a linked luciferase reporter.
  • Induction of PyMT in beta cells causes beta-cell hyperplastic lesions that do not progress to malignant neoplasms.
  • When PyMT is de-induced, beta cell proliferation and growth cease; however, regression does not occur, suggesting that continued production of PyMT is not required to maintain the viable expanded beta cell population.
  • In contrast, induction of PyMT in early pancreatic progenitor cells under the control of Pdx1 produces acinar cell carcinomas and beta-cell hyperplasia.
  • The survival of acinar tumor cells is dependent on continued expression of PyMT.
  • Our findings indicate that PyMT can induce exocrine tumors from pancreatic progenitor cells, but cells in the beta cell lineage are not transdifferentiated toward exocrine cell types by PyMT; instead, they undergo oncogene-dependent hyperplastic growth, but do not require PyMT for survival.

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  • (PMID = 19812721.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA105492; United States / NCI NIH HHS / CA / P30 CA08748; United States / NCI NIH HHS / CA / P01 CA94060; United States / NCI NIH HHS / CA / P30 CA008748; United States / NCI NIH HHS / CA / P30-CA 08748; United States / NCI NIH HHS / CA / P01 CA094060; United States / NCI NIH HHS / CA / R24 CA83084; United States / NCI NIH HHS / CA / 5U01CA105492; United States / NCI NIH HHS / CA / R24 CA083084
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; EC 1.13.12.- / Luciferases; F8VB5M810T / Tetracycline
  • [Other-IDs] NLM/ PMC2758666
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55. Yang TM, Han SC, Wu CJ, Mo LR: Acinar cell carcinomas with exophytic growth and intraductal pancreatic duct invasion: peculiar multislice computed tomographic picture. J Hepatobiliary Pancreat Surg; 2009;16(2):238-41
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  • [Title] Acinar cell carcinomas with exophytic growth and intraductal pancreatic duct invasion: peculiar multislice computed tomographic picture.
  • MSCT showed 8.4 cm well-enhancing exophytic tumor of the pancreatic head which also protruded into the duodenum.
  • The pathological diagnosis was acinar cell carcinoma (ACC) originating in the pancreatic head and directly invading through the duodenal wall and the main pancreatic duct, without any lymph node involvement.
  • [MeSH-major] Carcinoma, Acinar Cell / radiography. Pancreatic Neoplasms / radiography. Tomography, X-Ray Computed
  • [MeSH-minor] Aged. Female. Humans. Neoplasm Invasiveness. Pancreatic Ducts / pathology

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  • (PMID = 19183830.001).
  • [ISSN] 1436-0691
  • [Journal-full-title] Journal of hepato-biliary-pancreatic surgery
  • [ISO-abbreviation] J Hepatobiliary Pancreat Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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56. Tatli S, Mortele KJ, Levy AD, Glickman JN, Ros PR, Banks PA, Silverman SG: CT and MRI features of pure acinar cell carcinoma of the pancreas in adults. AJR Am J Roentgenol; 2005 Feb;184(2):511-9
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  • [Title] CT and MRI features of pure acinar cell carcinoma of the pancreas in adults.
  • OBJECTIVE: We sought to describe the CT and MRI features of pure acinar cell carcinoma of the pancreas in adults.
  • MATERIALS AND METHODS: Eleven patients (six women and five men; mean age, 64 years) with acinar cell carcinoma, documented by pathologic examination of resected specimens, underwent CT (n=9) or MRI (n=2) examinations.
  • Two radiologists evaluated imaging studies and determined, by consensus, the following data for each tumor: size, location, margination, internal density or signal intensity, and contrast enhancement pattern.
  • CONCLUSION: Pure acinar cell carcinoma of the pancreas is usually an exophytic, oval or round, well-marginated, and hypovascular mass on CT and MRI.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Magnetic Resonance Imaging. Pancreatic Neoplasms / pathology. Tomography, X-Ray Computed

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  • (PMID = 15671372.001).
  • [ISSN] 0361-803X
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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57. Chowdhury P, Udupa KB: Nicotine as a mitogenic stimulus for pancreatic acinar cell proliferation. World J Gastroenterol; 2006 Dec 14;12(46):7428-32
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  • [Title] Nicotine as a mitogenic stimulus for pancreatic acinar cell proliferation.
  • Cell proliferation is an important process in life for growth of normal and cancer cells.
  • This editorial focuses on the role of nicotine, a mitogen, in the induction of signaling pathways resulting in proliferation of pancreatic tumor cells and compares these events with those in normal acinar cells isolated from the rat pancreas.
  • In addition, the editorial reviews very recent literature of the contribution of MAPK signaling in cell lines associated with human diseases.
  • [MeSH-minor] Animals. Cell Line. Cell Proliferation / drug effects. Humans. In Vitro Techniques. MAP Kinase Signaling System / drug effects. Models, Biological. Rats

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  • (PMID = 17167829.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Mitogens; 6M3C89ZY6R / Nicotine
  • [Number-of-references] 66
  • [Other-IDs] NLM/ PMC4087586
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58. Rembao-Bojórquez D, Vega R, Bermúdez-Maldonado L, Gutiérrez R, Salinas C, Tena-Suck M: Choroid plexus acinar adenoma: a case report. J Neurooncol; 2007 Jun;83(2):191-7
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  • [Title] Choroid plexus acinar adenoma: a case report.
  • Mucus-secreting adenomas or acinar adenoma of the choroid plexus are very rare.
  • He was admitted to the hospital with significant tumor expansion and clinical deterioration.
  • Pathological findings were consistent with an acinar choroid plexus adenoma.
  • The tumor was attached to the ependymal lining and was strongly adhered to the walls and floor of the IV ventricle.
  • Post-operative bleeding complicated partial removal of this tumor.
  • [MeSH-major] Adenoma / pathology. Carcinoma, Acinar Cell / pathology. Cerebral Ventricle Neoplasms / pathology. Choroid Plexus Neoplasms / pathology

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  • (PMID = 17406790.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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59. Sequeira SJ, Wen HC, Avivar-Valderas A, Farias EF, Aguirre-Ghiso JA: Inhibition of eIF2alpha dephosphorylation inhibits ErbB2-induced deregulation of mammary acinar morphogenesis. BMC Cell Biol; 2009 Sep 15;10:64
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  • [Title] Inhibition of eIF2alpha dephosphorylation inhibits ErbB2-induced deregulation of mammary acinar morphogenesis.
  • We have shown that forced phosphorylation of eIF2alpha can suppress head and neck, colorectal carcinoma and multiple myeloma tumor growth and/or survival.
  • Here we explore whether ErbB2 modulates eIF2alpha phosphorylation and whether forced phosphorylation of the latter can antagonize ErbB2 deregulation of mammary acinar morphogenesis.
  • RESULTS: We tested whether ErbB2 signaling influenced eIF2alpha signaling and whether enhanced phosphorylation of the latter affected ErbB2-deregulated mammary acinar development.
  • We obtained stable MCF10A cells overexpressing wild-type (Wt) Neu/ErbB2 or a constitutively active (CA) variant via retroviral delivery or mammary tumor cells from MMTV-Neu tumors.
  • However, inhibition of eIF2alpha dephosphorylation with salubrinal was sufficient to inhibit Wt- and CA-ErbB2- as well as MMTV-Neu-induced deregulation of acinar growth.

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  • (PMID = 19754954.001).
  • [ISSN] 1471-2121
  • [Journal-full-title] BMC cell biology
  • [ISO-abbreviation] BMC Cell Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109182; United States / NCI NIH HHS / CA / R01 CA119018; United States / NCI NIH HHS / CA / CA109182; United States / NCI NIH HHS / CA / CA119018
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Atf4 protein, mouse; 0 / Ccnd1 protein, mouse; 0 / DDIT3 protein, human; 0 / Eukaryotic Initiation Factor-2; 136601-57-5 / Cyclin D1; 145891-90-3 / Activating Transcription Factor 4; 147336-12-7 / Transcription Factor CHOP; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC2754445
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60. Lin YC, Lee PH, Yao YT, Hsiao JK, Sheu JC, Chen CH: Alpha-fetoprotein-producing pancreatic acinar cell carcinoma. J Formos Med Assoc; 2007 Aug;106(8):669-72
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  • [Title] Alpha-fetoprotein-producing pancreatic acinar cell carcinoma.
  • A pancreatic tail tumor, instead of liver tumor, was detected.
  • He underwent elective distal pancreatectomy and splenectomy and the pathology turned out to be acinar cell carcinoma of the pancreas.
  • Alpha-fetoprotein is commonly used as a tumor marker to screen for hepatocellular carcinoma in high-risk patients.
  • However, elevated alpha-fetoprotein could occur in a much rarer disease, acinar cell carcinoma of the pancreas.

