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1. Cariaga-Martinez AE, Lorenzati MA, Riera MA, Cubilla MA, De La Rossa A, Giorgio EM, Tiscornia MM, Gimenez EM, Rojas ME, Chaneton BJ, Rodríguez DI, Zapata PD: Tumoral prostate shows different expression pattern of somatostatin receptor 2 (SSTR2) and phosphotyrosine phosphatase SHP-1 (PTPN6) according to tumor progression. Adv Urol; 2009;:723831
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  • [Title] Tumoral prostate shows different expression pattern of somatostatin receptor 2 (SSTR2) and phosphotyrosine phosphatase SHP-1 (PTPN6) according to tumor progression.
  • Many studies on SHP-1 revealed that the expression of this protein was diminished or abolished in several of the cancer cell lines and tissues examined.
  • However, it is necessary to confront the cell lines data with real situation in cancer cases.
  • Our studies have shown that epithelial expressions of both proteins, SHP-1 and SSTR2, in normal and benign hyperplasia are localized in the luminal side of duct and acinar cells.

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  • (PMID = 19365586.001).
  • [ISSN] 1687-6369
  • [Journal-full-title] Advances in urology
  • [ISO-abbreviation] Adv Urol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2667939
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2. Xu M, Yuan Y, Xia Y, Achilefu S: Monoclonal antibody CC188 binds a carbohydrate epitope expressed on the surface of both colorectal cancer stem cells and their differentiated progeny. Clin Cancer Res; 2008 Nov 15;14(22):7461-9
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  • Targeting both CSCs and differentiated, rapidly proliferating tumor cells with therapeutic drugs provides a focused strategy to treat cancer.
  • We characterized mAb CC188 binding epitope and examined the epitope distribution in normal and tumor tissues, particularly in CSCs using tissue arrays and immunofluorescence staining method.
  • We also evaluated the effect of mAb CC188 on invasiveness of NSY tumor cells.
  • In contrast, the expression of the carbohydrate epitope was low in normal prostate muscle and pancreatic acinar cells, as well as in some normal epithelial cells of the breast duct, cervix, and skin.
  • A functional study indicated that mAb CC188 suppressed the invasiveness of NSY tumor cells.
  • CONCLUSION: mAb CC188 selectively targets a carbohydrate epitope expressed on cancer cells, providing a viable method for specific tumor imaging and targeted therapy.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antigens, Neoplasm / immunology. Carbohydrates / immunology. Colorectal Neoplasms / immunology. Epitopes, B-Lymphocyte / immunology. Neoplastic Stem Cells / immunology
  • [MeSH-minor] Antibody Specificity. Cell Differentiation. Cell Line, Tumor. Fluorescent Antibody Technique. Humans. Immunohistochemistry. Immunomagnetic Separation. Neoplasm Invasiveness / immunology. Tissue Array Analysis

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  • (PMID = 19010863.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109754; United States / NIBIB NIH HHS / EB / R01 EB1430; United States / NCI NIH HHS / CA / R21 CA123537
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Carbohydrates; 0 / Epitopes, B-Lymphocyte
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3. Kitoh H, Ryozawa S, Harada T, Kondoh S, Furuya T, Kawauchi S, Oga A, Okita K, Sasaki K: Comparative genomic hybridization analysis for pancreatic cancer specimens obtained by endoscopic ultrasonography-guided fine-needle aspiration. J Gastroenterol; 2005 May;40(5):511-7
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  • Tumor cells were selected by microdissection.
  • Both of the patients with acinar cell carcinoma showed gains of 2q and 5p, and losses of 1p, 9p, 9q, 11p, 11q, 14q, 17p, 17q, and 18q.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / ultrasonography. Biopsy, Fine-Needle / methods. Nucleic Acid Hybridization. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / ultrasonography

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  • (PMID = 15942717.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
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4. Wilcox RA: Measurement of calcium fluxes in permeabilized cells using a ⁴⁵Ca²+ uptake and release assay. Methods Mol Biol; 2005;312:205-12
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  • Many cell surface receptors activate phosphoinositidase(s) C, via G proteins that catalyze the hydrolysis of phosphatidylinositol 4,5-biphosphate to produce the second messengers, inositol(1,4,5)trisphosphate [Ins(1,4,5)P(3)] and diacylglycerol.
  • Consequently, Ins(1,4,5)P(3)-induced Ca(2+) release was initially demonstrated in permeabilized pancreatic acinar cells, and all subsequent studies in cells have involved the introduction of Ins(1,4,5)P(3) by rendering a cell population permeable, using microinjection techniques or by the presentation of chemically modified membrane-permeable Ins(1,4,5)P(3) analogs, such as photolabile "caged Ins(1,4,5)P(3)" (5).
  • The author will describe a (45)Ca(2+)-release assay used to monitor Ins(1,4,5)P(3)-induced Ca(2+) mobilization from nonmitochondrial intracellular Ca(2+) stores using "cytosol-like" buffer (CLB) and permeabilized SH-SY5Y neuroblastoma cell populations.
  • [MeSH-major] Calcium / metabolism. Calcium Radioisotopes / metabolism. Cell Membrane Permeability. Inositol 1,4,5-Trisphosphate / pharmacology
  • [MeSH-minor] Calcium Channels / metabolism. Cell Line, Tumor. Cytosol / metabolism. Humans. Inositol 1,4,5-Trisphosphate Receptors / metabolism. Neuroblastoma

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  • (PMID = 21341101.001).
  • [ISSN] 1940-6029
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium Channels; 0 / Calcium Radioisotopes; 0 / Inositol 1,4,5-Trisphosphate Receptors; 85166-31-0 / Inositol 1,4,5-Trisphosphate; SY7Q814VUP / Calcium
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5. 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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6. Li S, Bobek LA: Functional analysis of human MUC7 mucin gene 5'-flanking region in lung epithelial cells. Am J Respir Cell Mol Biol; 2006 Nov;35(5):593-601
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  • MUC7 gene expression is tissue- and cell-specific, with dominant expression in salivary gland acinar cells.
  • To begin to understand the molecular mechanisms responsible for controlling MUC7 gene expression, we analyzed the promoter activity of MUC7 5'-flanking region in a human lung epithelial cell line A549.
  • We demonstrated that MUC7 gene is expressed constitutively in this cell line and is upregulated by TNF-alpha stimulation.

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  • (PMID = 16778149.001).
  • [ISSN] 1044-1549
  • [Journal-full-title] American journal of respiratory cell and molecular biology
  • [ISO-abbreviation] Am. J. Respir. Cell Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / DE009820; United States / NIDCR NIH HHS / DE / T32-DE007034
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MUC7 protein, human; 0 / Mucins; 0 / NF-kappa B; 0 / Salivary Proteins and Peptides; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2643277
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7. De Lisle RC, Xu W, Roe BA, Ziemer D: Effects of Muclin (Dmbt1) deficiency on the gastrointestinal system. Am J Physiol Gastrointest Liver Physiol; 2008 Mar;294(3):G717-27
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  • Functions proposed for Dmbt1 include it being a tumor suppressor, having roles in innate immune defense and inflammation, and being a Golgi-sorting receptor in the exocrine pancreas.
  • The Muclin-deficient mice did not develop GI tumors, even when crossed with mice lacking the known tumor suppressor p53.
  • Exocrine pancreatic function was impaired, as measured by attenuated neurohormonal-stimulated amylase release from Muclin-deficient acinar cells.


8. Yang H, Lu X, Qian J, Xu F, Hu Y, Yu Y, Bast RC, Li J: Imprinted tumor suppressor gene ARHI induces apoptosis correlated with changes in DNA methylation in pancreatic cancer cells. Mol Med Rep; 2010 Jul-Aug;3(4):581-7
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  • [Title] Imprinted tumor suppressor gene ARHI induces apoptosis correlated with changes in DNA methylation in pancreatic cancer cells.
  • Six pancreatic cancer cell lines, tumor xenografts in nude mice and 20 pancreatic cancer tissue sections were analyzed.
  • ARHI is widely expressed in ductal and acinar cells of normal pancreatic tissue, but is down-regulated or lost in approximately 50% of pancreatic cancers.
  • Aberrant methylation of the ARHI locus was found in five pancreatic cancer cell lines, which exhibited down-regulation or loss of ARHI expression.
  • Hypermethylation was detected in five cell lines (5/5, 100%) at CpG island I, in two cell lines (2/5, 40%) at CpG island II and in four cell lines (4/5, 80%) at CpG island III.
  • Treatment with the demethylating agent 5-aza-2'deoxycytidine (5-aza-dC) restored ARHI mRNA expression, inhibited cell growth and induced apoptosis in PANC-1 and P3 human pancreatic cancer cells in culture.
  • A demethylation agent reduced human pancreatic cancer cell line growth in conjunction with ARHI re-expression.

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  • (PMID = 21472283.001).
  • [ISSN] 1791-3004
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA016672-36; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P30 CA016672-36
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Other-IDs] NLM/ NIHMS292087; NLM/ PMC3097896
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9. Lewis CM, Herbert BS, Bu D, Halloway S, Beck A, Shadeo A, Zhang C, Ashfaq R, Shay JW, Euhus DM: Telomerase immortalization of human mammary epithelial cells derived from a BRCA2 mutation carrier. Breast Cancer Res Treat; 2006 Sep;99(1):103-15
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  • A novel human mammary epithelial cell line, HME348, was established from benign breast tissue from a 44-year-old germ-line BRCA2 mutation carrier with a history of stage 1 breast cancer.
  • Three clones derived from this culture were also p63(+)/ESA(+)/EMA(+/-) on glass but formed similar acinar structures with both luminal and myoepithelial cell differentiation in Matrigel confirming the mammary progenitor nature of these cells.
  • As this is the first report establishing and characterizing a benign human mammary epithelial cell line derived from a BRCA2 patient without the use of viral oncogenes, these cells may be useful for the study of BRCA2 function in breast morphogenesis and carcinogenesis.
  • [MeSH-minor] Animals. Cell Culture Techniques / methods. Collagen / pharmacology. Comet Assay. Drug Combinations. Humans. Laminin / pharmacology. Mice. Mice, Nude. Neoplasm Transplantation. Proteoglycans / pharmacology. Telomere / ultrastructure. Tumor Cells, Cultured

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  • (PMID = 16541310.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [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] Netherlands
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 2.7.7.49 / Telomerase
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10. Li T, Sotgia F, Vuolo MA, Li M, Yang WC, Pestell RG, Sparano JA, Lisanti MP: Caveolin-1 mutations in human breast cancer: functional association with estrogen receptor alpha-positive status. Am J Pathol; 2006 Jun;168(6):1998-2013
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  • Here, we developed a novel allele-specific real-time PCR assay to detect the Cav-1 P132L mutation in mammary tumor cells isolated by laser capture microdissection from formalin-fixed paraffin-embedded breast cancer samples.
  • To mechanistically dissect the functional relationship between Cav-1 gene inactivation and ERalpha expression, we isolated primary mammary epithelial cells from wild-type and Cav-1-/- mice and cultured them in a three-dimensional system, allowing them to form mammary acinar-like structures.
  • [MeSH-major] Breast Neoplasms / genetics. Caveolin 1 / genetics. Caveolin 1 / physiology. Cyclin D1 / genetics. Estrogen Receptor alpha / genetics. Mammary Neoplasms, Animal / genetics. Mutation


11. 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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12. 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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13. Erkan M, Kleeff J, Esposito I, Giese T, Ketterer K, Büchler MW, Giese NA, Friess H: Loss of BNIP3 expression is a late event in pancreatic cancer contributing to chemoresistance and worsened prognosis. Oncogene; 2005 Jun 23;24(27):4421-32
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  • In the present study, the hypoxia-inducible proapoptotic gene, BNIP3, was analysed in terms of expression, effect on patient survival, and chemo-responsiveness in pancreatic cancer cell lines. cDNA microarray, real-time light cycler quantitative polymerase chain reaction, laser-capture microdissection, and immunohistochemistry analyses were used to evaluate BNIP3 expression in normal and diseased pancreatic specimens.
  • By immunohistochemistry, BNIP3 was predominantly expressed in the acinar cells of the normal and diseased pancreas.
  • Hypoxia induced BNIP3 expression in four out of eight pancreatic cancer cell lines, while it was absent under normoxic and hypoxic conditions in the remaining four.
  • [MeSH-major] Deoxycytidine / analogs & derivatives. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Membrane Proteins / deficiency. Membrane Proteins / genetics. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology. Proto-Oncogene Proteins / deficiency. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Cell Line, Tumor. Fluorouracil / pharmacology. Humans. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Survival Rate

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  • (PMID = 15856026.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BNIP3 protein, human; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; U3P01618RT / Fluorouracil
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14. Sisto M, Lisi S, Lofrumento DD, Ingravallo G, Mitolo V, D'Amore M: Expression of pro-inflammatory TACE-TNF-α-amphiregulin axis in Sjögren's syndrome salivary glands. Histochem Cell Biol; 2010 Oct;134(4):345-53
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  • The tumor-necrosis-factor-converting-enzyme (TACE)-TNF-α-Amphiregulin (AREG) axis plays an important pathogenic role in inflammatory and autoimmune disorders.
  • This study showed that Furin, TACE, TNF-α, and AREG proteins, detected in acinar and ductal cells of human salivary glands from SS patients, increased remarkably in comparison with biopsies of labial salivary glands from healthy controls.
  • [MeSH-minor] ADAM17 Protein. Amphiregulin. Base Sequence. Blotting, Western. Cytokines / genetics. Cytokines / metabolism. DNA, Complementary. EGF Family of Proteins. Humans. Immunohistochemistry. Inflammation. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 20811902.001).
  • [ISSN] 1432-119X
  • [Journal-full-title] Histochemistry and cell biology
  • [ISO-abbreviation] Histochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / AREG protein, human; 0 / Amphiregulin; 0 / Cytokines; 0 / DNA, Complementary; 0 / EGF Family of Proteins; 0 / Glycoproteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Tumor Necrosis Factor-alpha; EC 3.4.21.75 / Furin; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.86 / ADAM17 Protein; EC 3.4.24.86 / ADAM17 protein, human
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15. Prieto-Rodríguez M, Artés-Martínez MJ, Navarro-Hervás M, Camañas-Sanz A, Vera-Sempere FJ: Cytological characteristics of acinic cell carcinoma (ACC) diagnosed by fine-needle aspiration biopsy (FNAB). A study of four cases. Med Oral Patol Oral Cir Bucal; 2005 Mar-Apr;10(2):103-8
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  • [Title] Cytological characteristics of acinic cell carcinoma (ACC) diagnosed by fine-needle aspiration biopsy (FNAB). A study of four cases.
  • OBJECTIVE: To present the cytopathological characteristics of acinic cell carcinoma (ACC) as well as its cyto-histological correlation, commenting on the differential diagnostic problems of this entity based on four observations studied using fine-needle aspiration biopsy (FNAB).
  • CYTOLOGICAL FINDINGS: The cytologic smears revealed abundant tumoral cellularity arranged in small monolayered sheets, forming acinar structures or isolated cells.
  • The diagnosis of ACCs frequently presents difficulties, owing to the great cytologic similarity of the tumor cells with the normal acinar component of the salivary gland.
  • The differential diagnosis is considered, fundamentally, with clear cell carcinomas, mucoepidermoid carcinomas, Warthin s tumor, and oncocytomas.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Salivary Gland Neoplasms / pathology. Salivary Glands / pathology

