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1. Doi Y, Kawamata H, Ono Y, Fujimori T, Imai Y: Expression and cellular localization of TSC-22 in normal salivary glands and salivary gland tumors: implications for tumor cell differentiation. Oncol Rep; 2008 Mar;19(3):609-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and cellular localization of TSC-22 in normal salivary glands and salivary gland tumors: implications for tumor cell differentiation.
  • TGF-beta-stimulated clone-22 (TSC-22) was reported to be a differentiation-inducing factor which negatively regulates the growth of salivary gland cancer cells.
  • In pleomorphic adenoma (PA), most of the sparse myoepithelial-like tumor cells, which are considered as the differentiated cells because they produce extracellular matrix, expressed TSC-22.
  • [MeSH-minor] Cell Differentiation. Humans. Immunohistochemistry

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  • (PMID = 18288391.001).
  • [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 / Repressor Proteins; 0 / TSC22D1 protein, human
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2. Zhang MZ, Xu J, Yao B, Yin H, Cai Q, Shrubsole MJ, Chen X, Kon V, Zheng W, Pozzi A, Harris RC: Inhibition of 11beta-hydroxysteroid dehydrogenase type II selectively blocks the tumor COX-2 pathway and suppresses colon carcinogenesis in mice and humans. J Clin Invest; 2009 Apr;119(4):876-85
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  • Furthermore, pharmacologic inhibition or gene silencing of 11betaHSD2 inhibited COX-2-mediated PGE2 production in tumors and prevented adenoma formation, tumor growth, and metastasis in mice.

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  • (PMID = 19307727.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA97386; United States / NIDDK NIH HHS / DK / DK48831; United States / NCI NIH HHS / CA / R01 CA094849; United States / NIDDK NIH HHS / DK / P50 DK039261; United States / NIDDK NIH HHS / DK / R01 DK048831; United States / NIDDK NIH HHS / DK / DK39261; United States / NIDDK NIH HHS / DK / R01 DK074359; United States / NCI NIH HHS / CA / R01 CA097386; United States / NIDDK NIH HHS / DK / DK74359; United States / NCI NIH HHS / CA / CA94849; United States / NIDDK NIH HHS / DK / DK62794; United States / NIDDK NIH HHS / DK / R01 DK062794
  • [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 / Cyclooxygenase 2 Inhibitors; 0 / Enzyme Inhibitors; 0 / RNA, Small Interfering; 0 / Receptors, Glucocorticoid; 6FO62043WK / Glycyrrhizic Acid; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenase Type 2; EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
  • [Other-IDs] NLM/ PMC2662561
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3. Spangelo BL, Roach JD, Hadi F, Damavandy AA, Plieskatt J, Badamchian M: Thymosin fraction-5 possesses antiproliferative properties in HL-60 human promyelocytic leukemia cells: characterization of an active peptide. Ann N Y Acad Sci; 2007 Sep;1112:305-16
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  • TF5 stimulates many assays of T cell-mediated immunity.
  • We found that TF5 substantially suppressed proliferation of the rat C6 glioma and MMQ pituitary adenoma cell lines.
  • Our current research using the promyelocytic cell line HL-60 suggests that TF5 also prevents proliferation of human myeloid leukemia cells.
  • Using the inhibition of HL-60 cell proliferation, we have chemically characterized TF5 using fast protein liquid chromatography (FPLC), reversed-phase high-performance liquid chromatography (RP-HPLC), and high-performance capillary electrophoresis (HPCE).
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Cell Division / drug effects. HL-60 Cells / cytology. Thymosin / analogs & derivatives
  • [MeSH-minor] Amino Acid Sequence. Animals. Apoptosis / drug effects. Cattle. Cell Line, Tumor. Glioma. Humans. Molecular Sequence Data. Myosins. Peptide Fragments / pharmacology. Pituitary Neoplasms. Thymus Gland