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  • (PMID = 17711801.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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61. Schmidt CM, Matos JM, Bentrem DJ, Talamonti MS, Lillemoe KD, Bilimoria KY: Acinar cell carcinoma of the pancreas in the United States: prognostic factors and comparison to ductal adenocarcinoma. J Gastrointest Surg; 2008 Dec;12(12):2078-86
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  • [Title] Acinar cell carcinoma of the pancreas in the United States: prognostic factors and comparison to ductal adenocarcinoma.
  • INTRODUCTION: Pancreatic acinar cell carcinoma (ACC) is a rare tumor with poorly defined prognosis.
  • OBJECTIVE: Our objective was to compare a large population of patients with ACC to pancreatic ductal cell adenocarcinoma (DCC) in order to determine distinguishing characteristics and to assess survival.
  • RESULTS: Median tumor size was 6.9 cm (vs. 4.6 cm DCC); 32.1% had nodal metastases (vs. 48.0% DCC); and 47% had high-grade tumors (vs. 37.3% DCC).
  • Patients with ACC were more likely to be male, white, and have larger tumor size, no nodal involvement, or pancreatic tail tumors.
  • [MeSH-major] Carcinoma, Acinar Cell / epidemiology. Carcinoma, Acinar Cell / surgery. Pancreatic Neoplasms / epidemiology. Pancreatic Neoplasms / surgery

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  • (PMID = 18836784.001).
  • [ISSN] 1873-4626
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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62. 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


63. Ambrosini-Spaltro A, Potì O, De Palma M, Filotico M: Pancreatic-type acinar cell carcinoma of the stomach beneath a focus of pancreatic metaplasia of the gastric mucosa. Hum Pathol; 2009 May;40(5):746-9
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  • [Title] Pancreatic-type acinar cell carcinoma of the stomach beneath a focus of pancreatic metaplasia of the gastric mucosa.
  • Acinar cell carcinoma is an uncommon type of carcinoma of the pancreas that can exceptionally arise in ectopic pancreatic tissue.
  • Herein, we report a case of a 52-year-old man with pancreatic-type acinar cell carcinoma of the stomach and concomitant pancreatic metaplasia of the adjacent nonneoplastic gastric mucosa.
  • There was neither clinical nor radiographic evidence of a tumor in the pancreas itself.
  • Macroscopically, an ulcerated tumor, measuring 4 x 1.7 cm, was found in the distal antrum.
  • Microscopically, the biopsy and the surgical specimen revealed a neoplasm with a predominantly trabecular architecture composed of moderately atypical cells with finely dispersed chromatin and indistinct nucleoli.
  • The neoplastic cells and those of the adjacent metaplastic mucosa were both strongly immunoreactive for alpha-1-antitrypsin, consistent with pancreatic acinar cell differentiation.
  • Ectopic pancreatic-type acinar cell carcinoma is an extremely rare condition, having been previously reported only in 5 occasions, none of them in association with pancreatic acinar cell metaplasia of the gastric mucosa.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Gastric Mucosa / pathology. Pancreas / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Cell Differentiation. Humans. Male. Metaplasia / pathology. Middle Aged. alpha 1-Antitrypsin / biosynthesis


64. Gallmeier E, Schäfer C, Moubarak P, Tietz A, Plössl I, Huss R, Göke B, Wagner AC: JAK and STAT proteins are expressed and activated by IFN-gamma in rat pancreatic acinar cells. J Cell Physiol; 2005 Apr;203(1):209-16
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  • [Title] JAK and STAT proteins are expressed and activated by IFN-gamma in rat pancreatic acinar cells.
  • The development of acute pancreatitis (AP) is triggered by acinar events, but the subsequent extra-acinar events, particularly a distinct immune response, appear to determine its severity.
  • Cytokines modulate this immune response and are derived not only from immunocytes but also from pancreatic acinar cells.
  • We studied whether pancreatic acinar cells were also capable of responding to cytokines.
  • Therefore, expression and regulation of JAK and STAT proteins were investigated in rat pancreatic acinar cells.
  • In addition, STAT1 was reversibly tyrosine-phosphorylated upon the procedure of acinar cell isolation.
  • Immunohistochemistry revealed cytoplasmic expression of unphosphorylated STAT1 in untreated acinar cells and nuclear translocation of phosphorylated STAT1 following IFN-gamma-treatment.
  • Interestingly, although CCK leads to the activation of multiple stress pathways in pancreatic acinar cells, we found no influence of CCK on phosphorylation of STAT1, STAT3, or STAT5 in the pancreas.
  • In conclusion, our data provide further evidence that pancreatic acinar cells are able to interact with immune cells.
  • Besides stimulating immune cells via cytokine secretion, acinar cells are in turn capable of responding to IFN-gamma via JAK2 and STAT1 which may have an impact on the development of AP.
  • [MeSH-minor] Animals. Cell Nucleus / metabolism. Cholecystokinin / pharmacology. Cytosol / metabolism. Enzyme Inhibitors / pharmacology. Epidermal Growth Factor / pharmacology. Interleukin-6 / pharmacology. Janus Kinase 1. Janus Kinase 2. Male. Milk Proteins / metabolism. Phosphorylation / drug effects. Proto-Oncogene Proteins / metabolism. Rats. Rats, Sprague-Dawley. STAT1 Transcription Factor. STAT2 Transcription Factor. STAT3 Transcription Factor. STAT5 Transcription Factor. STAT6 Transcription Factor. TYK2 Kinase. Tumor Necrosis Factor-alpha / pharmacology. Tyrphostins / pharmacology

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  • [Copyright] 2004 Wiley-Liss, Inc.
  • (PMID = 15493010.001).
  • [ISSN] 0021-9541
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Interleukin-6; 0 / Milk Proteins; 0 / Proto-Oncogene Proteins; 0 / STAT1 Transcription Factor; 0 / STAT2 Transcription Factor; 0 / STAT3 Transcription Factor; 0 / STAT5 Transcription Factor; 0 / STAT6 Transcription Factor; 0 / Stat1 protein, rat; 0 / Stat3 protein, rat; 0 / Trans-Activators; 0 / Tumor Necrosis Factor-alpha; 0 / Tyrphostins; 0 / alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide; 62229-50-9 / Epidermal Growth Factor; 82115-62-6 / Interferon-gamma; 9011-97-6 / Cholecystokinin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Jak1 protein, rat; EC 2.7.10.2 / Jak2 protein, rat; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.10.2 / TYK2 Kinase; EC 2.7.10.2 / Tyk2 protein, rat
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65. Herawi M, Epstein JI: Immunohistochemical antibody cocktail staining (p63/HMWCK/AMACR) of ductal adenocarcinoma and Gleason pattern 4 cribriform and noncribriform acinar adenocarcinomas of the prostate. Am J Surg Pathol; 2007 Jun;31(6):889-94
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  • [Title] Immunohistochemical antibody cocktail staining (p63/HMWCK/AMACR) of ductal adenocarcinoma and Gleason pattern 4 cribriform and noncribriform acinar adenocarcinomas of the prostate.
  • Overexpression of alpha-methylacyl coenzyme A racemase (AMACR) in combination with absence of basal cell markers [ie, p63 and high molecular weight cytokeratin (HMWCK)] is typical of classic acinar prostatic adenocarcinoma.
  • We studied the expression and diagnostic utility of p63/HMWCK/AMACR immunohistochemical cocktail staining in ductal adenocarcinoma and cribriform Gleason pattern 4 acinar prostate cancer and compared it to noncribriform Gleason pattern 4 acinar prostate cancer.
  • One to 4 representative formalin-fixed paraffin-embedded archival tissue blocks from 62 radical prostatectomy specimens harboring prostate cancer of ductal (n=51), cribriform Gleason pattern 4 acinar (n=27), and noncribriform Gleason pattern 4 acinar adenocarcinoma (n=48) were included in this study.
  • Seventy-seven percent of ductal prostatic adenocarcinoma, 67% of cribriform acinar prostatic carcinoma, and 81% of noncribriform acinar prostatic carcinoma showed positive staining for AMACR.
  • There was no statistically significant difference between AMACR staining among the 3 histologic types, although there was a trend for noncribriform acinar prostatic carcinoma to have greater expression of AMACR than cribriform acinar prostatic carcinoma (P=0.07).
  • Basal cells were detectable by p63 and HMWCK in a patchy fashion in 31.4% (16/51) of ductal and 29.6% (8/27) of cribriform acinar carcinomas compared with 2.1% (1/48) of noncribriform acinar carcinomas. In summary:.
  • (1) the majority of prostatic ductal and cribriform acinar carcinomas strongly expressed AMACR, however, subpopulations of these prostatic carcinoma were either completely negative or only weakly positive;.
  • (2) AMACR staining was often heterogeneous in intensity in the same histologic type of tumor, even within the same case;.
  • (3) patchy basal cell staining in noncribriform acinar prostatic carcinoma is rare.
  • In contrast, remnants of basal cells identified by p63/HMWCK were seen in a patchy fashion in a significant minority of both ductal and cribriform acinar prostatic adenocarcinoma, which most likely represents intraductal spread of tumor.
  • [MeSH-major] Adenocarcinoma / diagnosis. Biomarkers, Tumor / analysis. Keratins / metabolism. Membrane Proteins / metabolism. Prostatic Neoplasms / diagnosis. Racemases and Epimerases / metabolism