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  • (PMID = 15735541.001).
  • [ISSN] 1698-6946
  • [Journal-full-title] Medicina oral, patología oral y cirugía bucal
  • [ISO-abbreviation] Med Oral Patol Oral Cir Bucal
  • [Language] eng; spa
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Spain
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16. Bonkhoff H: [Differential diagnosis of prostate cancer: impact of pattern analysis and immunohistochemistry]. Pathologe; 2005 Nov;26(6):405-21
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  • Basal cell markers (34betaE12 and P63) are very useful to analyze histo-architectural features of small and large glandular lesions.
  • AMACR (P504 s) is helpful not only in identifying small amount of cancer in needle biopsies but also in the diagnosis of high grade prostatic intra epithelial neoplasia (HGPIN).
  • A number of lesions which may be confused with small acinar adenocarcinoma (Cowper's gland, nephrogenic metaplasia, mesonephric glands) and poorly differentiated prostate cancer (urothelial neoplasia, mucinous colon cancer and other metastatic lesions) lacks convincing PSA immunoreactivity.
  • Basal cell markers and the nuclear androgen receptors are important markers to differentiate Gleason grade 5 A und 5 B patterns from prostatic involvement by transitional cell carcinoma.
  • [MeSH-major] Biomarkers, Tumor / analysis. Prostate / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Carcinoma, Basal Cell / pathology. Cell Division / physiology. Diagnosis, Differential. Humans. Male. Prostatic Hyperplasia / pathology. Prostatic Intraepithelial Neoplasia / pathology


17. Perez EA, Gutierrez JC, Koniaris LG, Neville HL, Thompson WR, Sola JE: Malignant pancreatic tumors: incidence and outcome in 58 pediatric patients. J Pediatr Surg; 2009 Jan;44(1):197-203
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  • RESULTS: Malignant pancreatic neoplasms were identified in 58 patients.
  • Exocrine tumors included pancreatoblastoma (n = 10), solid-cystic tumor (SCT) (n = 10), ductal adenocarcinoma (DA) (n = 7), and acinar cell carcinoma (ACC) (n = 4).
  • Ductal adenocarcinoma, SCT, acinar cell carcinoma, sarcomas, and endocrine tumors were more common in children older than 10 years, whereas pancreatoblastoma was more common in younger children (P = .045).
  • There was a significant difference in tumor type 15-year survival with DA having the worst (23%) and SCT the best (100%).
  • CONCLUSIONS: Pediatric pancreatic neoplasms are uncommon and carry a variable prognosis.
  • [MeSH-major] Pancreatic Neoplasms / epidemiology. Pancreatic Neoplasms / surgery

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  • (PMID = 19159743.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Sakai A, Sugawara Y, Kuroishi T, Sasano T, Sugawara S: Identification of IL-18 and Th17 cells in salivary glands of patients with Sjögren's syndrome, and amplification of IL-17-mediated secretion of inflammatory cytokines from salivary gland cells by IL-18. J Immunol; 2008 Aug 15;181(4):2898-906
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  • This study showed that the expression of IL-18 was detected in acinar cells, intraducts, and CD68(+) macrophages in salivary glands of SS patients, but not in those of healthy subjects or patients with chronic graft-vs-host disease, by immunohistochemistry, and immunoblot analysis revealed that 24-kDa precursor form of IL-18 (proIL-18) and 18-kDa mature IL-18 were detected in SS salivary glands.
  • Human salivary gland HSY and acinar AZA3 cells constitutively expressed proIL-18 and caspase-1, and a calcium ionophore A23187 induced the secretion of IL-18 from the cells.
  • HSY and AZA3 cells expressed IL-18R and IL-17R on the cell surface, and IL-18 amplified the secretion of IL-6 and IL-8 that were induced by low amounts of IL-17.
  • [MeSH-minor] Adult. Cell Line, Tumor. Cell Movement / immunology. Cells, Cultured. Humans

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  • (PMID = 18684981.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Inflammation Mediators; 0 / Interleukin-17; 0 / Interleukin-18
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19. 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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20. 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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21. Fehr A, Stenman G, Bullerdiek J, Löning T: [Molecular markers in salivary gland tumors: their use in diagnostic and prognostic workup]. Pathologe; 2009 Nov;30(6):466-71
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  • The molecular genetic background of salivary gland neoplasms has not been characterized in detail to date.
  • One of the major advantages of molecular tumor markers is that valid results are obtained on minute cell and/or tissue samples.
  • This is also true for the most frequent malignant salivary gland tumors after the mucoepidermoid carcinoma, i.e. adenoid cystic carcinomas and acinic cell carcinomas.
  • [MeSH-major] Biomarkers, Tumor / genetics. Neoplasm Proteins / genetics. Salivary Gland Neoplasms / diagnosis. Salivary Gland Neoplasms / genetics. Salivary Gland Neoplasms / pathology
  • [MeSH-minor] Adenoma, Pleomorphic / diagnosis. Adenoma, Pleomorphic / genetics. Adenoma, Pleomorphic / pathology. Carcinoma, Acinar Cell. Carcinoma, Adenoid Cystic. Carcinoma, Mucoepidermoid / diagnosis. Carcinoma, Mucoepidermoid / genetics. Carcinoma, Mucoepidermoid / pathology. Chromosome Aberrations. Comparative Genomic Hybridization. DNA Mutational Analysis. DNA-Binding Proteins. Gene Fusion. HMGA2 Protein. Humans. Nuclear Proteins. Prognosis. Protein Array Analysis. Salivary Glands / pathology. Transcription Factors

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  • (PMID = 19784654.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CRTC1 protein, human; 0 / DNA-Binding Proteins; 0 / HMGA2 Protein; 0 / MAML2 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / PLAG1 protein, human; 0 / Transcription Factors
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22. Stanger BZ, Stiles B, Lauwers GY, Bardeesy N, Mendoza M, Wang Y, Greenwood A, Cheng KH, McLaughlin M, Brown D, Depinho RA, Wu H, Melton DA, Dor Y: Pten constrains centroacinar cell expansion and malignant transformation in the pancreas. Cancer Cell; 2005 Sep;8(3):185-95
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  • [Title] Pten constrains centroacinar cell expansion and malignant transformation in the pancreas.
  • Knockout mice display progressive replacement of the acinar pancreas with highly proliferative ductal structures that contain abundant mucins and express Pdx1 and Hes1, two markers of pancreatic progenitor cells.
  • We provide evidence that ductal metaplasia results from the expansion of centroacinar cells rather than transdifferentiation of acinar cells.
  • These results indicate that Pten actively maintains the balance between different cell types in the adult pancreas and that misregulation of the PI3-K pathway in centroacinar cells may contribute to the initiation of pancreatic carcinoma in vivo.
  • [MeSH-major] Pancreatic Neoplasms / pathology. Protein Tyrosine Phosphatases / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Animals. Cell Differentiation. Cell Transformation, Neoplastic. Metaplasia / pathology. Mice. PTEN Phosphohydrolase. Pancreas / pathology. Pancreas / physiopathology. Pancreas / ultrastructure

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  • (PMID = 16169464.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK064136
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
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23. Hansel DE, Nakayama M, Luo J, Abukhdeir AM, Park BH, Bieberich CJ, Hicks JL, Eisenberger M, Nelson WG, Mostwin JL, De Marzo AM: Shared TP53 gene mutation in morphologically and phenotypically distinct concurrent primary small cell neuroendocrine carcinoma and adenocarcinoma of the prostate. Prostate; 2009 May 1;69(6):603-9
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  • [Title] Shared TP53 gene mutation in morphologically and phenotypically distinct concurrent primary small cell neuroendocrine carcinoma and adenocarcinoma of the prostate.
  • BACKGROUND: Small cell carcinoma of the prostate is an uncommon neoplasm, the origin of which has been controversial.
  • To address this, we performed transcriptome profiling and TP53 sequencing of concurrent small cell and prostatic adenocarcinoma to determine the relationship between these entities.
  • METHODS: We identified an unusual case of primary prostate cancer that contained adjacent acinar adenocarcinoma (Gleason score 4 + 3 = 7) and small cell carcinoma.
  • We performed laser capture microdissection to isolate tumor components and performed gene expression and TP53 gene sequence analysis on each component, with results validated by immunohistochemistry for PSA, PSAP, PSMA, androgen receptor, NKX 3.1 and neuroendocrine markers.
  • RESULTS: Transcriptome profiling of the carcinoma components identified 99 genes with a greater than 10-fold differential expression between prostatic adenocarcinoma and small cell carcinoma, many of which have not been previously reported in prostate cancer.
  • The small cell carcinoma component demonstrated upregulation of proliferative and neuroendocrine markers and tyrosine kinase receptors, and downregulation of cell adhesion molecules, supporting the aggressive nature of this form of carcinoma.
  • CONCLUSIONS: This is the first report of a primary small cell carcinoma of the prostate subjected to extensive molecular analysis and the first to show a clonal relation between two morphologically distinct prostate cancer types.
  • The evidence of progression to small cell carcinoma may yield important insights into the pathogenesis of this entity and provide a novel spectrum of molecular markers to further dissect cellular pathways important in tumor progression.

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
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  • (PMID = 19125417.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA058236-10; United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P50 CA058236; United States / NCI NIH HHS / CA / P50 CA058236-10
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Other-IDs] NLM/ NIHMS285484; NLM/ PMC3170854
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24. Siveke JT, Lubeseder-Martellato C, Lee M, Mazur PK, Nakhai H, Radtke F, Schmid RM: Notch signaling is required for exocrine regeneration after acute pancreatitis. Gastroenterology; 2008 Feb;134(2):544-55
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  • To investigate Notch and beta-catenin interaction, acinar 266-6 cells were analyzed using transfection and biochemical assays.
  • RESULTS: Loss of Notch signaling results in impaired regeneration after acute pancreatitis with fewer mature acinar cells in dibenzazepine-treated and Notch1-deficient mice in the regenerative phase 3 days after induction. beta-catenin expression was increased and prolonged during exocrine regeneration.
  • Our results suggest an interaction of Notch and Wnt signaling in pancreatic acinar cells, providing evidence for a role of these pathways in the regulation of the maturation process of acinar cells.
  • [MeSH-minor] Acute Disease. Amyloid Precursor Protein Secretases / antagonists & inhibitors. Animals. Cell Line, Tumor. Ceruletide. Dibenzazepines / pharmacology. Disease Models, Animal. Mice. Mice, Inbred C57BL. Mice, Knockout. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / physiopathology. Signal Transduction / physiology. Wnt Proteins / physiology

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  • (PMID = 18242220.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dibenzazepines; 0 / Notch1 protein, mouse; 0 / Receptor, Notch1; 0 / Wnt Proteins; 0 / beta Catenin; 888Y08971B / Ceruletide; EC 3.4.- / Amyloid Precursor Protein Secretases
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25. Zhao J, Epstein JI: High-grade foamy gland prostatic adenocarcinoma on biopsy or transurethral resection: a morphologic study of 55 cases. Am J Surg Pathol; 2009 Apr;33(4):583-90
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  • [Title] High-grade foamy gland prostatic adenocarcinoma on biopsy or transurethral resection: a morphologic study of 55 cases.
  • The morphologic features of high foamy gland carcinoma have not been previously studied.
  • On average, 84% of the total tumor volume was foamy gland carcinoma, with high-grade foamy gland cancer averaging 73% of the total foamy gland carcinoma.
  • Concurrent ordinary acinar nonfoamy adenocarcinoma was encountered in 26 of 55 cases (47%) with the following Gleason scores: Gleason 6 (27%); Gleason 7 (27%); and Gleason 8 to 10 (46%).
  • Associated ordinary high-grade prostatic intraepithelial neoplasia and foamy gland variant of high-grade prostatic intraepithelial neoplasia/intraductal adenocarcinoma were seen in 13 cases (24%) and 11 cases (20%), respectively.
  • Of the 19 cases with available immunohistochemical stains for high molecular weight cytokeratin, 7 (37%) showed nonspecific labeling of cancer cells in a nonbasal cell pattern.
  • High-grade foamy gland cancer shares certain morphologic features with more typical lower-grade foamy gland cancer including relatively bland nuclei with more difficult to identify nucleoli and frequent intraluminal dense pink secretions.
  • [MeSH-major] Adenocarcinoma / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Biopsy, Needle. Cell Nucleolus / pathology. Humans. Keratin-7 / analysis. Male. Middle Aged. Mitosis. Neoplasm Invasiveness / pathology. Prostatic Intraepithelial Neoplasia / pathology. Transurethral Resection of Prostate