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  • (PMID = 17600287.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / 1R15NS051198-01A
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Peptide Fragments; 0 / thymosin fraction 5; 61512-21-8 / Thymosin; 77591-33-4 / thymosin beta(4); EC 3.6.4.1 / Myosins
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4. Smith DL, Keshavan P, Avissar U, Ahmed K, Zucker SD: Sodium taurocholate inhibits intestinal adenoma formation in APCMin/+ mice, potentially through activation of the farnesoid X receptor. Carcinogenesis; 2010 Jun;31(6):1100-9
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  • [Title] Sodium taurocholate inhibits intestinal adenoma formation in APCMin/+ mice, potentially through activation of the farnesoid X receptor.
  • Tissue specimens were analyzed by light microscopy, TUNEL staining, immunohistochemistry for beta-catenin and Ki-67 and quantitative polymerase chain reaction for farnesoid X receptor (FXR)-dependent gene expression.
  • Both treatment groups exhibited reduced levels of cellular proliferation in the ileum (by Ki-67 staining), but no differences in TUNEL staining or the percentage of beta-catenin-positive crypts.
  • Bilirubin feeding reduced intestinal inducible nitric oxide synthase expression, but did not alter adenoma multiplicity in APC(Min/+) mice or in AOM-treated j/j versus +/+ rats.

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  • (PMID = 20194350.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA119006; United States / NCI NIH HHS / CA / CA119006
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Cytoplasmic and Nuclear; 0 / beta Catenin; 0 / farnesoid X-activated receptor; 5E090O0G3Z / Taurocholic Acid; RFM9X3LJ49 / Bilirubin
  • [Other-IDs] NLM/ PMC2878362
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5. Nigawara T, Iwasaki Y, Asai M, Yoshida M, Kambayashi M, Sashinami H, Hashimoto K, Suda T: Inhibition of 11beta-hydroxysteroid dehydrogenase eliminates impaired glucocorticoid suppression and induces apoptosis in corticotroph tumor cells. Endocrinology; 2006 Feb;147(2):769-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We conclude that ectopic expression of 11beta-HSD2 is, at least in part, responsible for the impaired glucocorticoid suppression in corticotroph adenoma.
  • [MeSH-major] 11-beta-Hydroxysteroid Dehydrogenases / metabolism. Adenoma / enzymology. Apoptosis. Glucocorticoids / metabolism. Hydrocortisone / metabolism. Pituitary ACTH Hypersecretion / enzymology. Pituitary Neoplasms / enzymology
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Animals. Carbenoxolone / pharmacology. Cell Line, Tumor. Feedback, Physiological. Mice

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  • (PMID = 16254034.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenases; MM6384NG73 / Carbenoxolone; WI4X0X7BPJ / Hydrocortisone
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6. Haas S, Merkelbach-Bruse S, Justenhoven C, Brauch H, Fischer HP: Expression of xenobiotic and steroid hormone metabolizing enzymes in hepatocellular tumors of the non-cirrhotic liver. Pathol Res Pract; 2009;205(10):716-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Adenoma, Liver Cell / enzymology. Carcinoma, Hepatocellular / enzymology. Cytochrome P-450 Enzyme System / biosynthesis. Glutathione Transferase / biosynthesis. Liver Neoplasms / enzymology
  • [MeSH-minor] Adolescent. Biomarkers, Tumor / analysis. Female. Gonadal Steroid Hormones / metabolism. Humans. Immunohistochemistry. Male. Mutation. Polymerase Chain Reaction. Xenobiotics / metabolism. beta Catenin / genetics

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  • (PMID = 19596526.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Gonadal Steroid Hormones; 0 / Xenobiotics; 0 / beta Catenin; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 2.5.1.18 / Glutathione Transferase
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7. Monga SP: Hepatic adenomas: presumed innocent until proven to be beta-catenin mutated. Hepatology; 2006 Mar;43(3):401-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hepatic adenomas: presumed innocent until proven to be beta-catenin mutated.
  • [MeSH-major] Adenoma, Liver Cell / genetics. Liver Neoplasms / genetics. beta Catenin / genetics