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  • (PMID = 17527076.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Membrane Proteins; 68238-35-7 / Keratins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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66. Wisnoski NC, Townsend CM Jr, Nealon WH, Freeman JL, Riall TS: 672 patients with acinar cell carcinoma of the pancreas: a population-based comparison to pancreatic adenocarcinoma. Surgery; 2008 Aug;144(2):141-8
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  • [Title] 672 patients with acinar cell carcinoma of the pancreas: a population-based comparison to pancreatic adenocarcinoma.
  • BACKGROUND: Acinar cell carcinoma (ACC) is a rare cancer of the pancreas accounting for approximately 1% of nonendocrine tumors.
  • The demographic factors, tumor characteristics, resection status, and long-term survival were compared between the 2 groups.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18656619.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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67. Machado MC, Machado MA, Perini MV, Herman P, Jukemura J, Leite KR, Bacchella T: Acinar cell carcinoma of the pancreas: is the absence of neuroendocrine component related to a more malignant behavior? Hepatogastroenterology; 2008 Mar-Apr;55(82-83):708-10
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  • [Title] Acinar cell carcinoma of the pancreas: is the absence of neuroendocrine component related to a more malignant behavior?
  • BACKGROUND/AIMS: Acinar cell carcinomas are uncommon malignant tumors of the pancreas, accounting for 1-2% of all the cases of exocrine pancreatic tumor.
  • Some authors have estimated acinar cell tumors to be as aggressive as ductal adenocarcinoma of the pancreas whereas other series showed acinar cell tumors to have a favorable clinical outcome.
  • This discrepancy in prognosis may be related to the cellular components of the tumor.
  • METHODOLOGY: With the aim to evaluate the possible relationship between the presence of neuroendocrine differentiation and behavior of these tumors, the authors reviewed all patients presenting acinar cell carcinoma of the pancreas in the last 5 years with emphasis in the immunohistochemical evaluation.
  • This data suggests that this tumor is less aggressive than ductal adenocarcinoma and even with nodal involvement, long-term survival after complete resection can be achieved.
  • Due to the rarity of this pancreatic tumor, this relationship remains to be confirmed with a multicentric study including a larger number of patients.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18613439.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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68. Rossetti S, Hoogeveen AT, Esposito J, Sacchi N: Loss of MTG16a (CBFA2T3), a novel rDNA repressor, leads to increased ribogenesis and disruption of breast acinar morphogenesis. J Cell Mol Med; 2010 Jun;14(6A):1358-70
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  • [Title] Loss of MTG16a (CBFA2T3), a novel rDNA repressor, leads to increased ribogenesis and disruption of breast acinar morphogenesis.
  • We also show that either knocking down MTG16a by RNA interference, or sequestering MTG16a outside the nucleolus of human breast epithelial cells, hampers acinar morphogenesis concomitant with up-regulation of rRNA synthesis and increased ribogenesis.
  • [MeSH-major] Breast / embryology. Breast / metabolism. DNA, Ribosomal / metabolism. Morphogenesis. Repressor Proteins / deficiency. Ribosomes / metabolism. Tumor Suppressor Proteins / deficiency
  • [MeSH-minor] Breast Neoplasms / genetics. Breast Neoplasms / pathology. Cell Nucleolus / metabolism. Down-Regulation / genetics. Epithelial Cells / metabolism. Female. Fibroblasts / metabolism. Gene Expression Regulation, Neoplastic. Gene Knockdown Techniques. HeLa Cells. Humans. Models, Biological. Nucleolus Organizer Region / genetics. Protein Transport. Proto-Oncogene Proteins c-myc / metabolism. Up-Regulation / genetics

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  • [ErratumIn] J Cell Mol Med. 2010 Aug;14(8):2186
  • (PMID = 19961547.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CBFA2T3 protein, human; 0 / DNA, Ribosomal; 0 / Proto-Oncogene Proteins c-myc; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC3828852
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69. Williard DE, Twait E, Yuan Z, Carter AB, Samuel I: Nuclear factor kappa B-dependent gene transcription in cholecystokinin- and tumor necrosis factor-alpha-stimulated isolated acinar cells is regulated by p38 mitogen-activated protein kinase. Am J Surg; 2010 Aug;200(2):283-90
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  • [Title] Nuclear factor kappa B-dependent gene transcription in cholecystokinin- and tumor necrosis factor-alpha-stimulated isolated acinar cells is regulated by p38 mitogen-activated protein kinase.
  • We investigated the relationship between the p38 MAP kinase and NF-kappaB in isolated acinar cells.
  • METHODS: Isolated rodent acinar cells were stimulated with agonists after infection with an adenovector containing a luciferase promoter driven only by NF-kappaB and an adenovector containing the dominant negative (DN) form of p38 (empty vector in controls).
  • RESULTS: Initial immunoblots confirmed that the agonist stimulated p38 activation in acinar cells was substantially attenuated by DN p38 overexpression.
  • Stimulation of native cholecystokinin (CCK)-A receptors or tumor necrosis factor-alpha (TNF-alpha) receptors promoted a significant increase in NF-kappaB-dependent gene transcription in cells infected with the empty vector, while overexpression of DN p38 significantly abrogated NF-kappaB-dependent luciferase activity.

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  • [Copyright] Published by Elsevier Inc.
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  • (PMID = 20413104.001).
  • [ISSN] 1879-1883
  • [Journal-full-title] American journal of surgery
  • [ISO-abbreviation] Am. J. Surg.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK071731-01A2; United States / NIEHS NIH HHS / ES / R01 ES014871; United States / NIEHS NIH HHS / ES / ES-014871; United States / NIEHS NIH HHS / ES / R01 ES015981; United States / NIDDK NIH HHS / DK / DK071731-01A2; United States / NIDDK NIH HHS / DK / DK-071731; United States / NIDDK NIH HHS / DK / R01 DK071731; United States / NIEHS NIH HHS / ES / ES-015981
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 9011-97-6 / Cholecystokinin; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS182891; NLM/ PMC2910146
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70. Hervieu V, Lombard-Bohas C, Dumortier J, Boillot O, Scoazec JY: Primary acinar cell carcinoma of the liver. Virchows Arch; 2008 Mar;452(3):337-41
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  • [Title] Primary acinar cell carcinoma of the liver.
  • We report a case of acinar cell carcinoma primary to the liver.
  • The tumor was diagnosed in a 35-year-old woman complaining of abdominal pain and asthenia; serum alpha-fetoprotein (AFP) levels were increased at 6,000 IU/mL; imaging studies showed a hypervascular mass located in the left lobe of the liver.
  • The tumor had a heterogeneous appearance.
  • In well-differentiated areas, tumor cells formed acinar structures, had a pyramidal shape and a highly eosinophilic, granular cytoplasm, PAS diastase resistant.
  • In less-differentiated areas, tumor cells were endocrinelike.
  • The immunohistochemical study showed that tumor cells expressed trypsin.
  • The final diagnosis, based on histological, immunohistochemical, and ultrastructural arguments, was extra-pancreatic acinar cell carcinoma, primary to the liver.
  • This unusual lesion is likely to be the result of an abnormal differentiation pathway involving a transformed multipotential progenitor cell.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Liver / pathology. Liver Neoplasms / pathology

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  • (PMID = 18193278.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / alpha 1-Antitrypsin; 0 / alpha-Fetoproteins
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71. Imamura M, Kimura Y, Ito H, Nobuoka T, Koito K, Sasaki A, Hirata K: Acinar cell carcinoma of the pancreas with intraductal growth: report of a case. Surg Today; 2009;39(11):1006-9
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  • [Title] Acinar cell carcinoma of the pancreas with intraductal growth: report of a case.
  • Acinar cell carcinomas (ACCs) of the pancreas are rare neoplasms, accounting for approximately 1% of all exocrine pancreatic tumors.
  • This type of tumor is known to be aggressive, although the survival rates are somewhat better than they are for ductal carcinoma.
  • The tumor tends to present nonspecific symptoms.
  • [MeSH-major] Carcinoma, Acinar Cell / surgery. Neoplasm Invasiveness. Pancreatectomy / methods. Pancreatic Ducts / pathology. Pancreatic Neoplasms / surgery

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  • (PMID = 19882327.001).
  • [ISSN] 1436-2813
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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72. 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.
  • 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