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  • (PMID = 19033862.001).
  • [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 / Keratin-7
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26. Zhang XP, Chen L, Hu QF, Tian H, Xu RJ, Wang ZW, Wang KY, Cheng QH, Yan W, Li Y, Li QY, He Q, Wang F: Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis. World J Gastroenterol; 2007 Nov 7;13(41):5506-11
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  • [Title] Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis.
  • Their contents of amylase and endotoxin in plasma and contents of tumor necrosis factor (TNF-alpha), phospholipase A(2) (PLA(2)) and IL-6 in serum were also determined.
  • CONCLUSION: The mechanism of dexamethasone treatment in acute pancreatitis is related to its inhibition of inflammatory mediator generation and induction of pancreatic acinar cell apoptosis.
  • [MeSH-minor] Acute Disease. Amylases / blood. Animals. Ascites / pathology. Ascites / prevention & control. Body Weight / drug effects. Disease Models, Animal. Dose-Response Relationship, Drug. Endotoxins / blood. Interleukin-6 / blood. Male. Phospholipases A2 / blood. Rats. Rats, Sprague-Dawley. Severity of Illness Index. Time Factors. Tissue Array Analysis. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 17907297.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Endotoxins; 0 / Inflammation Mediators; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 7S5I7G3JQL / Dexamethasone; EC 3.1.1.4 / Phospholipases A2; EC 3.2.1.- / Amylases
  • [Other-IDs] NLM/ PMC4171288
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27. Hammami B, Dhouib H, Sallemi M, Ben Hmida A, Ben Mahfoudh K, Daoud J, Ghorbel A: [Acinic cell carcinoma of the nasal septum]. Rev Stomatol Chir Maxillofac; 2010 Apr;111(2):88-90
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  • [Title] [Acinic cell carcinoma of the nasal septum].
  • INTRODUCTION: Nasal cavity acinic carcinoma are exceptional and often of turbinal origin.
  • We report a case of acinic carcinoma of septal origin and discuss this histological type rare in this site.
  • The surgical treatment was endonasal tumor resection.
  • The histological examination revealed a nasal fossa acinic carcinoma completely resected.
  • DISCUSSION: Acinic carcinoma is rarely located in the nasal cavity.
  • The prognosis is related to tumor extension and quality of resection.
  • [MeSH-major] Carcinoma, Acinar Cell / surgery. Nasal Septum / pathology. Nose Neoplasms / surgery

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  • (PMID = 19942241.001).
  • [ISSN] 1776-257X
  • [Journal-full-title] Revue de stomatologie et de chirurgie maxillo-faciale
  • [ISO-abbreviation] Rev Stomatol Chir Maxillofac
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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28. 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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29. Machado MC, Coelho AM, Martins JO, Sampietre SN, Molan NA, Patzina RA, Machado MA, Jancar S: CO2 abdominal insufflation decreases local and systemic inflammatory response in experimental acute pancreatitis. Pancreas; 2010 Mar;39(2):175-81
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  • Inflammatory parameters were evaluated in the peritoneum (ascites, cell number, and tumor necrosis factor alpha [TNF-alpha]), serum (amylase, TNF-alpha, interleukin-6 [IL-6], and IL-10), pancreas (myeloperoxidase [MPO] activity, cyclo-oxygenase 2 and inducible nitric oxide synthase expression, and histological diagnosis), liver, and lung (mitochondria dysfunction and MPO activity).
  • In the pancreas, this treatment reduced MPO activity, acinar and fat necrosis, and the expression of inducible nitric oxide synthase and cyclo-oxygenase 2.
  • [MeSH-minor] Amylases / blood. Animals. Ascites / immunology. Ascites / prevention & control. Cyclooxygenase 2 / metabolism. Disease Models, Animal. Inflammation Mediators / blood. Interleukin-10 / blood. Interleukin-6 / blood. Lung / immunology. Male. Mitochondria, Liver / metabolism. Nitric Oxide Synthase Type II / metabolism. Oxidation-Reduction. Oxidative Phosphorylation. Peroxidase / metabolism. Rats. Rats, Wistar. Taurocholic Acid. Time Factors. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 19924017.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Inflammation Mediators; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 142M471B3J / Carbon Dioxide; 5E090O0G3Z / Taurocholic Acid; EC 1.11.1.7 / Peroxidase; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, rat; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Ptgs2 protein, rat; EC 3.2.1.- / Amylases
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30. Parikh B, Jojo A, Shah B, Bansal R, Trivedi P, Shah MJ: Fine needle aspiration cytology of hepatoblastoma: a study of 20 cases. Indian J Pathol Microbiol; 2005 Jul;48(3):331-6
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  • Hepatoblastoma (HBL) is the most common primary malignant hepatic tumor in children.
  • Morphologically, the tumor cells were commonly arranged in acinar pattern, papillary pattern, or in sheets.
  • Hence, cytoarchitecture in combination with clinicalfeatures, imaging techniques and serum a-fetoprotein levels were helpful for specific diagnosis of HBL and to rule out various others differential diagnosis of small round cell tumor.
  • [MeSH-major] Hepatoblastoma. Liver Neoplasms

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  • (PMID = 16761744.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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31. Shet T, Ramadwar M, Sharma S, Laskar S, Arora B, Kurkure P: An eyelid sialoblastoma-like tumor with a sarcomatoid myoepithelial component. Pediatr Dev Pathol; 2007 Jul-Aug;10(4):309-14
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  • [Title] An eyelid sialoblastoma-like tumor with a sarcomatoid myoepithelial component.
  • Nonround cell tumors are rare in children and often difficult to diagnose.
  • Histologically, the tumor had nests of basaloid and relatively round cells with immature acinar or ductular structures similar to those seen in a conventional sialoblastoma, but these nests were embedded in a malignant spindle cell stroma.
  • Overall histologic features suggested a tumor similar to a sialoblastoma with sarcomatoid transformation of the myoepithelial component, hitherto not described in literature.
  • This tumor probably arose from the palpebral lobe of the lacrimal gland.
  • Awareness of this unusual histology of sialoblastoma will help in avoiding misdiagnosis and also refine treatment-related issues on this rare tumor.
  • [MeSH-major] Eyelid Neoplasms / pathology. Myoepithelioma / pathology. Sarcoma / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Combined Modality Therapy. Desmosomes / ultrastructure. Disease-Free Survival. Humans. Immunohistochemistry. Infant. Treatment Outcome

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  • (PMID = 17638426.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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32. 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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33. Uzaslan E, Stuempel T, Ebsen M, Freudenberg N, Nakamura S, Costabel U, Guzman J: Surfactant protein A detection in primary pulmonary adenocarcinoma without bronchioloalveolar pattern. Respiration; 2005 May-Jun;72(3):249-53
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  • BACKGROUND: Immunohistochemical studies in human lung carcinoma reported positive staining of tumor cells for surfactant protein A (SP-A), especially in peripheral airway cell carcinoma, which include bronchioloalveolar carcinoma and in some reports also papillary subtypes.
  • OBJECTIVE: The purpose of this study was to determine the SP-A expression in tumor cells of lung adenocarcinoma without a bronchioloalveolar pattern, classified according to the WHO.
  • METHODS: In total, 169 primary adenocarcinomas of the lung (109 acinar, 32 solid with mucin, 24 papillary and 4 mucinous) were examined by immunohistochemistry for SP-A expression.
  • RESULTS: Twenty-five percent of acinar, 38% of papillary and 3% of solid adenocarcinoma with mucin showed a positive intracytoplasmic SP-A reaction of the tumor cells.
  • This study included the largest number of acinar adenocarcinomas and solid adenocarcinomas with mucin studied for SP-A.
  • A positive staining of hyperplastic type II cells surrounding the tumors or entrapped in the tumor could clearly be differentiated from the SP-A-positive stain of tumor cells.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Lung Neoplasms / metabolism. Pulmonary Surfactant-Associated Protein A / metabolism
  • [MeSH-minor] Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Mucinous / pathology. Adenocarcinoma, Papillary / metabolism. Adenocarcinoma, Papillary / pathology. Carcinoma, Acinar Cell / metabolism. Carcinoma, Acinar Cell / pathology. Humans

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  • [Copyright] Copyright 2005 S. Karger AG, Basel
  • (PMID = 15942293.001).
  • [ISSN] 0025-7931
  • [Journal-full-title] Respiration; international review of thoracic diseases
  • [ISO-abbreviation] Respiration
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Pulmonary Surfactant-Associated Protein A
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34. Thrall M, Jessurun J, Stelow EB, Adsay NV, Vickers SM, Whitson AK, Saltzman DA, Pambuccian SE: Multicystic adenomatoid hamartoma of the pancreas: a hitherto undescribed pancreatic tumor occurring in a 3-year-old boy. Pediatr Dev Pathol; 2008 Jul-Aug;11(4):314-20
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  • [Title] Multicystic adenomatoid hamartoma of the pancreas: a hitherto undescribed pancreatic tumor occurring in a 3-year-old boy.
  • This report describes an unusual pancreatic tumor in a 3-year-old boy.
  • Acinar and endocrine cells were often seen budding into the ducts forming "ductulo-insular bodies."
  • [MeSH-minor] Biomarkers / metabolism. Cell Proliferation. Child, Preschool. Disease-Free Survival. Humans. Immunoenzyme Techniques. Keratin-7 / metabolism. Magnetic Resonance Imaging. Male. Pancreas / metabolism. Pancreas / pathology. Pancreaticoduodenectomy

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  • (PMID = 17990924.001).
  • [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; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Keratin-7
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35. Go JH: A spindle cell predominant pancreatic solid-pseudopapillary tumor. Yonsei Med J; 2008 Aug 30;49(4):672-5
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  • [Title] A spindle cell predominant pancreatic solid-pseudopapillary tumor.
  • A hitherto unrecognized variant of solid-pseudopapillary tumor (SPT) of the pancreas is reported.
  • The tumor presented in the pancreatic tail of a 44-year-old female patient.
  • Histologically, the neoplasm was mostly composed of sheets of spindle cells.
  • The periphery of the tumor showed typical feature of SPT.
  • Immunohistochemically, the tumor cells were positive for vimentin, CD10, CD56, beta-catenin, and alpha1-antichymotrypsin, but negative for cytokeratin, chromogranin, synaptophysin and S-100 protein.
  • Ultrastructurally, the tumor showed a few acinar spaces with microvilli between tumor cells.
  • This case is peculiar in that the tumor did not show gross cystic change and predominantly consists of spindle shaped tumor cells, so may cause difficult diagnostic problem.
  • [MeSH-major] Pancreatic Neoplasms / pathology

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  • (PMID = 18729314.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2615298
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36. Gülben K, Ozdemir H, Berberoğlu U, Mersin H, Yrkin F, Cakýr E, Aksaray S: Melatonin modulates the severity of taurocholate-induced acute pancreatitis in the rat. Dig Dis Sci; 2010 Apr;55(4):941-6
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  • The aim of this study was to investigate the effects of melatonin on serum amylase, tumor necrosis factor-alpha (TNF-alpha) and histological changes in rats with taurocholate-induced acute pancreatitis.
  • The total histological score, including edema, inflammation, perivascular infiltrate, acinar necrosis, fat necrosis and hemorrhage, was also significantly lower in the melatonin group as compared to the control (P < 0.0001).
  • [MeSH-minor] Amylases / blood. Animals. Injections, Intraperitoneal. Male. Pancreas / drug effects. Pancreas / pathology. Rats. Rats, Wistar. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 19399617.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 5E090O0G3Z / Taurocholic Acid; EC 3.2.1.- / Amylases; JL5DK93RCL / Melatonin
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37. Sultan AS, Brim H, Sherif ZA: Co-overexpression of Janus kinase 2 and signal transducer and activator of transcription 5a promotes differentiation of mammary cancer cells through reversal of epithelial-mesenchymal transition. Cancer Sci; 2008 Feb;99(2):272-9
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  • Signal transducer and activator of transcription (Stat) 5 appears to play a vital role in prolactin (PRL)-induced cell differentiation and normal mammary gland development.
  • Jak2 and Stat5a-co-overexpressing cells treated with cocktail (PRL, dexamethasone, and insulin), effectively reverse epithelial-mesenchymal transition by stimulating 3D organoids more reminiscent of the acinar growth of normal mammary epithelial cells, compared with cells overexpressing only Stat5a or Jak2.
  • [MeSH-major] Breast Neoplasms / metabolism. Epithelial Cells / cytology. Janus Kinase 2 / metabolism. Mesoderm / cytology. STAT5 Transcription Factor / metabolism. Signal Transduction. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Cell Differentiation. Cell Line, Transformed. Cell Line, Tumor. Female. Humans

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  • (PMID = 18271926.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5K01CA087554-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / STAT5 Transcription Factor; 0 / STAT5A protein, human; 0 / Tumor Suppressor Proteins; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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38. Tavora F, Rassaei N, Shilo K, Foss RD, Galvin JR, Travis WD, Franks TJ: Occult primary parotid gland acinic cell adenocarcinoma presenting with extensive lung metastasis. Arch Pathol Lab Med; 2007 Jun;131(6):970-3
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  • [Title] Occult primary parotid gland acinic cell adenocarcinoma presenting with extensive lung metastasis.
  • Acinic cell adenocarcinoma is a malignant salivary gland neoplasm with a relatively low rate of lymphangitic spread to regional lymph nodes.
  • We encountered an unusual example of acinic cell adenocarcinoma that initially presented in the lung, whereas the primary parotid carcinoma, despite extensive clinical evaluation, only became apparent 1 year after initial diagnosis.
  • The histologic, immunohistochemical, and ultrastructural features of the tumor in the parotid gland and lung were similar.
  • The tumor displayed an aggressive behavior resulting in death within 2 years of the initial presentation.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Lung Neoplasms / secondary. Parotid Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Fatal Outcome. Female. Humans. Palliative Care