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  • [CommentOn] Hepatology. 2006 Mar;43(3):515-24 [16496320.001]
  • (PMID = 16496344.001).
  • [ISSN] 0270-9139
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / beta Catenin
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8. Braeuning A, Singh Y, Rignall B, Buchmann A, Hammad S, Othman A, von Recklinghausen I, Godoy P, Hoehme S, Drasdo D, Hengstler JG, Schwarz M: Phenotype and growth behavior of residual β-catenin-positive hepatocytes in livers of β-catenin-deficient mice. Histochem Cell Biol; 2010 Nov;134(5):469-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The remaining β-catenin-positive hepatocytes showed approximately 25% higher cell volumes compared to the β-catenin-negative cells and exhibited a marker protein expression profile similar to that of normal perivenous hepatocytes or hepatoma cells with mutationally activated β-catenin.
  • Surprisingly, the expression pattern was observed independent of the cell's position within the liver lobule, suggesting a malfunction of physiological periportal repression of perivenously expressed genes in β-catenin-deficient liver.
  • Nonetheless, β-catenin-positive hepatocytes had no striking proliferative advantage, but started to grow out on treatment with phenobarbital, a tumor-promoting agent known to facilitate the formation of mouse liver adenoma with activating mutations of Ctnnb1.
  • [MeSH-major] Hepatocytes / pathology. beta Catenin / metabolism
  • [MeSH-minor] Animals. Carcinogens / pharmacology. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cell Proliferation. Cell Separation. Cell Size. Connexins / deficiency. Cytochrome P-450 CYP2E1 / metabolism. DNA Mutational Analysis. Disease Models, Animal. Female. Gene Expression. Glutamate-Ammonia Ligase / metabolism. Liver / drug effects. Liver / enzymology. Liver / pathology. Liver Neoplasms / genetics. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Male. Mice. Mice, Inbred C3H. Mice, Knockout. Phenobarbital / pharmacology. Phenotype. RNA, Messenger / metabolism

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  • (PMID = 20886225.001).
  • [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 / CTNNB1 protein, mouse; 0 / Carcinogens; 0 / Connexins; 0 / RNA, Messenger; 0 / beta Catenin; EC 1.14.13.- / Cytochrome P-450 CYP2E1; EC 6.3.1.2 / Glutamate-Ammonia Ligase; YQE403BP4D / Phenobarbital
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9. Bioulac-Sage P, Blanc JF, Rebouissou S, Balabaud C, Zucman-Rossi J: Genotype phenotype classification of hepatocellular adenoma. World J Gastroenterol; 2007 May 21;13(19):2649-54
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  • [Title] Genotype phenotype classification of hepatocellular adenoma.
  • Based on two molecular criteria (presence of a TCF1/HNF1 alpha or beta-catenin mutation), and an additional histological criterion (presence or absence of an inflammatory infiltrate), subgroups of hepatocellular adenoma can be defined and distinguished from focal nodular hyperplasia.
  • Analysis of 96 hepatocellular adenomas performed by a French collaborative network showed that they can be divided into four broad subgroups: the first one is defined by the presence of mutations in TCF1 gene inactivating the hepatocyte nuclear factor 1 (HNF1 alpha); the second by the presence of beta-catenin activating mutations; the category without mutations of HNF1 alpha or beta-catenin is further divided into 2 subgroups depending on the presence or absence of inflammation.
  • It is hoped that immunohistological tools will improve significantly diagnosis of liver biopsy in our ability to distinguish hepatocellular adenoma from focal nodular hyperplasia (FNH), and to delineate clinically meaningful entities within each group to define the best clinical management.
  • [MeSH-major] Adenoma, Liver Cell / classification. Genotype. Liver Neoplasms / classification. Phenotype
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Focal Nodular Hyperplasia / diagnosis. Hepatocyte Nuclear Factor 1-alpha / genetics. Humans. Liver / pathology. Mutation / genetics. beta Catenin / genetics

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  • (PMID = 17569132.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / beta Catenin
  • [Number-of-references] 23
  • [Other-IDs] NLM/ PMC4147112
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10. Murray NR, Weems J, Braun U, Leitges M, Fields AP: Protein kinase C betaII and PKCiota/lambda: collaborating partners in colon cancer promotion and progression. Cancer Res; 2009 Jan 15;69(2):656-62
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  • Our previous data indicated that PKCbetaII drives tumorigenesis and proliferation by activating beta-catenin/Apc signaling.