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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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73. Arcolino FO, Ribeiro DL, Gobbo MG, Taboga SR, Góes RM: Proliferation and apoptotic rates and increased frequency of p63-positive cells in the prostate acinar epithelium of alloxan-induced diabetic rats. Int J Exp Pathol; 2010 Apr;91(2):144-54
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  • [Title] Proliferation and apoptotic rates and increased frequency of p63-positive cells in the prostate acinar epithelium of alloxan-induced diabetic rats.
  • The effects of experimental type 1 diabetes were investigated in the acinar epithelium of rat ventral prostate, focusing on the rates of cell proliferation and the frequency of apoptosis and p63-positive cells.
  • Immunocytochemical methods for the localization of cell proliferation antigen (PCNA), androgen receptor (AR) and p63 protein were carried out, and apoptotic cells were identified by TUNEL essay.
  • In short-term diabetic rats, cell proliferation decreased, and in medium-term, epithelial apoptotic rates increased.
  • Insulin treatment was effective in preventing testosterone decrease, p63-positive cell increase and apoptotic rates, but did not interfere in cell proliferation.
  • This investigation shows that, soon after diabetes onset, there are important modifications in cell proliferation within the acinar prostatic epithelium, and in longer term, there is a marked impact on kinetics of differentiation and cell death, which may initially be attributable to an androgenic fall, but is probably also because of other factors related to diabetes, as changes are considerably different from those resulting from castration.
  • [MeSH-major] Apoptosis. Diabetes Mellitus, Experimental / pathology. Prostate / pathology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Animals. Blood Glucose / biosynthesis. Body Weight. Cell Proliferation / drug effects. Epithelium / metabolism. Epithelium / pathology. Gonadal Steroid Hormones / blood. Insulin / therapeutic use. Male. Organ Size. Proliferating Cell Nuclear Antigen / metabolism. Rats. Rats, Wistar. Receptors, Androgen / metabolism

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  • (PMID = 20041964.001).
  • [ISSN] 1365-2613
  • [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 / Blood Glucose; 0 / Gonadal Steroid Hormones; 0 / Insulin; 0 / Proliferating Cell Nuclear Antigen; 0 / Receptors, Androgen; 0 / Trp63 protein, rat; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC2965900
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74. Guo L, Lichten LA, Ryu MS, Liuzzi JP, Wang F, Cousins RJ: STAT5-glucocorticoid receptor interaction and MTF-1 regulate the expression of ZnT2 (Slc30a2) in pancreatic acinar cells. Proc Natl Acad Sci U S A; 2010 Feb 16;107(7):2818-23
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  • [Title] STAT5-glucocorticoid receptor interaction and MTF-1 regulate the expression of ZnT2 (Slc30a2) in pancreatic acinar cells.
  • Rat AR42J acinar cells when induced into a secretory phenotype, using the glucocorticoid analog dexamethasone (DEX), exhibited increased ZnT2 expression and labile zinc as measured with a fluorophore.
  • We conclude, based upon experiments with intact mice and pancreatic acinar cells in culture, that ZnT2 participates in zinc transport into pancreatic zymogen granules through a glucocorticoid pathway requiring glucocorticoid receptor and STAT5, and zinc-regulated signaling pathways requiring MTF-1.

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  • (PMID = 20133611.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R37 DK031127; United States / NIDDK NIH HHS / DK / R56 DK031127; United States / NIDDK NIH HHS / DK / Z01 DK031127; United States / NIDDK NIH HHS / DK / DK31127; United States / NIDDK NIH HHS / DK / R01 DK031127
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cation Transport Proteins; 0 / DNA-Binding Proteins; 0 / Receptors, Glucocorticoid; 0 / STAT5 Transcription Factor; 0 / Slc30a2 protein, rat; 0 / Transcription Factors; 0 / transcription factor MTF-1; 7S5I7G3JQL / Dexamethasone; EC 1.13.12.- / Luciferases; J41CSQ7QDS / Zinc
  • [Other-IDs] NLM/ PMC2840329
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75. Peng HQ, Darwin P, Papadimitriou JC, Drachenberg CB: Liver metastases of pancreatic acinar cell carcinoma with marked nuclear atypia and pleomorphism diagnosed by EUS FNA cytology: a case report with emphasis on FNA cytological findings. Cytojournal; 2006;3:29
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  • [Title] Liver metastases of pancreatic acinar cell carcinoma with marked nuclear atypia and pleomorphism diagnosed by EUS FNA cytology: a case report with emphasis on FNA cytological findings.
  • BACKGROUND: Acinar cell carcinoma of the pancreas is a rare neoplasm.
  • Although this tumor has been well characterized histologically, the morphological patterns in Fine Needle Aspiration Cytology have not been well defined.
  • Unlike ductal adenocarcinomas, endocrine tumors, and solid pseudopapillary tumors of the pancreas with their characteristic FNA cytological features, acinar cell carcinomas pose a particular diagnostic challenge by sharing many cytomorphologic features with endocrine tumors of the pancreas.
  • FNA cytology revealed abundant, loosely cohesive clusters of malignant epithelial cells with vaguely acinar and trabecular formations.
  • Scattered, strikingly large tumor cells with giant nuclei, prominent mitoses and associated necrosis were evident.
  • A pancreatic endocrine tumor was suspected initially, but acinar cell carcinoma of the pancreas was confirmed by immunohistochemistry, cytochemical and ultrastructural studies.
  • CONCLUSION: We describe a case of pancreatic acinar cell carcinoma with unusual cytomorphologic features mimicking an endocrine tumor of pancreas, encountered in endoscopic ultrasound-guided fine needle aspiration of a metastatic liver mass and discuss the diagnostic approach for this unusual pancreatic tumor in fine needle aspiration cytology.

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  • (PMID = 17196112.001).
  • [ISSN] 1742-6413
  • [Journal-full-title] CytoJournal
  • [ISO-abbreviation] Cytojournal
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1779360
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76. Dimri M, Naramura M, Duan L, Chen J, Ortega-Cava C, Chen G, Goswami R, Fernandes N, Gao Q, Dimri GP, Band V, Band H: Modeling breast cancer-associated c-Src and EGFR overexpression in human MECs: c-Src and EGFR cooperatively promote aberrant three-dimensional acinar structure and invasive behavior. Cancer Res; 2007 May 1;67(9):4164-72
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  • [Title] Modeling breast cancer-associated c-Src and EGFR overexpression in human MECs: c-Src and EGFR cooperatively promote aberrant three-dimensional acinar structure and invasive behavior.
  • Using a combination of morphologic analysis and confocal imaging of polarity markers in three-dimensional Matrigel culture together with functional analyses of early oncogenic traits, we show for the first time that EGFR and c-Src co-overexpression but not EGFR or c-Src overexpression alone unleashes an oncogenic signaling program that leads to hyperproliferation and loss of polarity in three-dimensional acinar cultures, marked enhancement of migratory and invasive behavior, and anchorage-independent growth.

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  • (PMID = 17483327.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096986-01A1; United States / NCI NIH HHS / CA / R01 CA095221-02; United States / NCI NIH HHS / CA / CA096986-01A1; United States / NCI NIH HHS / CA / R01 CA095221-01A1; United States / NCI NIH HHS / CA / R01 CA096986-04; United States / NCI NIH HHS / CA / R01 CA095221-05; United States / NCI NIH HHS / CA / CA 94143; United States / NCI NIH HHS / CA / R01 CA096986-05; United States / NCI NIH HHS / CA / CA095221-01A1; United States / NCI NIH HHS / CA / R01 CA096986-02; United States / NCI NIH HHS / CA / CA 87986; United States / NCI NIH HHS / CA / CA 81076; United States / NCI NIH HHS / CA / CA 99163; United States / NCI NIH HHS / CA / 1U54 CA 119341-01; United States / NCI NIH HHS / CA / CA 96844; United States / NCI NIH HHS / CA / CA 76118; United States / NCI NIH HHS / CA / CA 99900; United States / NCI NIH HHS / CA / R01 CA095221-03; United States / NCI NIH HHS / CA / R01 CA096986-03; United States / NCI NIH HHS / CA / R01 CA095221-04
  • [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 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / src-Family Kinases
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77. Gerasimenko J, Ferdek P, Fischer L, Gukovskaya AS, Pandol SJ: Inhibitors of Bcl-2 protein family deplete ER Ca2+ stores in pancreatic acinar cells. Pflugers Arch; 2010 Oct;460(5):891-900
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  • [Title] Inhibitors of Bcl-2 protein family deplete ER Ca2+ stores in pancreatic acinar cells.
  • Physiological stimulation of pancreatic acinar cells by cholecystokinin and acetylcholine activate a spatial-temporal pattern of cytosolic [Ca(+2)] changes that are regulated by a coordinated response of inositol 1,4,5-trisphosphate receptors (IP(3)Rs), ryanodine receptors (RyRs) and calcium-induced calcium release (CICR).