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  • (PMID = 17550329.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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39. Sanlioglu AD, Dirice E, Elpek O, Korcum AF, Ozdogan M, Suleymanlar I, Balci MK, Griffith TS, Sanlioglu S: High TRAIL death receptor 4 and decoy receptor 2 expression correlates with significant cell death in pancreatic ductal adenocarcinoma patients. Pancreas; 2009 Mar;38(2):154-60
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  • [Title] High TRAIL death receptor 4 and decoy receptor 2 expression correlates with significant cell death in pancreatic ductal adenocarcinoma patients.
  • OBJECTIVES: The importance of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and TRAIL receptor expression in pancreatic carcinoma development is not known.
  • Lastly, the tumor grade, tumor stage, tumor diameter, perineural invasion, and number of lymph node metastasis were used for comparison purposes.
  • In addition, acinar cells from PDAC patients had higher DcR2 expression but lower death receptor 4 expression.
  • [MeSH-major] Adenocarcinoma / pathology. Apoptosis. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / pathology. Receptors, Tumor Necrosis Factor / physiology. Tumor Necrosis Factor Decoy Receptors / physiology

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  • (PMID = 18981952.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF10A protein, human; 0 / TNFRSF10D protein, human; 0 / Tumor Necrosis Factor Decoy Receptors
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40. Psalla D, Geigy C, Konar M, Café Marçal V, Oevermann A: Nasal acinic cell carcinoma in a cat. Vet Pathol; 2008 May;45(3):365-8
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  • [Title] Nasal acinic cell carcinoma in a cat.
  • This case report describes the clinical, magnetic resonance imaging (MRI)-related, and pathologic features of a nasal acinic cell carcinoma in a cat.
  • Evaluation by MRI revealed an heterogeneous, space-occupying lesion that filled the left nasal cavity and was diagnosed by histopathologic examination as an acinic cell carcinoma arising from a minor salivary gland of the nasal cavity.
  • Acinic cell carcinoma is a rare tumor in veterinary medicine.
  • The tumor is composed mainly of cells resembling serous cells of salivary glands and originates from major or minor salivary glands.
  • Clinicians and pathologists should be aware of the occurrence of acinic cell carcinoma in the sinonasal tract and include the tumor in the differential diagnosis of feline nasal diseases.
  • [MeSH-major] Carcinoma, Acinar Cell / veterinary. Paranasal Sinus Neoplasms / veterinary

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  • (PMID = 18487495.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 68238-35-7 / Keratins
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41. Thomas PB, Samant DM, Wang Y, Selvam S, Stevenson D, Gray JD, Schechter JE, Mircheff AK, Trousdale MD: Distinct dacryoadenitides autoadoptively transferred to rabbits by different subpopulations of lymphocytes activated ex vivo. Cornea; 2010 Oct;29(10):1153-62
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  • PURPOSE: To test whether CD4+ T cells proliferate in mixed cell reactions with autologous lacrimal gland (LG) acinar cells and whether these cells can autoadoptively transfer disease.
  • METHODS: Purified acinar cells were gamma irradiated and cocultured with peripheral blood lymphocytes.
  • Activated CD4+ T cells were sorted by fluorescence-activated cell sorting (FACS).
  • Unfractionated activated peripheral blood lymphocytes (UF), CD4+-enriched and CD4+-depleted T cells from an autologous mixed cell reaction were injected into the donor rabbit's remaining LG.
  • RESULTS: CD4 T cells increased in the autologous mixed cell reaction from 20% to 80%.
  • All LGs exhibited significant histopathology and increased messenger RNAs for tumor necrosis factor α.
  • The ID/CD4+-enriched group contained fewer infiltrating CD4 cells but more eosinophils, severely altered acinar morphology, and increased fibrosis.
  • The CD4+-depleted cell fraction also contained pathogenic effector cells capable of inducing disease.

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  • (PMID = 20577087.001).
  • [ISSN] 1536-4798
  • [Journal-full-title] Cornea
  • [ISO-abbreviation] Cornea
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY10550; United States / NEI NIH HHS / EY / R01 EY012689; United States / NEI NIH HHS / EY / R56 EY010550; United States / NEI NIH HHS / EY / R01 EY010550; United States / NEI NIH HHS / EY / EY05801; United States / NEI NIH HHS / EY / P30 EY003040; United States / NEI NIH HHS / EY / EY03040; United States / NEI NIH HHS / EY / EY12689; United States / NEI NIH HHS / EY / R01 EY005801
  • [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 / Cytokines; 0 / RNA, Messenger
  • [Other-IDs] NLM/ NIHMS181101; NLM/ PMC2945426
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42. van Furth W, Smyth HS, Horvath E, Kovacs K, Salehi F, Cusimano MD: Salivary gland-like tumor of the sella. Can J Neurol Sci; 2007 Nov;34(4):478-82
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  • [Title] Salivary gland-like tumor of the sella.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / physiopathology. Sella Turcica / pathology. Skull Neoplasms / pathology. Skull Neoplasms / physiopathology
  • [MeSH-minor] Angioplasty, Balloon, Coronary. Aortic Aneurysm / pathology. Diabetes Insipidus / etiology. Diagnosis, Differential. Humans. Hypernatremia / etiology. Immunohistochemistry. Magnetic Resonance Imaging. Male. Microscopy, Electron, Transmission. Middle Aged. Myocardial Infarction / pathology. Myocardial Infarction / surgery. Pituitary Neoplasms / pathology. Salivary Gland Neoplasms / pathology. Stomach Ulcer / pathology

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  • (PMID = 18062459.001).
  • [ISSN] 0317-1671
  • [Journal-full-title] The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques
  • [ISO-abbreviation] Can J Neurol Sci
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Canada
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43. Lin WN, Huang HC, Wu CC, Liao CT, Chen IH, Kan CJ, Huang SF: Analysis of acinic cell carcinoma of the parotid gland - 15 years experience. Acta Otolaryngol; 2010 Dec;130(12):1406-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of acinic cell carcinoma of the parotid gland - 15 years experience.
  • CONCLUSION: In our experience, the prognosis for parotid gland acinic cell carcinoma (AciCC) is good.
  • Surgery alone would be sufficient in early-stage tumor.
  • OBJECTIVES: AciCC is a rare tumor in parotid gland malignancy.
  • The tumor stage distributions of the patients were 24%, 44%, 28%, and 4% for stages I, II, III, and IV, respectively.
  • [MeSH-major] Carcinoma, Acinar Cell / surgery. Parotid Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Disease-Free Survival. Dose Fractionation. Female. Follow-Up Studies. Humans. Lymphatic Irradiation. Male. Middle Aged. Neoplasm Staging. Parotid Gland / pathology. Parotid Gland / surgery. Prognosis. Radiotherapy, Adjuvant. Retrospective Studies. Young Adult

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  • (PMID = 20809887.001).
  • [ISSN] 1651-2251
  • [Journal-full-title] Acta oto-laryngologica
  • [ISO-abbreviation] Acta Otolaryngol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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44. Cui W, De Jesus K, Zhao H, Takasawa S, Shi B, Srikant CB, Liu JL: Overexpression of Reg3alpha increases cell growth and the levels of cyclin D1 and CDK4 in insulinoma cells. Growth Factors; 2009 Jun;27(3):195-202
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  • [Title] Overexpression of Reg3alpha increases cell growth and the levels of cyclin D1 and CDK4 in insulinoma cells.
  • Regenerating gene (Reg) family protein Reg3alpha is normally expressed in pancreatic acinar and endocrine cells.
  • In order to explore its effect on islet beta-cell replication, insulinoma MIN6 cells were stably transfected with murine Reg3alpha cDNA.
  • In MTT cell proliferation assay, Reg3alpha-overexpressing cells exhibited a 2-fold increase in the rate of cell growth.
  • In order to investigate the intracellular mechanism, we studied cell cycle regulatory proteins.
  • It is established that beta-cell replication is associated with increased cyclin D1 and CDK4 levels; deficiency in CDK4 or cyclin D2 results in reduced beta-cell mass and diabetes.
  • Our results suggest that Reg3alpha stimulates beta-cell replication, by activating Akt kinase and increasing the levels of cyclin D1/CDK4.
  • [MeSH-minor] Animals. Antigens, Neoplasm. Biomarkers, Tumor. Cell Line, Tumor. Cell Proliferation. Lectins, C-Type. Mice. Phosphorylation. Proto-Oncogene Proteins c-akt / metabolism

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  • (PMID = 19343564.001).
  • [ISSN] 1029-2292
  • [Journal-full-title] Growth factors (Chur, Switzerland)
  • [ISO-abbreviation] Growth Factors
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / Proteins; 0 / pancreatitis-associated protein; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / Akt1 protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.22 / Cdk4 protein, mouse; EC 2.7.11.22 / Cyclin-Dependent Kinase 4
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45. Isakoff SJ, Engelman JA, Irie HY, Luo J, Brachmann SM, Pearline RV, Cantley LC, Brugge JS: Breast cancer-associated PIK3CA mutations are oncogenic in mammary epithelial cells. Cancer Res; 2005 Dec 1;65(23):10992-1000
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  • Herein, we examine the activity of the two most common variants, E545K and H1047R, in the MCF-10A immortalized breast epithelial cell line.
  • In addition, expression of p110alpha mutants in mammary epithelial cells induces multiple phenotypic alterations characteristic of breast tumor cells, including anchorage-independent proliferation in soft agar, growth factor-independent proliferation, and protection from anoikis.
  • Expression of these mutant p110alpha isoforms also confers increased resistance to paclitaxel and induces abnormal mammary acinar morphogenesis in three-dimensional basement membrane cultures.

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  • (PMID = 16322248.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA089393; United States / NCI NIH HHS / CA / CA89021; United States / NCI NIH HHS / CA / 5T32 CA09172-30; United States / NCI NIH HHS / CA / T32 CA009172; United States / NCI NIH HHS / CA / CA105134; United States / NIGMS NIH HHS / GM / R01 GM041890; United States / NCI NIH HHS / CA / 5T32 CA09172-29; United States / NIGMS NIH HHS / GM / GM41890
  • [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] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human
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46. Kusafuka K, Bando E, Muramatsu K, Ito H, Tanizawa Y, Kawamura T, Mochizuki T, Terashima M, Nakajima T: Pancreatic-type mixed acinar-endocrine carcinoma with alpha-fetoprotein production arising from the stomach: a report of an extremely rare case. Med Mol Morphol; 2009 Sep;42(3):167-74
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  • [Title] Pancreatic-type mixed acinar-endocrine carcinoma with alpha-fetoprotein production arising from the stomach: a report of an extremely rare case.
  • An extremely rare case of mixed acinar-endocrine carcinoma (MAEC) arising from the stomach in a 56-year-old Japanese woman is herein presented.
  • An endoscopic examination and computed tomography showed a protruding gastric tumor and a large extragastric mass, respectively.
  • Macroscopic observation on the surgical specimen revealed the extragastric cystic mass was continued to the intragastric tumor.
  • Histologically, the intragastric tumor consisted of large or small solid nests with acinar appearance.
  • This tumor was finally diagnosed to be MAEC with AFP production of the stomach.
  • Although no ectopic pancreas was found in the stomach, this tumor may originate from ectopic pancreas.
  • As another theory, it is possible for this tumor to originate from the pluripotent stem cells in the stomach.
  • [MeSH-major] Carcinoma, Acinar Cell. Endocrine Gland Neoplasms. Stomach Neoplasms. alpha-Fetoproteins / metabolism
  • [MeSH-minor] Female. Humans. Middle Aged. Pancreatic Neoplasms / pathology

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  • [CommentIn] Med Mol Morphol. 2010 Mar;43(1):65 [20340009.001]
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  • (PMID = 19784744.001).
  • [ISSN] 1860-1499
  • [Journal-full-title] Medical molecular morphology
  • [ISO-abbreviation] Med Mol Morphol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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47. Kaifi JT, Heidtmann S, Schurr PG, Reichelt U, Mann O, Yekebas EF, Wachowiak R, Strate T, Schachner M, Izbicki JR: Absence of L1 in pancreatic masses distinguishes adenocarcinomas from poorly differentiated neuroendocrine carcinomas. Anticancer Res; 2006 Mar-Apr;26(2A):1167-70
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  • BACKGROUND: Pancreatic adenocarcinoma is a tumor with fatal outcome.
  • Cell adhesion molecules, such as L1 (CD171), have an essential function in tumor progression.
  • No expression was found in acinar or ductal cells of normal pancreatic tissue.
  • Since L1 was previously found to be expressed specifically in neuroendocrine pancreatic carcinomas, its absence in unclear pancreatic masses might hint at a ductal origin for a malignant pancreatic tumor.
  • [MeSH-major] Adenocarcinoma / immunology. Adenocarcinoma / pathology. Carcinoma, Neuroendocrine / immunology. Carcinoma, Neuroendocrine / pathology. Leukocyte L1 Antigen Complex / biosynthesis. Pancreatic Neoplasms / immunology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Female. Humans. Male. Middle Aged. Neoplasm Staging

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  • (PMID = 16619519.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Leukocyte L1 Antigen Complex
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48. Gigoux V, Clerc P, Sanchez D, Coll MG, Corominola H, Leung-Theung-Long S, Pénicaud L, Gomis R, Seva C, Fourmy D, Dufresne M: Reg genes are CCK2 receptor targets in ElasCCK2 mice pancreas. Regul Pept; 2008 Feb 7;146(1-3):88-98
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  • We previously demonstrated that expression of the gastrin receptor, CCK2R, in pancreatic acini of transgenic ElasCCK2 mice induced alteration of acinar morphology and differentiation, increased sensitivity to a carcinogen and development of preneoplastic lesions and tumours.
  • The expression of Reg III proteins is increased in ElasCCK2 pancreas before the development of preneoplastic lesions in a subpopulation of islet cells and in small islet-like cell clusters dispersed within the acinar tissue.
  • [MeSH-minor] Animals. Antigens, Neoplasm. Biomarkers, Tumor. Gene Expression Regulation. Glucose Tolerance Test. Immunohistochemistry. Insulin / blood. Insulin / secretion. Lectins, C-Type. Mice. Mice, Transgenic. Organ Size. Protein Array Analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17888528.001).
  • [ISSN] 0167-0115
  • [Journal-full-title] Regulatory peptides
  • [ISO-abbreviation] Regul. Pept.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Insulin; 0 / Lectins, C-Type; 0 / Pap protein, mouse; 0 / Proteins; 0 / Receptor, Cholecystokinin B; 0 / pancreatitis-associated protein
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49. Hasegawa M, Hagiwara S, Sato T, Jijiwa M, Murakumo Y, Maeda M, Moritani S, Ichihara S, Takahashi M: CD109, a new marker for myoepithelial cells of mammary, salivary, and lacrimal glands and prostate basal cells. Pathol Int; 2007 May;57(5):245-50
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  • The CD109 gene encodes a glycosylphosphatidylinositol (GPI)-anchored cell surface protein.
  • The anti-CD109 antibody generated by the authors was available for formalin-fixed paraffin section, and it strongly stained myoepithelial cells and basal cells but not ductal, acinar, and secretory cells in these glands.
  • [MeSH-major] Antigens, CD / analysis. Biomarkers / analysis. Neoplasm Proteins / analysis
  • [MeSH-minor] Blotting, Western. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Line. Cell Line, Tumor. Female. GPI-Linked Proteins. Humans. Immunohistochemistry. Lacrimal Apparatus / chemistry. Lacrimal Apparatus / cytology. Male. Mammary Glands, Human / chemistry. Mammary Glands, Human / cytology. Prostate / chemistry. Prostate / cytology. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. RNA Interference. Salivary Gland Neoplasms / metabolism. Salivary Gland Neoplasms / pathology. Salivary Glands / chemistry. Salivary Glands / cytology. Transfection