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  • (PMID = 19147581.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA081436; United States / NCI NIH HHS / CA / CA081436-11; United States / NCI NIH HHS / CA / CA094122; United States / NCI NIH HHS / CA / R01 CA094122; United States / NCI NIH HHS / CA / CA081436; United States / NCI NIH HHS / CA / R01 CA081436-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Isoenzymes; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C beta; EC 2.7.11.13 / protein kinase C lambda; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ NIHMS79085; NLM/ PMC2688739
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11. Bioulac-Sage P, Balabaud C, Zucman-Rossi J: Subtype classification of hepatocellular adenoma. Dig Surg; 2010;27(1):39-45
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  • [Title] Subtype classification of hepatocellular adenoma.
  • The expression of FABP1 (which is a HNF1A target gene) is downregulated and the absence of L-FABP expression diagnosed this subgroup. beta-Catenin-mutated HCA: beta-catenin mutations leading to activation of the Wnt/beta-catenin pathway represented 10-15% of HCA.
  • They are characterized by overexpression of glutamine synthetase and aberrant nuclear beta-catenin staining.
  • These beta-catenin-activated HCA are at greater risk of malignant transformation; they are difficult to differentiate from well-differentiated HCC.
  • Inflammatory HCA occurred more frequently in patients with high body mass index; they can be also mutated for beta-catenin and therefore are probably at risk of HCC.
  • [MeSH-major] Adenoma, Liver Cell / classification. Liver Neoplasms / classification
  • [MeSH-minor] Biomarkers, Tumor / analysis. Female. Hepatocyte Nuclear Factor 1 / genetics. Histocytochemistry. Humans. beta Catenin / genetics

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20357450.001).
  • [ISSN] 1421-9883
  • [Journal-full-title] Digestive surgery
  • [ISO-abbreviation] Dig Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / beta Catenin; 126548-29-6 / Hepatocyte Nuclear Factor 1
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12. Qian CN, Knol J, Igarashi P, Lin F, Zylstra U, Teh BT, Williams BO: Cystic renal neoplasia following conditional inactivation of apc in mouse renal tubular epithelium. J Biol Chem; 2005 Feb 04;280(5):3938-45
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  • Alterations in Wnt/beta-catenin signaling have been linked to abnormal kidney development and tumorigenesis.
  • As expected, the loss of Apc leads to increased levels of beta-catenin protein in renal epithelium.
  • Our results confirm an important role for proper regulation of Wnt/beta-catenin signaling in renal development and provide evidence that dysregulation of the pathway can initiate tumorigenesis in the kidney.
  • [MeSH-major] Adenoma / physiopathology. Genes, APC / physiology. Kidney Neoplasms / physiopathology. Polycystic Kidney Diseases / physiopathology
  • [MeSH-minor] Animals. Cytoplasm / metabolism. Cytoskeletal Proteins / metabolism. Integrases / genetics. Intercellular Signaling Peptides and Proteins / metabolism. Kidney Tubules / pathology. Kidney Tubules / physiopathology. Mice. Mice, Transgenic. Trans-Activators / metabolism. Urothelium / pathology. Urothelium / physiopathology. Wnt Proteins. beta Catenin

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  • (PMID = 15550389.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P50 DK057328; United States / NIDDK NIH HHS / DK / R01 DK067565; United States / NIDDK NIH HHS / DK / DK-42921; United States / NIDDK NIH HHS / DK / DK-57328; United States / NIDDK NIH HHS / DK / R01 DK042921; United States / NIDDK NIH HHS / DK / DK-67565
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, mouse; 0 / Cytoskeletal Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Trans-Activators; 0 / Wnt Proteins; 0 / beta Catenin; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
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13. Barker N, Ridgway RA, van Es JH, van de Wetering M, Begthel H, van den Born M, Danenberg E, Clarke AR, Sansom OJ, Clevers H: Crypt stem cells as the cells-of-origin of intestinal cancer. Nature; 2009 Jan 29;457(7229):608-11
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  • As in most cancers, the cell of origin has remained elusive.
  • The distribution of Lgr5(+) cells within stem-cell-derived adenomas indicates that a stem cell/progenitor cell hierarchy is maintained in early neoplastic lesions.
  • We conclude that stem-cell-specific loss of Apc results in progressively growing neoplasia.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / deficiency. Adenomatous Polyposis Coli Protein / genetics. Cell Lineage. Cell Transformation, Neoplastic. Intestinal Neoplasms / genetics. Intestinal Neoplasms / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Animals. Cell Proliferation. Colonic Neoplasms / genetics. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Genes, APC. Mice. Receptors, G-Protein-Coupled / analysis. Receptors, G-Protein-Coupled / genetics. Receptors, G-Protein-Coupled / metabolism. beta Catenin / metabolism