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  • (PMID = 20617337.001).
  • [ISSN] 1432-2013
  • [Journal-full-title] Pflugers Archiv : European journal of physiology
  • [ISO-abbreviation] Pflugers Arch.
  • [Language] ENG
  • [Grant] United States / NIAAA NIH HHS / AA / P50 AA011999; United Kingdom / Medical Research Council / / G8801575; United States / NIAAA NIH HHS / AA / P60 AA11999; United Kingdom / Wellcome Trust / /
  • [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] Germany
  • [Chemical-registry-number] 0 / 3-iodo-5-chloro-N-(2-chloro-5-((4-chlorophenyl)sulphonyl)phenyl)-2-hydroxybenzamide; 0 / Bcl2l1 protein, mouse; 0 / Benzamides; 0 / Benzopyrans; 0 / Inositol 1,4,5-Trisphosphate Receptors; 0 / Nitriles; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Ryanodine Receptor Calcium Release Channel; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; 0 / ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC2937140
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78. Lee JH, Lee KG, Park HK, Lee KS: [Acinar cell carcinoma of the pancreas in Korea--clinicopathologic analysis of 27 patients from korean literature and 2 cases from our hospital--]. Korean J Gastroenterol; 2010 Apr;55(4):245-51
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  • [Title] [Acinar cell carcinoma of the pancreas in Korea--clinicopathologic analysis of 27 patients from korean literature and 2 cases from our hospital--].
  • BACKGROUND/AIMS: Acinar cell carcinoma (ACC) of the pancreas is a rare malignancy.
  • The mean tumor size was 7.0 cm, and most common location was tail.
  • CONCLUSIONS: In Korea, the clinical features of ACC include young age, large size, tail location, and nonspecific tumor markers.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Age Factors. Aged. Biomarkers, Tumor / analysis. Female. Humans. Male. Middle Aged. Prognosis. Republic of Korea. Survival Analysis

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  • (PMID = 20389178.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 22
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79. Kobayashi S, Asakura T, Ohike N, Enomoto T, Sakurai J, Koizumi S, Watanabe T, Nakano H, Otsubo T: Mixed acinar-endocrine carcinoma of the pancreas with intraductal growth into the main pancreatic duct: Report of a case. Surg Today; 2010 Apr;40(4):380-4
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  • [Title] Mixed acinar-endocrine carcinoma of the pancreas with intraductal growth into the main pancreatic duct: Report of a case.
  • The patient was a 75-year-old asymptomatic man, in whom a tumor mass in the pancreatic tail had been found 6 months earlier.
  • Computed tomography revealed a mass 7 cm in diameter, and an enhancement with contrast medium was observed at the periphery and partially inside the mass, but not in most parts of the tumor.
  • A distal pancreatectomy was performed because of the possibility of a malignant tumor.
  • The tumor consisted of a lobular invasive growth component and a component with intraductal growth into the main pancreatic duct, and histologically the tumor cells had solid acinar to partially trabecular/tubular patterns.
  • Trypsin (an acinic cell marker) expression was widely observed, followed by the expression of chromogranin A (an endocrine cell marker) in about 30% of the tumor cells.
  • The tumor was diagnosed as mixed acinar-endocrine carcinoma according to the WHO classification.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Endocrine Gland Neoplasms / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 20339996.001).
  • [ISSN] 1436-2813
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Chromogranin A
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80. Lim JW, Song JY, Seo JY, Kim H, Kim KH: Role of pancreatitis-associated protein 1 on oxidative stress-induced cell death of pancreatic acinar cells. Ann N Y Acad Sci; 2009 Aug;1171:545-8
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  • [Title] Role of pancreatitis-associated protein 1 on oxidative stress-induced cell death of pancreatic acinar cells.
  • Previously we showed that oxidative stress induces apoptosis of pancreatic acinar cells with nuclear loss of DNA repair proteins.
  • In this study, we investigated the role of PAP-1 on oxidative stress-induced cell death of pancreatic acinar AR42J cells.
  • PAP-1 mRNA expression and cell viability were determined.
  • Cell viability decreased with the concentration of glucose oxides delivered to the cells that had received glucose.
  • Cell death caused by oxidative stress was inhibited in the cells transfected with PAP-1 S cDNA, but it increased in the cells transfected with PAP-1 AS cDNA.
  • These results indicate that PAP-1 may be a defensive gene for oxidative stress-induced cell death of pancreatic acinar cells.
  • [MeSH-major] Antigens, Neoplasm / physiology. Apoptosis / physiology. Biomarkers, Tumor / physiology. Lectins, C-Type / physiology. Oxidative Stress / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / physiology. DNA, Antisense / genetics. DNA, Complementary / genetics. Gene Expression Regulation, Neoplastic. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 19723102.001).
  • [ISSN] 1749-6632
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA, Antisense; 0 / DNA, Complementary; 0 / Lectins, C-Type; 0 / RNA, Messenger; 0 / pancreatitis-associated protein
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81. Martin SK, Agarwal G, Lynch GR: Subcutaneous fat necrosis as the presenting feature of a pancreatic carcinoma: the challenge of differentiating endocrine and acinar pancreatic neoplasms. Pancreas; 2009 Mar;38(2):219-22
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  • [Title] Subcutaneous fat necrosis as the presenting feature of a pancreatic carcinoma: the challenge of differentiating endocrine and acinar pancreatic neoplasms.
  • In our review of the published reports of tumor types associated with pancreatic panniculitis, we found that immunohistochemical staining and electron microscopy can and should be used in conjunction with clinical correlation to accurately differentiate neuroendocrine tumors from carcinomas with acinar cell features.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Fat Necrosis / pathology. Neuroendocrine Tumors / pathology. Pancreatic Neoplasms / pathology. Panniculitis / pathology. Skin / pathology

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  • (PMID = 19238022.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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82. Jang SH, Choi SY, Min JH, Kim TW, Lee JA, Byun SJ, Lee JW: [A case of acinar cell carcinoma of pancreas, manifested by subcutaneous nodule as initial clinical symptom]. Korean J Gastroenterol; 2010 Feb;55(2):139-43
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  • [Title] [A case of acinar cell carcinoma of pancreas, manifested by subcutaneous nodule as initial clinical symptom].
  • Pancreas acinar cell carcinoma (ACC) accounts for only 1-2% of pancreatic exocrine malignant tumor.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Neoplasms / diagnosis. Subcutaneous Fat / pathology

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  • (PMID = 20168061.001).
  • [ISSN] 2233-6869
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Synaptophysin; 68238-35-7 / Keratins
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83. Williams CM, Engler AJ, Slone RD, Galante LL, Schwarzbauer JE: Fibronectin expression modulates mammary epithelial cell proliferation during acinar differentiation. Cancer Res; 2008 May 1;68(9):3185-92
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  • [Title] Fibronectin expression modulates mammary epithelial cell proliferation during acinar differentiation.
  • Essential roles for the epithelial basement membrane during acinar differentiation, in particular laminin and its integrin receptors, have been identified using mammary epithelial cells cultured on a reconstituted basement membrane.
  • Alterations in fibronectin levels perturbed acinar organization.
  • During acinar development, increased fibronectin levels resulted in overproliferation of mammary epithelial cells and increased acinar size.
  • Addition of fibronectin to differentiated acini stimulated proliferation and reversed growth arrest of mammary epithelial cells negatively affecting maintenance of proper acinar morphology.
  • These results show that expression of fibronectin creates a permissive environment for cell growth that antagonizes the differentiation signals from the basement membrane.
  • These effects suggest a link between fibronectin expression and epithelial cell growth during development and oncogenesis in the mammary gland.

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  • (PMID = 18451144.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM059383-08; United States / NCI NIH HHS / CA / P01 CA41086; United States / NIGMS NIH HHS / GM / GM059383-08; United States / NCI NIH HHS / CA / P01 CA041086-200009; United States / NIGMS NIH HHS / GM / T32 GM07388; United States / NIGMS NIH HHS / GM / GM007388-32; United States / NIGMS NIH HHS / GM / T32 GM007388; United States / NIGMS NIH HHS / GM / T32 GM007388-32; United States / NCI NIH HHS / CA / CA041086-200009; United States / NCI NIH HHS / CA / T32 CA009528; United States / NIGMS NIH HHS / GM / R01 GM059383; United States / NCI NIH HHS / CA / P01 CA041086
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fibronectins
  • [Other-IDs] NLM/ NIHMS106353; NLM/ PMC2748963
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84. Sun LK, Reding T, Bain M, Heikenwalder M, Bimmler D, Graf R: Prostaglandin E2 modulates TNF-alpha-induced MCP-1 synthesis in pancreatic acinar cells in a PKA-dependent manner. Am J Physiol Gastrointest Liver Physiol; 2007 Dec;293(6):G1196-204
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  • [Title] Prostaglandin E2 modulates TNF-alpha-induced MCP-1 synthesis in pancreatic acinar cells in a PKA-dependent manner.
  • The aim of our study is to identify mechanisms by which macrophages and acinar cells maintain an inflammatory reaction.
  • PGE(2) modulates the TNF-alpha-induced MCP-1 synthesis and secretion from acinar cells.
  • [MeSH-major] Chemokine CCL2 / metabolism. Cyclic AMP-Dependent Protein Kinases / metabolism. Dinoprostone / metabolism. Pancreas / metabolism. Pancreatitis / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cell Line. Rats. Rats, Wistar