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  • (PMID = 17493171.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers; 0 / CD109 protein, human; 0 / GPI-Linked Proteins; 0 / Neoplasm Proteins
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50. Shigeishi H, Yoneda S, Taki M, Nobumori T, Ohta K, Higashikawa K, Yasui W, Kamata N: Correlation of human Bub1 expression with tumor-proliferating activity in salivary gland tumors. Oncol Rep; 2006 Apr;15(4):933-8
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  • [Title] Correlation of human Bub1 expression with tumor-proliferating activity in salivary gland tumors.
  • Human Bub1 plays an important role at the spindle assembly check-point to prevent cell cycle progression following spindle damage.
  • We examined the expression of Bub1 mRNA and protein in 21 human salivary gland tumors (7 pleomorphic adenomas, 2 warthin tumors, 5 mucoepidermoid carcinomas, 3 adenoid cystic carcinomas and 4 acinic cell carcinomas) and 3 normal submandibular glands using real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) or western blotting.
  • We analyzed its relation with the proliferative activity monitored by the Ki-67 labeling index by immunohistochemistry as well as the expression of proliferating cell nuclear antigen (PCNA) by Western blotting.
  • These results indicate that increased expression of the human Bub1 gene is closely linked to abnormal cell proliferation in malignant conditions.
  • [MeSH-major] Cell Proliferation. Protein Kinases / genetics. Salivary Gland Neoplasms / pathology
  • [MeSH-minor] Adenolymphoma / genetics. Adenolymphoma / metabolism. Adenolymphoma / pathology. Adenoma, Pleomorphic / genetics. Adenoma, Pleomorphic / metabolism. Adenoma, Pleomorphic / pathology. Blotting, Western. Carcinoma, Acinar Cell / genetics. Carcinoma, Acinar Cell / metabolism. Carcinoma, Acinar Cell / pathology. Carcinoma, Adenoid Cystic / genetics. Carcinoma, Adenoid Cystic / metabolism. Carcinoma, Adenoid Cystic / pathology. Carcinoma, Mucoepidermoid / genetics. Carcinoma, Mucoepidermoid / metabolism. Carcinoma, Mucoepidermoid / pathology. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Ki-67 Antigen / analysis. Neoplasm Staging. Proliferating Cell Nuclear Antigen / analysis. Protein-Serine-Threonine Kinases. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16525682.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA, Messenger; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / BUB1 protein, human; EC 2.7.11.1 / Bub1 spindle checkpoint protein; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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51. Sheng L, Weixia Z, Longhai Y, Jinming Y: Clinical and biologic analysis of pancreatoblastoma. Pancreas; 2005 Jan;30(1):87-90
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  • Since the first description of pancreatoblastoma as a malignant pancreatic tumor of childhood in 1957, approximately 200 cases have been reported.
  • During laparotomy, a 10 x 8 x 8-cm3 tumor was discovered in the pancreatic body and tail, and with 3 cystic masses, 15, 10, and 8 cm in diameter, respectively, involving the right lobe of the liver.
  • Pathologic examination of the resected tumor revealed findings characteristic of pancreatoblastoma.
  • The tumor formed acinar and glandular structures and solid areas and contained many "squamoid corpuscles," a defining feature of pancreatoblastoma.
  • Unfortunately, the patient died 26 months later from disseminated tumor progression.
  • A review of the literature reveals that pancreatoblastoma in childhood must be considered malignant but usually has a favorable prognosis in contrast to pancreatic neoplasms in adult patients.
  • Biologic study will investigate the molecular biology of this rare tumor.
  • The biology may help define prognosis and therapy for this kind of tumor.
  • [MeSH-major] Pancreas / pathology. Pancreas / radiography. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / radiography
  • [MeSH-minor] Adolescent. Cell Division. Flow Cytometry. G2 Phase. Humans. Male. Microscopy, Electron. S Phase

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  • (PMID = 15632705.001).
  • [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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52. 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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53. Zhang HZ, Jiang ZM, Shi L: [Pathologic characteristics of pseudohyperplastic prostatic adenocarcinoma]. Zhonghua Bing Li Xue Za Zhi; 2007 Nov;36(11):742-5
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  • The incidence, morphology, pathologic differential diagnosis, tumor volume, preferred location and Gleason's score were studied.
  • Histologically, 66.7% of PHPA demonstrated direct transition with conventional acinar adenocarcinoma; and 76.7% of cases had coexisting conventional acinar adenocarcinoma in the remaining tissue blocks.
  • The tumor volume accounted for 5% to 100% of total carcinoma among core needle biopsy and 1% to 30% of total carcinoma among radical prostatectomy.
  • The tumor was primarily located in the peripheral zone.
  • Majority of cases have concurrent conventional acinar adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Prostatic Hyperplasia / pathology. Prostatic Neoplasms / pathology. Racemases and Epimerases / metabolism
  • [MeSH-minor] Biopsy, Needle. Carcinoma, Acinar Cell / metabolism. Carcinoma, Acinar Cell / pathology. Diagnosis, Differential. Follow-Up Studies. Humans. Immunohistochemistry. Male. Prostatectomy

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  • (PMID = 18307877.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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54. Maeda K, Hirota M, Kimura Y, Ichihara A, Ohmuraya M, Sugita H, Ogawa M: Proinflammatory role of trypsin and protease-activated receptor-2 in a rat model of acute pancreatitis. Pancreas; 2005 Jul;31(1):54-62
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  • We hypothesize that trypsin may activate acinar cells or inflammatory cells through PAR-2 signals in acute pancreatitis.
  • METHODS: We immunochemically analyzed the expression of PAR-2 in the rat acinar cell line, ARIP, and the rat pancreas, using anti-rat PAR-2 cleavage site (PCS) and anti-rat PAR-2 N-terminal fragment (PNF) antibodies.
  • We also showed that PAR-2 is strongly expressed in pancreatic acinar and duct cells and that it is activated in rat cerulein-induced acute pancreatitis.
  • [MeSH-minor] Acute Disease. Amylases / blood. Animals. Blotting, Western. Calcium / metabolism. Cell Line, Tumor. Cytokines / blood. Disease Models, Animal. Immunohistochemistry. Lipase / blood. Male. Rabbits. Rats. Rats, Wistar

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  • (PMID = 15968248.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Receptor, PAR-2; EC 3.1.1.3 / Lipase; EC 3.2.1.- / Amylases; EC 3.4.21.4 / Trypsin; SY7Q814VUP / Calcium
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55. Foschini MP, Krausz T: Salivary gland-type tumors of the breast: a spectrum of benign and malignant tumors including "triple negative carcinomas" of low malignant potential. Semin Diagn Pathol; 2010 Feb;27(1):77-90
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  • Salivary gland-type neoplasms of the breast are uncommon and comprise numerous entities analogous to that more commonly seen in salivary glands.
  • In the breast, benign adenomyoepithelioma is recognized in addition to malignant one, whereas in the salivary gland a histologically similar tumor is designated as epithelial-myoepithelial carcinoma without a separate benign subgroup.
  • Mammary adenoid cystic carcinoma is a low-grade neoplasm compared with its salivary equivalent.
  • It is also important to appreciate that in contrast to "triple negative" conventional breast carcinomas with aggressive course, most salivary-type malignant breast neoplasms behave in a low-grade manner.
  • Another family of salivary gland-type mammary epithelial neoplasms is devoid of myoepithelial cells.
  • Key examples include mucoepidermoid carcinoma and acinic cell carcinoma.
  • The number of cases of salivary gland-type mammary neoplasms in the published data is constantly increasing but some of the rarest subtypes like polymorphous low-grade adenocarcinoma and oncocytic carcinoma are "struggling" to become clinically relevant entities in line with those occurring more frequently in salivary glands.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Breast Neoplasms / pathology. Neoplasms, Complex and Mixed / pathology. Salivary Gland Neoplasms / pathology
  • [MeSH-minor] Adenoma, Pleomorphic / metabolism. Adenoma, Pleomorphic / pathology. Adenomyoepithelioma / metabolism. Adenomyoepithelioma / pathology. Breast Neoplasms, Male / metabolism. Breast Neoplasms, Male / pathology. Carcinoma, Acinar Cell / metabolism. Carcinoma, Acinar Cell / pathology. Carcinoma, Adenoid Cystic / metabolism. Carcinoma, Adenoid Cystic / pathology. Carcinoma, Mucoepidermoid / metabolism. Carcinoma, Mucoepidermoid / pathology. Female. Humans. Male. Receptor, ErbB-2 / metabolism. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism

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  • (PMID = 20306833.001).
  • [ISSN] 0740-2570
  • [Journal-full-title] Seminars in diagnostic pathology
  • [ISO-abbreviation] Semin Diagn 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 / Receptors, Estrogen; 0 / Receptors, Progesterone; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
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56. Jiang X, Zhang W, Kayed H, Zheng P, Giese NA, Friess H, Kleeff J: Loss of ONECUT1 expression in human pancreatic cancer cells. Oncol Rep; 2008 Jan;19(1):157-63
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  • mRNA levels of ONECUT1, TCF2, PKHD1 and CYS1 were measured in pancreatic tissues and pancreatic cancer cell lines by quantitative reverse-transcriptase polymerase chain reaction (QRT-PCR).
  • ONECUT1 protein was expressed in normal acinar and ductal cells, but neither in the cancer cells of PDAC tissues nor in 7 of 8 cultured pancreatic cancer cell lines.
  • In conclusion, ONECUT1 expression is lost in pancreatic cancer cells, suggesting a tumor suppressor function in this malignancy.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Hepatocyte Nuclear Factor 6 / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Movement / physiology. Gene Expression. Hepatocyte Nuclear Factor 1-beta / metabolism. Humans. Immunoblotting. Immunohistochemistry. Lasers. Membrane Proteins / metabolism. Microdissection. Oligonucleotide Array Sequence Analysis. RNA, Messenger / analysis. Receptors, Cell Surface / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 18097590.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / CYS1 protein, human; 0 / HNF1B protein, human; 0 / Hepatocyte Nuclear Factor 6; 0 / Membrane Proteins; 0 / ONECUT1 protein, human; 0 / PKHD1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 138674-15-4 / Hepatocyte Nuclear Factor 1-beta
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57. 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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58. 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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59. Herrema H, Czajkowska D, Théard D, van der Wouden JM, Kalicharan D, Zolghadr B, Hoekstra D, van Ijzendoorn SC: Rho kinase, myosin-II, and p42/44 MAPK control extracellular matrix-mediated apical bile canalicular lumen morphogenesis in HepG2 cells. Mol Biol Cell; 2006 Jul;17(7):3291-303
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  • Prolonged cell culture results in extensive organizational changes, including cell clustering, multilayering, and apical lumen morphogenesis.
  • The latter includes the development of large acinar structures and subsequent elongated canalicular lumens that span multiple cells.
  • These morphological changes closely resemble the early organizational pattern during development, regeneration, and neoplasia of the liver and are rapidly induced when cells are cultured on predeposited extracellular matrix (ECM).
  • Consistently, stimulation of Rho kinase and subsequent myosin-II ATPase activity by lipoxygenase-controlled eicosatetranoic acid metabolism inhibits ECM-mediated cell multilayering and apical lumen morphogenesis but not initial apical lumen formation.
  • Furthermore, apical lumen remodeling but not cell multilayering requires basal p42/44 MAPK activity.
  • [MeSH-minor] Cell Membrane / metabolism. Cell Membrane / ultrastructure. Enzyme Inhibitors / pharmacology. Extracellular Matrix / enzymology. Extracellular Matrix / ultrastructure. Humans. Intracellular Signaling Peptides and Proteins. Tumor Cells, Cultured. rho-Associated Kinases

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  • (PMID = 16687572.001).
  • [ISSN] 1059-1524
  • [Journal-full-title] Molecular biology of the cell
  • [ISO-abbreviation] Mol. Biol. Cell
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Intracellular Signaling Peptides and Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / rho-Associated Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.6.1.- / Myosin Type II
  • [Other-IDs] NLM/ PMC1552049
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60. 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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61. Khanna AK, Yadav SK, Dixit VK, Kumar M: AgNOR count and subjective AgNOR pattern assessment (SAPA) score in carcinoma of the pancreatic head including periampullary tumors. JOP; 2005 Nov;6(6):575-80
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  • MAIN OUTCOME MEASURES: Patients were studied for the AgNOR count and the SAPA score, and the values were correlated with the size of the tumor, the type of tumor and histological type and grade of tumor.
  • Well-differentiated carcinomas had significantly lower AgNOR counts as compared to other tumors except acinar cell carcinomas since acinar cell carcinomas are also well-differentiated tumors.
  • The SAPA score was also higher in moderately-differentiated tumors and the difference between moderately-differentiated tumor and other types of tumors was significant although there was no significant difference between cystadenocarcinomas and unclassified tumors, and between acinar cell carcinomas and well-differentiated tumors on SAPA scoring.
  • CONCLUSIONS: The values of the AgNOR count and the SAPA score are well-correlated with the size of the tumor, the type of tumor and the histological grade.
  • [MeSH-major] Antigens, Nuclear. Nuclear Proteins. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Cell Count. Female. Humans. Male. Middle Aged. Pancreatectomy