14. Sidibé EH: [Pituitary carcinoma. Anatomic and clinical features of cases reported in literature]. Neurochirurgie; 2007 Aug;53(4):284-8
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  • METHODS: We reviewed 67 cases reported in the literature [44 corticotropic pituitary tumors, 11 PRL tumors, 3 GH tumors, 1 TSH tumor, 3 gonadotropic cell tumors and 5 non-functioning tumors].
  • ACTH, beta-lipotrophin, betaendorphin, alphamelano-stimulating hormone, CRH, and beta-gamma MSH were contributive while ultrastructural microscopy provided little information, as did an equimolar Lph/ACTH ratio.
  • The characteristic feature is a time interval from the initial diagnosis of adenoma to that of cancer, which has ranged from 0.3 to 18 years (mean: 6.6 years; median: 5.0 years).
  • GH tumors appear to predominate although it is known that these cancers can develop in association with corticotrophin cancers or with prolactin cell tumors.
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adult. Aged. Female. Gonadotropins / metabolism. Growth Hormone-Secreting Pituitary Adenoma / diagnosis. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Humans. Male. Middle Aged. Prolactinoma / diagnosis. Prolactinoma / metabolism. Prolactinoma / pathology. Thyrotropin / metabolism

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  • (PMID = 17524431.001).
  • [ISSN] 0028-3770
  • [Journal-full-title] Neuro-Chirurgie
  • [ISO-abbreviation] Neurochirurgie
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Gonadotropins; 9002-71-5 / Thyrotropin
  • [Number-of-references] 50
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15. Meyer SE, Waltz SE, Goss KH: The Ron receptor tyrosine kinase is not required for adenoma formation in Apc(Min/+) mice. Mol Carcinog; 2009 Nov;48(11):995-1004
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  • [Title] The Ron receptor tyrosine kinase is not required for adenoma formation in Apc(Min/+) mice.
  • Nearly all colon tumors demonstrate loss of the adenomatous polyposis coli (APC) tumor suppressor, an early initiating event, subsequently leading to beta-catenin stabilization.
  • Even though baseline levels of intestinal crypt proliferation were increased in the Apc(Min/+) Ron-deficient mice, loss of Ron did not influence tumor size or histological appearance of the Apc(Min/+) adenomas, nor was beta-catenin localization changed compared to Apc(Min/+) mice with Ron.