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  • (PMID = 17916652.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ccl2 protein, rat; 0 / Chemokine CCL2; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; K7Q1JQR04M / Dinoprostone
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85. Ramudo L, Manso MA, Vicente S, De Dios I: Pro- and anti-inflammatory response of acinar cells during acute pancreatitis. Effect of N-acetyl cysteine. Cytokine; 2005 Nov 3;32(3-4):125-31
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  • [Title] Pro- and anti-inflammatory response of acinar cells during acute pancreatitis. Effect of N-acetyl cysteine.
  • We investigate the ability of acinar cells to produce tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) at different stages of acute pancreatitis (AP).
  • Acinar cells were incubated for 4 h at 37 degrees C in 5% CO2 atmosphere in absence and presence of 24-h BPDO-PAAF (20%, v/v) as stimulant agent.
  • Acinar production of TNF-alpha and IL-10 was analysed by flow cytometry.
  • PAAF significantly stimulated the acinar production of TNF-alpha and IL-10 in control rats.
  • TNF-alpha production was also significantly stimulated in acinar cells of rats with AP, although a decrease in the pro-inflammatory response was found from 6 h after BPDO onwards.
  • However, acinar cells failed to produce IL-10 from 3 h after BPDO.
  • The protective effect of NAC treatment against oxidative cell damage reduced the pancreatic injury and maintained and enhanced the ability of acinar cells to produce IL-10 at early AP stages.
  • As long as acinar cells were not severely damaged in the course of AP, greater ability to produce cytokines in response to PAAF was found in those with higher forward scatter (R2 cells).
  • We suggest that the capability of acinar cells to maintain an appropriate balance between the production of pro- and anti-inflammatory mediators could contribute to determine the degree of severity of AP.
  • [MeSH-minor] Acute Disease. Animals. Bile Ducts / surgery. Cells, Cultured. Flow Cytometry. Hyperamylasemia / metabolism. Hyperamylasemia / pathology. Interleukin-10 / biosynthesis. Male. Pancreatic Ducts / surgery. Rats. Rats, Wistar. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16263306.001).
  • [ISSN] 1043-4666
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Inflammation Mediators; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; WYQ7N0BPYC / Acetylcysteine
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86. Ramudo L, Manso MA, Sevillano S, de Dios I: Kinetic study of TNF-alpha production and its regulatory mechanisms in acinar cells during acute pancreatitis induced by bile-pancreatic duct obstruction. J Pathol; 2005 May;206(1):9-16
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  • [Title] Kinetic study of TNF-alpha production and its regulatory mechanisms in acinar cells during acute pancreatitis induced by bile-pancreatic duct obstruction.
  • Cytokines play a critical role in acute pancreatitis (AP) but the contribution of different cell sources to cytokine production is unclear.
  • For this reason, the aim of this study was to analyse the ability of acinar cells, in comparison with leukocytes, to produce TNF-alpha at different stages of AP induced in rats by bile-pancreatic duct obstruction (BPDO) and to investigate the time course of oxidant-sensitive mechanisms involved in cytokine production.
  • The role of oxygen free radicals as messengers of the mechanisms underlying acinar cell TNF-alpha production was assessed in BPDO rats treated with N-acetylcysteine (NAC).
  • While monocytes were not able to produce TNF-alpha until 12 h after inducing AP, acinar cells triggered TNF-alpha production from 6 h after BPDO, at which time the pancreas develops maximal oxidative stress.
  • Phosphorylated p38-MAPK and activated NF-kappaB were detected in acinar cells from 6 h after BPDO.
  • As a result, acinar cells in NAC-treated rats failed to produce TNF-alpha during AP.
  • In conclusion, acinar cells contribute directly to the inflammatory response during BPDO-induced AP by producing TNF-alpha even before inflammatory cells in the peripheral blood.
  • The blockade of oxidant-mediated signal transduction pathways induced by NAC treatment prevented acinar cell TNF-alpha production.
  • [MeSH-major] Pancreas / metabolism. Pancreatitis / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Acute Disease. Animals. Blotting, Western / methods. Cell Culture Techniques. Cholestasis / complications. Cholestasis / metabolism. Flow Cytometry. Male. Models, Animal. NF-kappa B / metabolism. Pancreatic Ducts / metabolism. Rats. Rats, Wistar

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  • [Copyright] 2005 Pathological Society of Great Britain and Ireland
  • (PMID = 15761843.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha
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87. Iczkowski KA: Current prostate biopsy interpretation: criteria for cancer, atypical small acinar proliferation, high-grade prostatic intraepithelial neoplasia, and use of immunostains. Arch Pathol Lab Med; 2006 Jun;130(6):835-43
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  • [Title] Current prostate biopsy interpretation: criteria for cancer, atypical small acinar proliferation, high-grade prostatic intraepithelial neoplasia, and use of immunostains.
  • CONCLUSIONS: Diagnosis begins by evaluating a focus of atypical single-cell layer lined acini according to the 3 minimal diagnostic criteria for cancer: an infiltrative pattern, nuclear enlargement and hyperchromasia, and prominent nucleoli.
  • Atypical small acinar proliferation suspicious for malignancy designates foci that have either qualitative or quantitative limitations in atypia precluding a definite cancer diagnosis.
  • Isolated high-grade prostatic intraepithelial neoplasia has a 3% to 14% incidence and predicts cancer on repeat biopsy in 23% of cases.
  • Immunostaining for a marker of benign prostate (cytoplasmic keratin 34betaE12 or nuclear p63) and a marker of cancer (alpha-methylacyl coA racemase, clone P504S) may or may not resolve atypical small acinar proliferation diagnoses.
  • Performance of 34betaE12 and P504S immunostains resolved 76% of atypical small acinar proliferation diagnoses per consensus of 3 urologic pathologists studied; a technical limitation is preservation of the focus in question on the levels used for immunostaining.
  • [MeSH-major] Immunohistochemistry / methods. Precancerous Conditions / pathology. Prostate / pathology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Biopsy, Needle. Cell Nucleus / pathology. Cell Proliferation. Humans. Male

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  • (PMID = 16740037.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 58
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88. Ramnath RD, Sun J, Bhatia M: Involvement of SRC family kinases in substance P-induced chemokine production in mouse pancreatic acinar cells and its significance in acute pancreatitis. J Pharmacol Exp Ther; 2009 May;329(2):418-28
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  • [Title] Involvement of SRC family kinases in substance P-induced chemokine production in mouse pancreatic acinar cells and its significance in acute pancreatitis.
  • To that end, we have used primary preparations of mouse pancreatic acinar cells as our model to show that substance P/neurokinin 1 receptor (NK1R) induced activation of SFKs.
  • SFKs mediated the activation of mitogen-activated protein kinases [extracellular signal-regulated kinase (ERK), c-Jun NH(2)-terminal kinase (JNK)], transcription factors [signal transducer and activator of transcription (STAT) 3, nuclear factor (NF) kappaB, activator protein-1 (AP-1)], and production of chemokines in pancreatic acinar cells.
  • [MeSH-minor] Acute Disease. Amylases / metabolism. Animals. Blotting, Western. Cell Survival. Cells, Cultured. Enzyme-Linked Immunosorbent Assay. Male. Mice. Peroxidase / metabolism. Phosphorylation. Time Factors

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  • (PMID = 19211920.001).
  • [ISSN] 1521-0103
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokines; 33507-63-0 / Substance P; EC 1.11.1.7 / Peroxidase; EC 2.7.10.2 / src-Family Kinases; EC 3.2.1.- / Amylases
  • [Other-IDs] NLM/ PMC2672875
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89. Lin YF, Nagasawa H, Peng Y, Chuang EY, Bedford JS: Comparison of several radiation effects in human MCF10A mammary epithelial cells cultured as 2D monolayers or 3D acinar stuctures in matrigel. Radiat Res; 2009 Jun;171(6):708-15
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  • [Title] Comparison of several radiation effects in human MCF10A mammary epithelial cells cultured as 2D monolayers or 3D acinar stuctures in matrigel.
  • It has been argued that the cell-cell and cell-matrix interaction networks in normal tissues are disrupted by radiation and that this largely controls many of the most important cellular radiation responses.
  • While many studies have shown that, in some cases, cell-cell contact in spheroids of transformed or tumor cell lines can alter radiation responses relative to those for the same cells in monolayer cultures, a question remains regarding the possible effect of the above-mentioned disruption of signaling networks that operate more specifically for cells in normal tissues or in a 3D tissue-like context.
  • To test the generality of this notion, we used human MCF-10A cells, an immortalized mammary epithelial cell line that produces acinar structures in culture with many properties of human mammary ducts.
  • We compared the dose responses for these cells in the 2D monolayer and in 3D ductal or acinar structures.
  • The responses examined were reproductive cell death, induction of chromosomal aberrations, and the levels of gamma-H2AX foci in cells after single acute gamma-ray doses and immediately after 20 h of irradiation at a dose rate of 0.0017 Gy/min.
  • [MeSH-minor] Bromodeoxyuridine. Bystander Effect. Cell Culture Techniques. Cell Death / radiation effects. Cell Line. Cell Survival / radiation effects. Cesium Radioisotopes / adverse effects. Chromosome Aberrations / radiation effects. Dose-Response Relationship, Radiation. Histones / metabolism. Humans. Immunohistochemistry. Microscopy, Fluorescence