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  • (PMID = 16286708.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Nuclear Proteins; 0 / nucleolar organizer region associated proteins
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62. 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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63. Andreadis D, Epivatianos A, Poulopoulos A, Nomikos A, Papazoglou G, Antoniades D, Barbatis C: Detection of C-KIT (CD117) molecule in benign and malignant salivary gland tumours. Oral Oncol; 2006 Jan;42(1):57-65
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  • C-KIT (CD117), a tyrosine kinase receptor, is involved in the growth and development of normal tissues and some types of neoplasms.
  • In addition five samples of chronic submandibular sialadenitis, five normal minor salivary glands and parotid or submandibular gland tissue adjacent to benign tumour were also studied.
  • C-KIT expression was observed in cases of adenoid cystic, acinic cell polymorphous low grade, epithelial-myoepithelial, carcinosarcoma and basal cell adenocarcinomas, as in luminal cells of pleomorphic adenomas, in serous acinar and only in intercalated and a small number of striated ductal cells of inflammatory salivary gland tissue, whereas normal salivary lobules were generally negative except a weak positivity of intercalated cells.
  • Contrary to other reports, this study suggests that, C-KIT protein does not appear to be an exclusively specific marker for benign or malignant salivary gland neoplasms, but may be useful in differential diagnosis of adenoid cystic carcinoma from polymorphous low grade adenocarcinoma.
  • Furthermore its expression in serous acinar cells in sialadenitis and intercalated ductal cells in normal and inflammatory lesions may indicate a possible participation in pathogenesis of both neoplastic and non-neoplastic salivary gland diseases.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Adenoid Cystic / chemistry. Proto-Oncogene Proteins c-kit / analysis. Salivary Gland Neoplasms / chemistry

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  • (PMID = 16140564.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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64. Kim SA, Mathog RH: Acinic cell carcinoma of the parotid gland: a 15-year review limited to a single surgeon at a single institution. Ear Nose Throat J; 2005 Sep;84(9):597-602
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  • [Title] Acinic cell carcinoma of the parotid gland: a 15-year review limited to a single surgeon at a single institution.
  • The course of acinic cell carcinoma of the parotid gland following surgical and nonsurgical interventions is variable.
  • The objective of this study was to report our experience in treating this disease and to evaluate the factors that might be involved in the treatment of the tumor and the prognosis of the patient.
  • The most prevalent morphologic pattern of these tumors was microcystic.
  • During that time, we found no recurrences of acinic cell carcinoma and no evidence of metastatic disease.
  • Therefore, we conclude that acinic cell carcinoma can be successfully treated with a superficial or total parotidectomy with sparing of the facial nerve.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / therapy. Parotid Gland / surgery. Parotid Neoplasms / diagnosis. Parotid Neoplasms / therapy

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  • (PMID = 16261761.001).
  • [ISSN] 0145-5613
  • [Journal-full-title] Ear, nose, & throat journal
  • [ISO-abbreviation] Ear Nose Throat J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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65. Letoha T, Somlai C, Takacs T, Szabolcs A, Jarmay K, Rakonczay Z Jr, Hegyi P, Varga I, Kaszaki J, Krizbai I, Boros I, Duda E, Kusz E, Penke B: A nuclear import inhibitory peptide ameliorates the severity of cholecystokinin-induced acute pancreatitis. World J Gastroenterol; 2005 Feb 21;11(7):990-9
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  • AIM: To assess the effect of our novel cell-permeable nuclear factor-kappaB (NF-kappaB) inhibitor peptide PN50 in an experimental model of acute pancreatitis.
  • PN50 was produced by conjugating the cell-penetrating penetratin peptide with the nuclear localization signal of the NF-kappaB p50 subunit.
  • According to the histological findings, PN50 protected the animals against acute pancreatitis by favoring the induction of apoptotic, as opposed to necrotic acinar cell death associated with severe acute pancreatitis.
  • [MeSH-minor] Active Transport, Cell Nucleus. Acute Disease. Amino Acid Sequence. Amylases / blood. Animals. Body Weight. Cell Line, Transformed. Electrophoretic Mobility Shift Assay. Glutathione / metabolism. Interleukin-6 / metabolism. Lipid Peroxidation / drug effects. Lung / metabolism. Male. Mice. Molecular Sequence Data. NF-kappa B / metabolism. Organ Size. Pancreas / metabolism. Pancreas / pathology. Peroxidase / metabolism. Rats. Rats, Wistar. Sincalide. Transcription, Genetic / drug effects. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 15742402.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / NF-kappa B; 0 / Peptides; 0 / SN50 peptide; 0 / Tumor Necrosis Factor-alpha; EC 1.11.1.7 / Peroxidase; EC 3.2.1.- / Amylases; GAN16C9B8O / Glutathione; M03GIQ7Z6P / Sincalide
  • [Other-IDs] NLM/ PMC4250791
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66. Günther T: Na+/Mg2+ antiport in non-erythrocyte vertebrate cells. Magnes Res; 2007 Jun;20(2):89-99
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  • Experiments, results and conclusions on Na+/Mg2, antiport in lymphocytes, HL60 cells, Ehrlich ascites tumor cells, platelets, pancreatic acinar cells, sublingual acini, hepatocytes, ruminal epithelial cells, kidney cells, smooth muscle cells, heart muscle cells and skeletal muscle cells were reviewed.
  • In most cell types, the Na+/Mg2+ antiport was investigated indirectly by measuring [Mg2+], and [Na+]i after changing the physiological Mg2+ homeostasis by effectors or by loading the cells with Mg2+.
  • By these methods, the Na+/Mg2+ antiport was found in all investigated mammalian cell types.
  • [MeSH-minor] Animals. Biological Transport / physiology. Cell Line, Tumor. Cells, Cultured. HL-60 Cells. Homeostasis / physiology. Humans

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  • (PMID = 18062583.001).
  • [ISSN] 0953-1424
  • [Journal-full-title] Magnesium research
  • [ISO-abbreviation] Magnes Res
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiporters; 9NEZ333N27 / Sodium; I38ZP9992A / Magnesium
  • [Number-of-references] 67
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67. 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. CDX2 Transcription Factor. Cell Differentiation. Fatal Outcome. Female. Homeodomain Proteins / metabolism. Humans. Immunohistochemistry. Keratin-20 / metabolism. Lymphatic Metastasis. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19908063.001).
  • [ISSN] 1432-2307
  • [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 / CDX2 Transcription Factor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Keratin-20; 0 / Tumor Suppressor Protein p53
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68. Borka K: [Claudin expression in different pancreatic cancers and its significance in differential diagnostics]. Magy Onkol; 2009 Sep;53(3):273-8
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  • The aim of our studies was to compare the different CLDN expression patterns in normal pancreas cells, pancreatic endocrine tumors, adenocarcinomas, mucinous cystic tumors and acinar cell carcinomas.
  • ) In addition to the well-known CLDN-1 and -4 expression CLDN-2, -3 and -7 proteins were demonstrated in ductal cells, while CLDN-3 and -7 proteins showed expression in acinar cells.
  • 4.) This is a first review on childhood acinar cell carcinoma causing Cushing syndrome.
  • The adenocarcinomas and cystic mucinous tumors of exocrine origin denoted CLDN-1, -2, -4 and -7 positivity, whereas acinar cell carcinomas expressed only CLDN-1 and -2.
  • Considering the CLDN expression observed in normal pancreas cells, it can be established that CLDN-1, -2 and -4 proteins are definitely markers of ductal differentiation, CLDN-1 protein of acinar and CLDN-3 of endocrine differentiation. 2).
  • [MeSH-major] Biomarkers, Tumor / metabolism. Claudins / metabolism. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / metabolism

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  • (PMID = 19793693.001).
  • [ISSN] 0025-0244
  • [Journal-full-title] Magyar onkologia
  • [ISO-abbreviation] Magy Onkol
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CLDN1 protein, human; 0 / CLDN2 protein, human; 0 / CLDN3 protein, human; 0 / CLDN4 protein, human; 0 / CLDN7 protein, human; 0 / Claudin-1; 0 / Claudin-3; 0 / Claudin-4; 0 / Claudins; 0 / Membrane Proteins
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69. Bhatia P, Srinivasan R, Rajwanshi A, Nijhawan R, Khandelwal N, Wig J, Vasishtha RK: 5-year review and reappraisal of ultrasound-guided percutaneous transabdominal fine needle aspiration of pancreatic lesions. Acta Cytol; 2008 Sep-Oct;52(5):523-9
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  • Of the 142 malignant aspirates, the cytodiagnosis was adenocarcinoma in 126, neuroendocrine/carcinoid tumor in 7, papillary solid epithelial neoplasm in 2, mucinous cystadenocarcinoma in 2, acinar cell carcinoma in 1 and metastatic small cell carcinoma in lung in 4 cases.
  • [MeSH-major] Pancreatic Neoplasms / pathology

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  • [CommentIn] Acta Cytol. 2008 Sep-Oct;52(5):521-2 [18833811.001]
  • (PMID = 18833812.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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70. Dobashi Y, Suzuki S, Matsubara H, Kimura M, Endo S, Ooi A: Critical and diverse involvement of Akt/mammalian target of rapamycin signaling in human lung carcinomas. Cancer; 2009 Jan 1;115(1):107-18
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  • In AC, the frequency of p-mTOR staining was higher in the well differentiated subtype, in particular, in the acinar structure.
  • Conversely, in squamous cell carcinomas, mTOR activation was associated with a significantly higher frequency of lymph node metastasis.
  • First, mTOR may function not only in the proliferation of tumor cells as an effector molecule downstream of EGFR but also possibly in the morphogenesis of AC.
  • Second, the activation of mTOR may play a key role in metastasis in squamous cell carcinoma.
  • [MeSH-major] Lung Neoplasms / metabolism. Protein Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Humans. Neoplasm Metastasis. Neoplasms, Squamous Cell / metabolism. Neoplasms, Squamous Cell / pathology. Phosphorylation. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction. TOR Serine-Threonine Kinases


71. Yu JH, Kim KH, Kim H: SOCS 3 and PPAR-gamma ligands inhibit the expression of IL-6 and TGF-beta1 by regulating JAK2/STAT3 signaling in pancreas. Int J Biochem Cell Biol; 2008;40(4):677-88
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  • We previously showed that cerulein induced IL-1beta expression through the Janus kinase (JAK) 2/signal transducer and activator of transcription (STAT) 3 pathway in pancreatic acinar cells.
  • In this study, we demonstrate that SOCS 3 is induced by cerulein in pancreatic acinar AR42J cells and in the rat pancreas.
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Ceruletide / pharmacology. Chromans / pharmacology. Enzyme-Linked Immunosorbent Assay. Janus Kinase 2 / metabolism. Male. Prostaglandin D2 / analogs & derivatives. Prostaglandin D2 / pharmacology. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction. STAT3 Transcription Factor / metabolism. Thiazolidinediones / pharmacology

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  • (PMID = 18035585.001).
  • [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 / 15-deoxyprostaglandin J2; 0 / Chromans; 0 / Interleukin-6; 0 / PPAR gamma; 0 / STAT3 Transcription Factor; 0 / Socs3 protein, rat; 0 / Stat3 protein, rat; 0 / Suppressor of Cytokine Signaling Proteins; 0 / Thiazolidinediones; 0 / Transforming Growth Factor beta1; 888Y08971B / Ceruletide; EC 2.7.10.2 / Jak2 protein, rat; EC 2.7.10.2 / Janus Kinase 2; I66ZZ0ZN0E / troglitazone; RXY07S6CZ2 / Prostaglandin D2
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72. Capurso G, Crnogorac-Jurcevic T, Milione M, Panzuto F, Campanini N, Dowen SE, Di Florio A, Sette C, Bordi C, Lemoine NR, Delle Fave G: Peanut-like 1 (septin 5) gene expression in normal and neoplastic human endocrine pancreas. Neuroendocrinology; 2005;81(5):311-21
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  • Normal pancreatic tissue, purified islets, 11 PETs and two cell lines were used to evaluate the presence of PNUTL1 by RT-PCR and Western blot.
  • The expression of the PNUTL1 protein was also evaluated by immunohistochemistry on normal pancreas, additional 26 PETs, eight pancreatic adenocarcinomas, one mixed endocrine-exocrine pancreatic neoplasm, a specimen of solid papillary pseudomucinous tumor, an adult islet cell hyperplasia and a case of neonatal nesidioblastosis.
  • In addition, a tissue array (LandMark High Density Cancer Tissue MicroArray) comprising 280 various tumor and matched normal specimens was utilized.
  • In the normal pancreas PNUTL1 expression is almost exclusively confined to the islet cells, weak expression was occasionally seen in some acinar cells, while immunoreactivity was completely absent in the ductal epithelia.
  • Weak immunoreactivity was also noted in a proportion of exocrine neoplasms.
  • [MeSH-major] Cell Cycle Proteins / metabolism. Gene Expression / physiology. Gene Expression Regulation, Neoplastic / physiology. Islets of Langerhans / metabolism. Pancreatic Neoplasms / metabolism