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  • (PMID = 19580477.001).
  • [ISSN] 0033-7587
  • [Journal-full-title] Radiation research
  • [ISO-abbreviation] Radiat. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cesium Radioisotopes; 0 / H2AFX protein, human; 0 / Histones; G34N38R2N1 / Bromodeoxyuridine
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90. Calafat M, Larocca L, Roca V, Hauk V, Pregi N, Nesse A, Pérez Leirós C: Vasoactive intestinal peptide inhibits TNF-alpha-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands. Arthritis Res Ther; 2009;11(2):R53
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  • [Title] Vasoactive intestinal peptide inhibits TNF-alpha-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands.
  • Our goal was to analyse the effect of TNF-alpha on apoptotic mediators in isolated acinar cells from NOD submandibular gland and their modulation by VIP.
  • METHODS: Acinar cells were isolated from submandibular glands of 16-week-old NOD females with salivary flow decline.
  • VIP effects in acinar cells were assessed at 100 nM in TNF-alpha-treated cultures and VIP receptor functional assays by radio immunoassay (cAMP) or enzymatic detection (amylase).
  • RESULTS: NOD acinar cells at 16 weeks present an increased expression of TNF-alpha receptor1 together with increased Bax, tumour protein 53-induced nuclear protein1alpha (TP53INP1alpha), caspase 3 activity and chromatin condensation.
  • CONCLUSIONS: Our results indicate that acinar cells isolated from submandibular glands of NOD mice with salivary dysfunction are more sensitive to apoptosis induced by TNF-alpha which could be prevented by VIP through a PKA-mediated pathway.
  • [MeSH-major] Apoptosis / physiology. Sjogren's Syndrome / metabolism. Submandibular Gland / metabolism. Tumor Necrosis Factor-alpha / metabolism. Vasoactive Intestinal Peptide / metabolism

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  • (PMID = 19356238.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 37221-79-7 / Vasoactive Intestinal Peptide; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Other-IDs] NLM/ PMC2688204
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91. 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.
  • At the beginning of this treatment, it seemed to be a stable disease, but CT revealed tumor progression in January 2007.
  • 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

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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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92. 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
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  • [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.
  • 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.

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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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93. Soltoff SP, Hedden L: Isoproterenol and cAMP block ERK phosphorylation and enhance [Ca2+]i increases and oxygen consumption by muscarinic receptor stimulation in rat parotid and submandibular acinar cells. J Biol Chem; 2010 Apr 30;285(18):13337-48
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  • [Title] Isoproterenol and cAMP block ERK phosphorylation and enhance [Ca2+]i increases and oxygen consumption by muscarinic receptor stimulation in rat parotid and submandibular acinar cells.
  • Here we report that the beta-adrenergic ligand isoproterenol blocks increases in extracellular signal-related kinase (ERK) phosphorylation, a protein kinase C-dependent event promoted by the muscarinic receptor ligand carbachol in freshly dispersed rat parotid acinar cells.
  • Inhibitory effects on ERK were also observed in freshly dispersed rat submandibular acinar cells but not in three immortalized/cancer salivary cell lines (Par-C10, HSY, HSG), indicating significant differences between native cells and cell lines.

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  • (PMID = 20207737.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / R01 DE010877; United States / NIDCR NIH HHS / DE / DE-10877
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic beta-Agonists; 0 / Carcinogens; 0 / Cholinergic Agonists; 0 / Guanine Nucleotide Exchange Factors; 0 / P2rx7 protein, rat; 0 / Receptors, Adrenergic, beta; 0 / Receptors, Muscarinic; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2X7; 1F7A44V6OU / Colforsin; 8Y164V895Y / Carbachol; E0399OZS9N / Cyclic AMP; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / raf Kinases; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; L628TT009W / Isoproterenol; NI40JAQ945 / Tetradecanoylphorbol Acetate; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC2859492
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94. Benkoël L, Bernard JP, Payan-Defais MJ, Crescence L, Franceschi C, Delmas M, Ouaissi M, Sastre B, Sahel J, Benoliel AM, Bongrand P, Silvy F, Gauthier L, Romagné F, Lombardo D, Mas E: Monoclonal antibody 16D10 to the COOH-terminal domain of the feto-acinar pancreatic protein targets pancreatic neoplastic tissues. Mol Cancer Ther; 2009 Feb;8(2):282-91
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  • [Title] Monoclonal antibody 16D10 to the COOH-terminal domain of the feto-acinar pancreatic protein targets pancreatic neoplastic tissues.
  • We have shown that the 16D10 antigen located on the mucin-like COOH-terminal domain of the feto-acinar pancreatic protein (FAPP) is expressed at the surface of human pancreatic tumor cell lines such as SOJ-6 cell line.
  • Furthermore, an in vivo study indicates that targeting this cell-membrane glycopeptide by the use of the monoclonal antibody (mAb) 16D10 inhibits the growth of SOJ-6 xenografts in nude mice.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Lipase / chemistry. Lipase / immunology. Pancreatic Neoplasms / immunology
  • [MeSH-minor] Adult. Aged. Antibody Specificity. Antigens, Neoplasm / immunology. Electrophoresis, Polyacrylamide Gel. Female. Fluorescence. Frozen Sections. Humans. Immunohistochemistry. Male. Microscopy, Confocal. Middle Aged. Neoplasm Metastasis. Organ Specificity. Preoperative Care. Protein Structure, Tertiary

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  • (PMID = 19190122.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; EC 3.1.1.3 / CEL protein, human; EC 3.1.1.3 / Lipase
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95. Fitzgerald TL, Hickner ZJ, Schmitz M, Kort EJ: Changing incidence of pancreatic neoplasms: a 16-year review of statewide tumor registry. Pancreas; 2008 Aug;37(2):134-8
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  • [Title] Changing incidence of pancreatic neoplasms: a 16-year review of statewide tumor registry.
  • OBJECTIVES: Although most pancreatic neoplasms are adenocarcinoma, there are many other histological types, some of which may be increasing in frequency.
  • To better define these trends, we reviewed 16 years of data from a statewide tumor registry.
  • METHODS: Using the State of Michigan tumor registry, all patients with primary pancreatic cancers from 1986 to 2002 were identified, and patients were excluded if there were insufficient data or the histological subtype was not clearly defined in the literature.
  • RESULTS: There were 17,610 pancreatic neoplasms identified, and 2425 were excluded, leaving a final population of 15,185.
  • Twenty-five types of primary pancreatic neoplasms were identified.
  • The most common were adenocarcinoma, mucinous cystadenocarcinoma, nonfunctional neuroendocrine, adenosquamous, anaplastic, intraductal papillary mucinous, and acinar cell (8.37, 0.43, 0.18, 0.05, 0.04, 0.04, and 0.02 per 100,000 per year, respectively).
  • The mean age at presentation was similar for tumor types, 69.2 years old, with the exception of endocrine neoplasms occurring at a younger age, 58.5 years old (P < 0.0005).
  • There was a significant change in the incidence of nonfunctional neuroendocrine neoplasms, greater than 2-fold increase (P = 0.0003).
  • CONCLUSIONS: The incidence of most pancreatic neoplasms has changed a little; however, nonfunctional neuroendocrine neoplasms increased greater than 2-fold.
  • [MeSH-major] Pancreatic Neoplasms / epidemiology
  • [MeSH-minor] Adenocarcinoma / epidemiology. Aged. Carcinoma, Acinar Cell / epidemiology. Carcinoma, Adenosquamous / epidemiology. Carcinoma, Pancreatic Ductal / epidemiology. Cystadenocarcinoma, Mucinous / epidemiology. Female. Humans. Male. Michigan / epidemiology. Middle Aged. Neuroendocrine Tumors / epidemiology. Registries. Time Factors

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  • (PMID = 18665072.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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96. Hsu SD, Dickinson DP, Qin H, Borke J, Ogbureke KU, Winger JN, Camba AM, Bollag WB, Stöppler HJ, Sharawy MM, Schuster GS: Green tea polyphenols reduce autoimmune symptoms in a murine model for human Sjogren's syndrome and protect human salivary acinar cells from TNF-alpha-induced cytotoxicity. Autoimmunity; 2007 Mar;40(2):138-47
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  • [Title] Green tea polyphenols reduce autoimmune symptoms in a murine model for human Sjogren's syndrome and protect human salivary acinar cells from TNF-alpha-induced cytotoxicity.
  • We reported previously that the major green tea polyphenol (GTP) epigallocatechin-3-gallate (EGCG) inhibits autoantigen expression in normal human keratinocytes and immortalized normal human salivary acinar cells (Hsu et al. 2005).
  • However, it is not known whether GTPs have this effect in vivo, if they can reduce lymphocytic infiltration, or protect salivary acinar cells from tumor necrosis factor-alpha (TNF-alpha)-induced cytotoxicity.
  • Further, we show that EGCG protected normal human salivary acinar cells from TNF-alpha-induced cytotoxicity.
  • [MeSH-major] Autoimmunity. Flavonoids / pharmacology. Phenols / pharmacology. Plant Extracts / pharmacology. Salivary Glands / drug effects. Sjogren's Syndrome / immunology. Tea / chemistry. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Animals. Catechin / analogs & derivatives. Catechin / pharmacology. Cell Line. Cell Survival / drug effects. Disease Models, Animal. Humans. Imidazoles / pharmacology. Lymphocytes / immunology. Lymphocytes / pathology. MAP Kinase Kinase 4 / metabolism. MAP Kinase Kinase Kinases / antagonists & inhibitors. Mice. Mice, Inbred NOD. Phosphorylation. Polyphenols. Pyridines / pharmacology. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors

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  • (PMID = 17364504.001).
  • [ISSN] 0891-6934
  • [Journal-full-title] Autoimmunity
  • [ISO-abbreviation] Autoimmunity
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 097258-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Flavonoids; 0 / Imidazoles; 0 / Phenols; 0 / Plant Extracts; 0 / Polyphenols; 0 / Pyridines; 0 / SB 203580; 0 / Tea; 0 / Tumor Necrosis Factor-alpha; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.12.2 / MAP Kinase Kinase 4
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97. Lee J, Hwan Kim K, Kim H: Role of vascular endothelial growth factor-D (VEGF-D) on IL-6 expression in cerulein-stimulated pancreatic acinar cells. Ann N Y Acad Sci; 2007 Jan;1095:129-33
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  • [Title] Role of vascular endothelial growth factor-D (VEGF-D) on IL-6 expression in cerulein-stimulated pancreatic acinar cells.
  • Cerulein pancreatitis is similar to human edematous pancreatitis with dysregulation of the digestive enzyme production and cytoplasmic vacuolization, the death of acinar cells, edema formation, and an infiltration of inflammatory cells into the pancreas.
  • Our preliminary proteomic analysis showed increased expression of vascular endothelial growth factor-D (VEGF-D) in cerulein (10(-8)M)-treated pancreatic acinar cells.
  • We hypothesized that VEGF-D may have a role in cerulein-induced cytokine expression in pancreatic acinar cells.
  • This article was designed to elucidate whether cerulein induces VEGF-D expression in pancreatic AR42J cells, and whether VEGF-D expression is related to interleukin-6 (IL-6) expression by transfecting antisense oligonucleotide (AS ODN) for VEGF-D into pancreatic acinar AR42J cells.
  • Cerulein-induced VEGF-D expression may have a role in AP-1 activation and IL-6 expression in pancreatic acinar cells.
  • [MeSH-minor] Animals. Cell Line, Tumor. Growth Inhibitors / physiology. Rats. Transcription Factor AP-1 / metabolism


98. Yu JH, Lim JW, Kim H, Kim KH: NADPH oxidase mediates interleukin-6 expression in cerulein-stimulated pancreatic acinar cells. Int J Biochem Cell Biol; 2005 Jul;37(7):1458-69
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  • [Title] NADPH oxidase mediates interleukin-6 expression in cerulein-stimulated pancreatic acinar cells.
  • However, the source of ROS in pancreatic acinar cells has not been clarified.
  • We investigated whether pancreatic acinar cells contain NADPH oxidase, and whether NADPH oxidase mediates interleukin-6 (IL-6) in pancreatic acinar AR42J cells stimulated with cerulein.
  • As a result, pancreatic acinar AR42J cells constitutively express NADPH oxidase subunits p67phox and p47phox in the cytosol and Nox1 and p22phox in the membrane.
  • In conclusion, NADPH oxidase may mediate the expression of inflammatory cytokines by stimulating NF-kappaB activation in pancreatic acinar cells during the course of pancreatitis.
  • [MeSH-minor] Animals. Cell Line, Tumor. Electrophoretic Mobility Shift Assay. Enzyme Activation. Onium Compounds / pharmacology. Protein Subunits / antagonists & inhibitors. Protein Subunits / metabolism. Rats

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  • (PMID = 15833277.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / NF-kappa B; 0 / Onium Compounds; 0 / Protein Subunits; 0 / Reactive Oxygen Species; 6HJ411TU98 / diphenyleneiodonium; 888Y08971B / Ceruletide; EC 1.6.3.1 / NADPH Oxidase
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99. Chen P, Huang L, Zhang Y, Qiao M, Yuan Y: SiRNA-mediated PIAS1 silencing promotes inflammatory response and leads to injury of cerulein-stimulated pancreatic acinar cells via regulation of the P38MAPK signaling pathway. Int J Mol Med; 2010 Oct;26(4):619-26
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  • [Title] SiRNA-mediated PIAS1 silencing promotes inflammatory response and leads to injury of cerulein-stimulated pancreatic acinar cells via regulation of the P38MAPK signaling pathway.
  • Our aim in this study was to investigate the changes of inflammatory response by protein inhibitor of activated signal transducer and activator of transcription 1 (PIAS1) gene silencing treatment in cerulein-stimulated AR42J cells, and relate them to changes in cell injury, thus providing evidence for developing clinical therapies.
  • Consequently, the markers including DNA ladder, cell apoptotic rat, cell cycles, levels of cell cycle and apoptotic related factors were used to determine the effects of PIAS1 gene silencing on the cerulein-induced cell injury.
  • The results indicated that in the cerulein-stimulated PIASI silencing cells, the activity of P38MAPK was enhanced, while at the same time, the levels of inflammatory mediators such as the tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6 and matrix metallopeptidase-9, were markedly higher than those of other cerulein-stimulated cells.
  • Thus, the cerulein-stimulated PIASI gene-silenced cells obviously increased cell arrest in the G1/M phase by increasing P21 and P27 expression, and also induced apoptosis by regulating the P53 signaling pathway.
  • This study suggests that the down-regulation of PIAS1 is efficacious at enhancing the expression of inflammatory mediators and inducing cell injury in acute pancreatitis (AP), thus deteriorating the severity of disease.
  • [MeSH-minor] Animals. Apoptosis. Cell Line. Inflammation / genetics. Inflammation / immunology. Interleukin-6 / immunology. JNK Mitogen-Activated Protein Kinases / immunology. Pancreatitis / genetics. Pancreatitis / immunology. RNA, Small Interfering / genetics. Rats. Signal Transduction. Tumor Necrosis Factor-alpha / immunology


100. Seo JY, Masamune A, Shimosegawa T, Kim H: Protective effect of lycopene on oxidative stress-induced cell death of pancreatic acinar cells. Ann N Y Acad Sci; 2009 Aug;1171:570-5
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  • [Title] Protective effect of lycopene on oxidative stress-induced cell death of pancreatic acinar cells.
  • In the present study, we aim to investigate whether lycopene protects oxidative stress-induced cell death of pancreatic acinar AR42J cells by preventing the loss of Ku70 in the nucleus.
  • Viable cell numbers, the levels of H(2)O(2) in the medium, level of Ku70 protein, and Ku-DNA-binding activity were determined.
  • As a result, glucose/glucose oxidase induced the decrease in cell viability, increase in H(2)O(2) production, decrease in Ku70 levels in whole-cell extracts and nuclear extracts, and decrease in Ku-DNA-binding activity of AR42J cells.
  • Lycopene inhibited glucose/glucose oxidase-induced cell death by preventing nuclear loss of Ku70 and a decrease in Ku-DNA-binding activity of AR42J cells.
  • In conclusion, lycopene may be beneficial for the treatment of oxidative stress-induced cell death by preventing loss of DNA repair protein Ku70.
  • [MeSH-minor] Animals. Antigens, Nuclear / metabolism. Antioxidants / pharmacology. Cell Line, Tumor. Cell Survival / drug effects. DNA-Binding Proteins / metabolism. Hydrogen Peroxide / metabolism. Oligonucleotides / genetics. Oligonucleotides / metabolism. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Protein Binding / drug effects. Rats. Time Factors

  • Hazardous Substances Data Bank. HYDROGEN PEROXIDE .
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  • [ErratumIn] Ann N Y Acad Sci. 2009 Oct;1178:319
  • (PMID = 19723106.001).
  • [ISSN] 1749-6632
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Antioxidants; 0 / DNA-Binding Proteins; 0 / Ku autoantigen; 0 / Oligonucleotides; 0 / Protective Agents; 36-88-4 / Carotenoids; BBX060AN9V / Hydrogen Peroxide; SB0N2N0WV6 / lycopene
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