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16179808.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / RNA, Messenger; EC 3.6.1.- / SEPT5 protein, human; EC 3.6.1.- / Septins
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73. Roskams T, Kojiro M: Pathology of early hepatocellular carcinoma: conventional and molecular diagnosis. Semin Liver Dis; 2010 Feb;30(1):17-25
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  • Next to classical morphologic criteria such as nucleocytoplasmic ratio, thickness of cell plates, mitotic index, and architectural disturbance like acinar structures, one of the most relevant criteria to diagnose early HCC is stromal invasion.
  • Because a structured basement membrane is lacking along the hepatocytes in the liver, invasion cannot be defined as tumor growth through the basement membrane as in other tissues.
  • [MeSH-major] Biomarkers, Tumor / genetics. Carcinoma, Hepatocellular / pathology. Liver Neoplasms / pathology
  • [MeSH-minor] Biopsy, Needle. Early Detection of Cancer. Female. Gene Expression Regulation, Neoplastic. Glutamate-Ammonia Ligase / genetics. Glypicans / genetics. HSP70 Heat-Shock Proteins / genetics. Humans. Immunohistochemistry. Male. Neoplasm Staging. Prognosis. Sensitivity and Specificity

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  • (PMID = 20175030.001).
  • [ISSN] 1098-8971
  • [Journal-full-title] Seminars in liver disease
  • [ISO-abbreviation] Semin. Liver Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glypicans; 0 / HSP70 Heat-Shock Proteins; EC 6.3.1.2 / Glutamate-Ammonia Ligase
  • [Number-of-references] 54
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74. Hasteh F, Pu R, Michael CW: A metastatic renal carcinoid tumor presenting as breast mass: a diagnostic dilemma. Diagn Cytopathol; 2007 May;35(5):306-10
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  • [Title] A metastatic renal carcinoid tumor presenting as breast mass: a diagnostic dilemma.
  • We present clinicopathological and cytological findings of a well-defined breast mass in a patient with history of primary renal carcinoid tumor.
  • Fine-needle aspiration (FNA) cytology showed monotonous tumor cells with plasmacytoid appearance arranged singly and in small clusters.
  • Occasional tumor cells were arranged in acinar architecture resembling glandular differentiation.
  • Tumor cells showed fine speckled chromatin.
  • The unusual location for metastasis of this rare type of carcinoid tumor and overlapping cytological features with primary mammary carcinoma led to an erroneous preliminary cytological diagnosis of primary breast carcinoma with plasmacytoid features.
  • Tumor cells in the corresponding cell block showed strong diffuse positivity for synapthophysin and pan-cytokeratin with weak focal positivity for chromogranin markers.
  • These patterns of immunostaining were similar to the original renal carcinoid tumor.
  • To the best of our knowledge, a few cases of carcinoid tumor metastatic to the breast have been reported in the literature and more than half of these cases were initially misdiagnosed as primary breast carcinoma causing unnecessary surgical treatment.
  • This is a first reported case of metastatic renal carcinoid tumor into breast diagnosed with FNA biopsy.
  • This report highlights the cytological features of well-differentiated neuroendocrine tumor (carcinoid tumor) and its potential diagnostic pitfalls.
  • [MeSH-major] Biopsy, Fine-Needle. Breast Neoplasms / secondary. Carcinoid Tumor / secondary. Kidney Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Chromogranins / analysis. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Keratins / analysis. Middle Aged. Synaptophysin / analysis

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17427210.001).
  • [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; 0 / Chromogranins; 0 / Synaptophysin; 68238-35-7 / Keratins
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75. Dessimoz J, Grapin-Botton A: Pancreas development and cancer: Wnt/beta-catenin at issue... Cell Cycle; 2006 Jan;5(1):7-10
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  • This raises the question of the cell type in which beta-catenin is mutated during tumor formation in acinar cell carcinomas, pancreatoblastomas and solid cystic papillary tumors of the pancreas.
  • [MeSH-major] Organogenesis. Pancreas / embryology. Pancreatic Neoplasms / metabolism. Wnt Proteins / metabolism. beta Catenin / metabolism

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  • (PMID = 16322692.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Wnt Proteins; 0 / beta Catenin
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76. 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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77. 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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78. 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):106-10
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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.
  • [MeSH-major] Biomarkers, Tumor. Carcinoma, Adenoid Cystic / metabolism. Gene Expression Regulation, Neoplastic. Kallikreins / biosynthesis. Mouth Mucosa / metabolism. Salivary Gland Neoplasms / genetics

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  • (PMID = 16847813.001).
  • [ISSN] 0393-6155
  • [Journal-full-title] The International journal of biological markers
  • [ISO-abbreviation] Int. J. Biol. Markers
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.21.- / KLK13 protein, human; EC 3.4.21.- / Kallikreins
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79. Chen Y, Yu G, Ma D, Ni C, Zhu M: Microadenocarcinoma of the pancreas. Eur J Gastroenterol Hepatol; 2009 Dec;21(12):1373-8
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  • BACKGROUND: Microadenocarcinoma (MA) of the pancreas is a rare kind of neoplasm, whose status as an independent tumor entity is still a matter of controversy.
  • Immunohistochemistry revealed that MA, though with a certain extent of epithelial differentiation, possesses a different immunological phenotype from those of ductal carcinoma, acinar cell carcinoma, and endocrine tumors.
  • Genetic analysis showed no abnormality of p53, K-ras, and beta-catenin, which were usually mutated in pancreatic ductal adenocarcinoma.
  • CONCLUSION: Therefore, we suggest that MA should be taken as an independent tumor entity rather than a kind of growth pattern, but a final decision should be reached after cautious differential diagnosis of other kinds of pancreatic neoplasms.
  • [MeSH-major] Adenocarcinoma / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 19916245.001).
  • [ISSN] 1473-5687
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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80. Samaratunga H, Delahunt B: Ductal adenocarcinoma of the prostate: current opinion and controversies. Anal Quant Cytol Histol; 2008 Aug;30(4):237-46
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  • OBJECTIVE: To evaluate the morphologic spectrum and clinical significance of ductal adenocarcinoma of the prostate (DAP).
  • A basal cell layer can be seen in some of these tumors, which is probably due to tumor growth into preexisting ducts.
  • This usually represents an advanced stage of tumor progression and is not a precursor of invasive carcinoma.
  • CONCLUSION: DAP are neoplasms of prostatic origin, and the terms endometrioid or endometrial adenocarcinoma are best avoided.
  • DAP are aggressive tumors with a shortened average time to progression compared with acinar adenocarcinoma.

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  • (PMID = 18773743.001).
  • [ISSN] 0884-6812
  • [Journal-full-title] Analytical and quantitative cytology and histology
  • [ISO-abbreviation] Anal. Quant. Cytol. Histol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 36
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81. Kosmahl M, Pauser U, Anlauf M, Klöppel G: Pancreatic ductal adenocarcinomas with cystic features: neither rare nor uniform. Mod Pathol; 2005 Sep;18(9):1157-64
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  • Their wide spectrum also includes cystic variants of otherwise solid tumors, such as cystic endocrine tumors, cystic acinar cell carcinomas and ductal adenocarcinomas with cystic changes.
  • In the third group of cystic tumors there were four pancreatic ductal adenocarcinomas containing tumor-related retention cysts.
  • The fourth group consisted of two pancreatic ductal adenocarcinomas showing closely attached pseudocysts caused by tumor-associated pancreatitis.
  • The results indicate that a considerable number of pancreatic ductal adenocarcinomas and their variants display cystic features and must therefore be considered in the differential diagnosis of cystic neoplasms of the pancreas.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / pathology. Cysts / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Carcinoembryonic Antigen / metabolism. Female. Humans. Immunohistochemistry. Male. Middle Aged. Mucin 5AC. Mucins / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15920540.001).
  • [ISSN] 0893-3952
  • [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] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinoembryonic Antigen; 0 / MUC5AC protein, human; 0 / Mucin 5AC; 0 / Mucins; 0 / Tumor Suppressor Protein p53
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82. Fu XM, Dai X, Ding J, Zhu BT: Pancreas-specific protein disulfide isomerase has a cell type-specific expression in various mouse tissues and is absent in human pancreatic adenocarcinoma cells: implications for its functions. J Mol Histol; 2009 Jun;40(3):189-99
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  • [Title] Pancreas-specific protein disulfide isomerase has a cell type-specific expression in various mouse tissues and is absent in human pancreatic adenocarcinoma cells: implications for its functions.
  • Notably, in the digestive organs, such as the stomach and pancreas, very high levels of PDIp were selectively expressed in the digestive enzyme-secreting cells (e.g., gastric chief cells and pancreatic acinar cells).
  • In addition, high levels of PDIp expression were also detected in normal human pancreas, but its expression was mostly absent in human pancreatic duct adenocarcinoma and pancreatic cancer cell lines.
  • [MeSH-major] Adenocarcinoma / enzymology. Pancreas / enzymology. Pancreatic Neoplasms / enzymology. Protein Disulfide-Isomerases / metabolism
  • [MeSH-minor] Animals. Blotting, Western. COS Cells. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Pancreatic Ductal / pathology. Cell Line, Tumor. Cercopithecus aethiops. Humans. Mice. Organ Specificity. Protein Transport. Subcellular Fractions / enzymology

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  • (PMID = 19821078.001).
  • [ISSN] 1567-2387
  • [Journal-full-title] Journal of molecular histology
  • [ISO-abbreviation] J. Mol. Histol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA097109; United States / NCI NIH HHS / CA / CA97109; United States / NCRR NIH HHS / RR / P20RR021940
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 5.3.4.1 / Protein Disulfide-Isomerases
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83. Kimura N, Komuro K, Uchino S, Yagihashi S, Ishidate T, Ishizaka M: Multiple endocrine neoplasia type 1-associated cystic pancreatic endocrine neoplasia and multifocal cholesterol granulomas. Pathol Int; 2010 Apr;60(4):321-5
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  • [Title] Multiple endocrine neoplasia type 1-associated cystic pancreatic endocrine neoplasia and multifocal cholesterol granulomas.
  • A novel combination of tumors was found in a 68 year-old female with Multiple Endocrine Neoplasia type-1 (MEN 1) that included a cystic pancreatic endocrine neoplasm (CPEN), a pituitary adenoma, and multifocal cholesterol granulomas (MCGs) in the breast, pleura, and the extremities.
  • The pancreatic tumor displayed a single central locule surrounded by a thin rim of neoplastic parenchyma.
  • The tumor showed heterogeneity in the architecture that included glandular, trabecular and solid patterns.
  • The tumor cells of the pancreas were immunohistochemically positive for both endocrine and pancreatic acinar markers including chromogranin A, synaptophysin, glucagon, lipase, and reg protein.
  • Electron microscopy revealed that there were numerous smaller dense-cored neurosecretory granules, larger zymogen-like granules and microvilli on the apical side of the tumor cells.
  • The pancreatic tumor was diagnosed as CPEN with acinar cell features.
  • Analysis of the DNA extracted from the tissues revealed that there is a MEN1 germline mutation in exon 10 codon 527, and somatic mutation in exon 2 codon 32 in the pancreatic tumor, and one base pair deletion in exon 2 codon 79 in the pituitary adenoma.
  • [MeSH-major] Adenoma / pathology. Breast Neoplasms / pathology. Cholesterol. Granuloma, Foreign-Body / pathology. Multiple Endocrine Neoplasia Type 1 / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology. Pituitary Neoplasms / pathology


84. 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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86. Inamura K, Takeuchi K, Togashi Y, Hatano S, Ninomiya H, Motoi N, Mun MY, Sakao Y, Okumura S, Nakagawa K, Soda M, Choi YL, Mano H, Ishikawa Y: EML4-ALK lung cancers are characterized by rare other mutations, a TTF-1 cell lineage, an acinar histology, and young onset. Mod Pathol; 2009 Apr;22(4):508-15
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  • [Title] EML4-ALK lung cancers are characterized by rare other mutations, a TTF-1 cell lineage, an acinar histology, and young onset.
  • In this study, we clinicopathologically examined the characteristics of the EML4-ALK-positive cases, including the mutation status of EGFR, KRAS, and TP53, and whether they were of thyroid transcription factor-1 (TTF-1) cell lineage or not.
  • EML4-ALK-positive lung adenocarcinomas were characterized by less-differentiated grade (P=0.0082) and acinar-predominant structure (P<0.0001) in histology.
  • Thus, EML4-ALK-positive tumors may form a distinct entity among lung adenocarcinomas, characterized by young onset, acinar histology, no or rare mutations in EGFR, KRAS, and TP53, and a TTF-1 cell lineage, all in agreement with the prevalence in non- or light smokers.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. DNA-Binding Proteins / metabolism. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Age of Onset. Cell Lineage. Genes, erbB-1. Humans. Immunohistochemistry. Middle Aged. Mutation. Polymerase Chain Reaction. Polymorphism, Single-Stranded Conformational. Proto-Oncogene Proteins / genetics. Tumor Suppressor Protein p53 / genetics. ras Proteins / genetics

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  • (PMID = 19234440.001).
  • [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] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / EML4-ALK fusion protein, human; 0 / KRAS protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / TTF1 protein, human; 0 / Tumor Suppressor Protein p53; EC 3.6.5.2 / ras Proteins
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87. Sandoval J, Escobar J, Pereda J, Sacilotto N, Rodriguez JL, Sabater L, Aparisi L, Franco L, López-Rodas G, Sastre J: Pentoxifylline prevents loss of PP2A phosphatase activity and recruitment of histone acetyltransferases to proinflammatory genes in acute pancreatitis. J Pharmacol Exp Ther; 2009 Nov;331(2):609-17
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  • Pentoxifylline is a phosphodiesterase inhibitor with marked anti-inflammatory properties through blockade of extracellular signal regulated kinase (ERK) phosphorylation and tumor necrosis factor alpha production.
  • Necrotizing pancreatitis induced by taurocholate in rats and taurocholate-treated AR42J acinar cells were studied.
  • The rapid loss in PP2A activity induced by taurocholate in acinar cells was due to a decrease in cAMP levels that was prevented by pentoxifylline.
  • [MeSH-minor] Acute Disease. Animals. Blotting, Western. Cell Line. Chromatin Immunoprecipitation. Cyclic AMP / metabolism. Enzyme Activation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Male. Mitogen-Activated Protein Kinases / metabolism. Phosphoprotein Phosphatases / metabolism. RNA / biosynthesis. RNA / genetics. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 19671881.001).
  • [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 / Anti-Inflammatory Agents; 0 / Phosphodiesterase Inhibitors; 0 / Tumor Necrosis Factor-alpha; 63231-63-0 / RNA; E0399OZS9N / Cyclic AMP; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.4.17 / Cyclic Nucleotide Phosphodiesterases, Type 2; SD6QCT3TSU / Pentoxifylline
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88. Skoulidis F, Cassidy LD, Pisupati V, Jonasson JG, Bjarnason H, Eyfjord JE, Karreth FA, Lim M, Barber LM, Clatworthy SA, Davies SE, Olive KP, Tuveson DA, Venkitaraman AR: Germline Brca2 heterozygosity promotes Kras(G12D) -driven carcinogenesis in a murine model of familial pancreatic cancer. Cancer Cell; 2010 Nov 16;18(5):499-509
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  • Unexpectedly, tumor cells retain a functional Brca2 allele.
  • Three tumors from these patients displaying LOH were acinar carcinomas, which also developed only in mice with biallelic Brca2 inactivation.
  • We suggest a revised model for tumor suppression by BRCA2 with implications for the therapeutic strategy targeting BRCA2 mutant cancer cells.
  • [MeSH-major] BRCA2 Protein / genetics. Carcinoma, Pancreatic Ductal / genetics. Disease Models, Animal. Genes, BRCA2. Germ-Line Mutation. Heterozygote. Pancreatic Neoplasms / genetics. Proto-Oncogene Proteins p21(ras) / genetics
  • [MeSH-minor] Alleles. Animals. Cell Line, Tumor. Codon, Nonsense. Gene Silencing. Loss of Heterozygosity. Mice. Mice, 129 Strain. Mice, Inbred C57BL. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21056012.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105359877; United Kingdom / Medical Research Council / / ; United Kingdom / Cancer Research UK / / ; United Kingdom / Medical Research Council / / G9900064; United Kingdom / Medical Research Council / / G0600332; United Kingdom / Medical Research Council / / G0700651
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BRCA2 Protein; 0 / Codon, Nonsense; 0 / Tumor Suppressor Protein p53; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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89. Merrick GS, Gutman S, Andreini H, Taubenslag W, Lindert DL, Curtis R, Adamovich E, Anderson R, Allen Z, Butler W, Wallner K: Prostate cancer distribution in patients diagnosed by transperineal template-guided saturation biopsy. Eur Urol; 2007 Sep;52(3):715-23
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  • OBJECTIVES: To determine the prostate cancer incidence, anatomic distribution, Gleason score profile, and tumor burden in patients diagnosed by transperineal template-guided saturation biopsy (TTSB).
  • [MeSH-major] Biopsy / methods. Carcinoma, Acinar Cell / epidemiology. Prostatic Neoplasms / epidemiology
  • [MeSH-minor] Aged. Biomarkers, Tumor / blood. Diagnosis, Differential. Humans. Incidence. Male. Middle Aged. Multivariate Analysis. Neoplasm Staging / methods. Perineum. Predictive Value of Tests. Prostate-Specific Antigen / blood. Retrospective Studies. United States / epidemiology


90. Strom A, Bonal C, Ashery-Padan R, Hashimoto N, Campos ML, Trumpp A, Noda T, Kido Y, Real FX, Thorel F, Herrera PL: Unique mechanisms of growth regulation and tumor suppression upon Apc inactivation in the pancreas. Development; 2007 Aug;134(15):2719-25
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  • [Title] Unique mechanisms of growth regulation and tumor suppression upon Apc inactivation in the pancreas.
  • In adult mice, Apc-deficient pancreata were enlarged, solely as a result of hyperplasia of acinar cells, which accumulated beta-catenin, with the sparing of islets.
  • Expression of a target of beta-catenin, the proto-oncogene c-myc (Myc), was increased in acinar cells lacking Apc, suggesting that c-myc expression is essential for hyperplasia.
  • In support of this hypothesis, we found that conditional inactivation of c-myc in pancreata lacking Apc completely reversed the acinar hyperplasia.
  • Apc loss in organs such as the liver, colon and kidney, as well as experimental misexpression of c-myc in pancreatic acinar cells, led to tumor formation with high penetrance.
  • In conclusion, our work shows that beta-catenin modulation of c-myc is an essential regulator of acinar growth control, and unveils an unprecedented example of Apc requirement in the pancreas that is both temporally restricted and cell-specific.
  • This provides new insights into the mechanisms of tumor pathogenesis and tumor suppression in the pancreas.
  • [MeSH-minor] Animals. Genes, Tumor Suppressor / physiology. Genes, myc / physiology. Hyperplasia / genetics. Hypertrophy / genetics. Mice. Mice, Transgenic. Organ Specificity. Pancreatic Neoplasms / genetics. Signal Transduction. beta Catenin / metabolism. beta Catenin / physiology


91. Cazares LH, Drake RR, Esquela-Kirscher A, Lance RS, Semmes OJ, Troyer DA: Molecular pathology of prostate cancer. Cancer Biomark; 2010;9(1-6):441-59
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  • In spite of the large number of tissue cores, the amount of tumor available for study is often quite limited.
  • With the exception of ductal variants, recognized subtypes of prostate cancer are largely confined to research applications, and most prostate cancers are acinar.
  • The chapter concludes with an overview of blood biomarkers such as circulating nucleic acids and tumor cells and bound/free isoforms of prostate specific antigen (PSA).
  • [MeSH-major] Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Early Detection of Cancer. Humans. Male. Proteomics


92. Abdul M, Mccray SD, Hoosein NM: Expression of gamma-aminobutyric acid receptor (subtype A) in prostate cancer. Acta Oncol; 2008;47(8):1546-50
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  • We have also examined the effect of several GABA agonists and antagonists on the in vitro proliferation of four human prostate cancer cell lines: LNCaP, MDA-PCA-2b, DU145 and PC3.
  • Also, low to moderate GABAar staining was observed in the acinar epithelium of 50 (33%) prostate cancer specimens.
  • A GABAa agonist isoguvacine, at doses between 5-50 microg/ml (31-310 microM), stimulated the proliferation of all four human prostate cancer cell lines, tested.
  • [MeSH-major] Prostatic Neoplasms / metabolism. Receptors, GABA-A / metabolism
  • [MeSH-minor] Bicuculline / pharmacology. Cell Proliferation / drug effects. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Dihydroergotoxine / pharmacology. GABA Agonists / pharmacology. GABA Antagonists / pharmacology. GABA-A Receptor Agonists. GABA-B Receptor Agonists. Humans. Isonicotinic Acids / pharmacology. Male. Picrotoxin / pharmacology. Prostate / metabolism. Prostate / pathology. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology. Receptors, GABA-B / metabolism. Tumor Cells, Cultured

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  • (PMID = 18607852.001).
  • [ISSN] 1651-226X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / RR16461
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / GABA Agonists; 0 / GABA Antagonists; 0 / GABA-A Receptor Agonists; 0 / GABA-B Receptor Agonists; 0 / Isonicotinic Acids; 0 / Receptors, GABA-A; 0 / Receptors, GABA-B; 11032-41-0 / Dihydroergotoxine; 124-87-8 / Picrotoxin; Y37615DVKC / Bicuculline; YTF580771Y / isoguvacine
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93. Jorgenson TC, Williams BR, Wendland A, Bilger A, Sandgren EP, Drinkwater NR: Identification of susceptibility loci in a mouse model of KRASG12D-driven pancreatic cancer. Cancer Res; 2010 Nov 1;70(21):8398-406
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  • In this model, KRAS oncogene expression is driven by an elastase promoter in acinar cells of the pancreas on an FVB/NTac (FVB) background [FVB-Tg(Ela-KRAS(G12D))] with the transgene carried on the Y chromosome.
  • Markers on chromosome 2 segregated with high tumor multiplicity in all three strains; these loci were designated Prsq1-3 (pancreatic ras susceptibility quantitative trait loci 1-3; combined F2 and N2 LOD(W), 6.0, 4.1, and 2.7, respectively).
  • A marker on chromosome 12 segregated with tumor multiplicity in a BALB × FVB-Tg(Ela-KRAS(G12D)) cross and was designated Prsq6 (LOD(W), ∼2.5).
  • Our findings provide evidence that regions of chromosomes 2, 4, and 12 influence the development and progression of pancreatic neoplasms initiated by an oncogenic allele of KRAS in mice.

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  • [Copyright] ©2010 AACR.
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  • (PMID = 20959479.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076361; United States / NCI NIH HHS / CA / P01 CA022484; United States / NCI NIH HHS / CA / P01CA022484; United States / NCI NIH HHS / CA / R01CA076361; United States / NCI NIH HHS / CA / T32 CA009135
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS305961; NLM/ PMC3141286
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94. Osunkoya AO, Hansel DE, Sun X, Netto GJ, Epstein JI: Aberrant diffuse expression of p63 in adenocarcinoma of the prostate on needle biopsy and radical prostatectomy: report of 21 cases. Am J Surg Pathol; 2008 Mar;32(3):461-7
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  • Needle biopsy cases ranged from Gleason patterns 3 to 5 with tumor identified on one or more cores, ranging from a minute focus to 80% of the core.
  • In all 8 radical prostatectomies p63 positive cancer was present, with in 2/8 cases both p63 positive cancer and usual p63 negative acinar prostate cancer.
  • Rarely, prostate cancer can aberrantly express diffuse p63 staining in a nonbasal cell distribution leading to the erroneous diagnosis of atrophy or atypical basal cell proliferation.
  • [MeSH-major] Adenocarcinoma / chemistry. Biopsy, Needle. Membrane Proteins / analysis. Prostatectomy. Prostatic Neoplasms / chemistry

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  • (PMID = 18300803.001).
  • [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 / CKAP4 protein, human; 0 / Membrane Proteins
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95. 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.


96. Volkan Adsay N: Cystic lesions of the pancreas. Mod Pathol; 2007 Feb;20 Suppl 1:S71-93
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  • The names of some existing entities were revised; for example, what was known as papillary-cystic tumor is now regarded as solid-pseudopapillary tumor.
  • New entities, in particular, intraductal papillary mucinous neoplasm and its variants, such as oncocytic and intestinal subtypes were recognized.
  • Consensus criteria for the distinction of these from the ordinary precursors of adenocarcinoma, the pancreatic intraepithelial neoplasia, were established.
  • The definition of mucinous cystic neoplasms was refined; ovarian-like stroma has now become almost a requirement for the diagnosis of mucinous cystic neoplasia, and defined as such, the propensity of these tumors to occur in perimenopausal women became even more striking.
  • Greater accessibility of the pancreas afforded by improved invasive as well as noninvasive modalities has also increased the detection of otherwise clinically silent cystic tumors, which has led to the recognition of more innocuous entities such as acinar cell cystadenoma and squamoid cyst of pancreatic ducts.
  • [MeSH-major] Cystadenocarcinoma, Mucinous / pathology. Cystadenocarcinoma, Papillary / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology. Pancreatic Pseudocyst / pathology

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  • (PMID = 17486054.001).
  • [ISSN] 0893-3952
  • [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] Journal Article
  • [Publication-country] United States
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97. Osumi D, Takahashi M, Miyoshi E, Yokoe S, Lee SH, Noda K, Nakamori S, Gu J, Ikeda Y, Kuroki Y, Sengoku K, Ishikawa M, Taniguchi N: Core fucosylation of E-cadherin enhances cell-cell adhesion in human colon carcinoma WiDr cells. Cancer Sci; 2009 May;100(5):888-95
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  • [Title] Core fucosylation of E-cadherin enhances cell-cell adhesion in human colon carcinoma WiDr cells.
  • It was revealed that the low molecular weight population of E-cadherin was significantly increased in alpha1,6-fucosyltransferase-transfected WiDr cells in dense culture, which resulted in an enhancement in cell-cell adhesion.
  • In alpha1,6-fucosyltransferase knock down mouse pancreatic acinar cell carcinoma TGP49 cells, the expression of E-cadherin and E-cadherin dependent cell-cell adhesion was decreased.
  • The introduction of alpha1,6-fucosyltransferase into kidney epithelial cells from alpha1,6-fucosyltransferase(-/-) mice restored the expression of E-cadherin and E-cadherin-dependent cell-cell adhesion.
  • These results suggest a possible role of core fucosylation in the regulation of cell-cell adhesion in cancer.
  • [MeSH-major] Cadherins / metabolism. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Fucose / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Adhesion. Cell Line, Tumor. Female. Fucosyltransferases / deficiency. Fucosyltransferases / genetics. Fucosyltransferases / metabolism. Humans. Male

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  • (PMID = 19302290.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cadherins; 3713-31-3 / Fucose; EC 2.4.1.- / Fucosyltransferases; EC 2.4.1.68 / Glycoprotein 6-alpha-L-fucosyltransferase
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98. Tanahashi C, Yabuki S, Akamine N, Yatabe Y, Ichihara S: Pure acinic cell carcinoma of the breast in an 80-year-old Japanese woman. Pathol Int; 2007 Jan;57(1):43-6
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  • [Title] Pure acinic cell carcinoma of the breast in an 80-year-old Japanese woman.
  • Acinic cell carcinoma of the breast is an uncommon neoplasm.
  • Reported herein is the first case of primary acinic cell carcinoma of the breast in a Japanese woman.
  • To the naked eye, the tumor appeared well circumscribed and the cut surface was grayish-pink and hemorrhaging.
  • Microscopically, the tumor was predominantly made up of a monotonous proliferation of cells with a finely granular cytoplasm, resembling acinic cells of the parotid gland.
  • In spite of extensive sampling, no common histological patterns of breast carcinoma such as in situ and invasive ductal carcinoma were recognized in the present case, indicating that the present case was pure acinic cell carcinoma.
  • In addition, the immunohistochemical profile of this tumor was identical to that of the acinic cell carcinoma of the salivary gland: estrogen receptor, progesterone receptor, HER2 and cytokeratin (CK)20 were negative and amylase and CK7 were positive.
  • The patient has been well for 22 months since the wide local excision of the tumor and no signs of salivary neoplasm are evident to date.
  • [MeSH-major] Breast Neoplasms / diagnosis. Breast Neoplasms / pathology. Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / pathology


99. 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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100. 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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