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  • (PMID = 19452510.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA059268; United States / NCI NIH HHS / CA / R01 CA125379; United States / NCI NIH HHS / CA / CA 100002; United States / NCI NIH HHS / CA / R01 CA100002; United States / NCI NIH HHS / CA / T32 CA 59268
  • [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 / DNA Primers; EC 2.7.1.- / RON protein; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ NIHMS600186; NLM/ PMC4102426
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16. Ago K, Saegusa Y, Nishimura J, Dewa Y, Kemmochi S, Kawai M, Harada T, Mitsumori K, Shibutani M: Involvement of glycogen synthase kinase-3beta signaling and aberrant nucleocytoplasmic localization of retinoblastoma protein in tumor promotion in a rat two-stage thyroid carcinogenesis model. Exp Toxicol Pathol; 2010 May;62(3):269-80
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  • To investigate the cell cycle kinetics during the tumor promotion process induced by hypothyroidism in a rat model of thyroid follicular cell carcinogenesis, immunohistochemical analysis of cell cycle molecules and related signaling molecules was performed in conjunction with analysis of cell proliferation activity in an initiation-promotion model.
  • At each time point, proliferative lesions increased the expression of cyclin A, cyclin D, cyclin E and cyclin-dependent kinase (Cdk)-2, in association with the development of lesion stages from the early focal hyperplasia to the late carcinoma, while a subpopulation of proliferative lesions showed decreased numbers of both cell division cycle-2- and Ki-67-positive cells at week 15 compared with that at week 10, suggesting a reduced promoting effect of serum thyroid-stimulating hormone in the sensitive cellular population after long-term exposure to PTU.
  • The results suggest that proliferative lesions activate the cell cycle machinery following tumor promotion via a regulatory mechanism involving inactivation of GSK3beta and Rb protein, the latter signaling mechanism involving its aberrant nucleocytoplasmic transport for the acquisition of a malignant phenotype.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Glycogen Synthase Kinase 3 / metabolism. Retinoblastoma Protein / metabolism. Signal Transduction / physiology. Thyroid Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma, Follicular / chemically induced. Adenocarcinoma, Follicular / metabolism. Adenoma / chemically induced. Adenoma / metabolism. Animals. Carcinogens / toxicity. Cell Cycle Proteins / biosynthesis. Cell Cycle Proteins / drug effects. Cell Nucleus / metabolism. Cytoplasm / metabolism. Disease Models, Animal. Immunohistochemistry. Male. Nitrosamines / toxicity. Protein Transport / physiology. Rats. Rats, Inbred F344. Thiouracil / toxicity

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  • (PMID = 19505811.001).
  • [ISSN] 1618-1433
  • [Journal-full-title] Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie
  • [ISO-abbreviation] Exp. Toxicol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Cell Cycle Proteins; 0 / Nitrosamines; 0 / Retinoblastoma Protein; 59X161SCYL / Thiouracil; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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17. Mutanen M, Pajari AM, Paivarinta E, Misikangas M, Rajakangas J, Marttinen M, Oikarinen S: Berries as chemopreventive dietary constituents--a mechanistic approach with the ApcMin/+ mouse. Asia Pac J Clin Nutr; 2008;17 Suppl 1:123-5
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  • We wanted to see if pure ellagic acid, natural ellagitannins and three wild berries have any effect on the adenoma formation in Apc- mutated Min/+ mice.
  • Min/+ mice were fed high-fat AIN93-G diets containing 10% (w/w) freeze-dried bilberry (Vaccinium myrtillus), lingonberry (Vaccinium vitis-idaea), cloudberry (Rubus chamaemorus), cloudberry seeds or cloudberry pulp or pure ellagic acid at 1564 mg/kg for 10 weeks. beta-Catenin and cyclin D1 protein levels in the adenomas and in the normal-appearing mucosa were determined by Western blotting and immunohistochemistry.
  • Cloudberry resulted in decreased levels of nuclear beta-catenin and cyclin D1 and lingonberry in the level of cyclin D1 in the large adenomas (p < 0.05).
  • Ellagic acid had no effect on the number or size of adenomas in the distal or total small intestine but it increased adenoma size in the duodenum when compared with the control diet (p < 0.05).
  • Neither cloudberry seed nor pulp had any effect on the adenoma formation.
  • [MeSH-major] Adenoma / prevention & control. Cell Transformation, Neoplastic / drug effects. Ellagic Acid / pharmacology. Fruit / chemistry. Hydrolyzable Tannins / pharmacology. Intestinal Neoplasms / prevention & control
  • [MeSH-minor] Animals. Antineoplastic Agents, Phytogenic / pharmacology. Cyclin D1 / metabolism. Genes, APC. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Mice. Mice, Mutant Strains. Random Allocation. beta Catenin / metabolism

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  • (PMID = 18296318.001).
  • [ISSN] 0964-7058
  • [Journal-full-title] Asia Pacific journal of clinical nutrition
  • [ISO-abbreviation] Asia Pac J Clin Nutr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Hydrolyzable Tannins; 0 / beta Catenin; 0 / ellagitannin; 136601-57-5 / Cyclin D1; 19YRN3ZS9P / Ellagic Acid
  • [Number-of-references] 10
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18. Krause K, Karger S, Schierhorn A, Poncin S, Many MC, Fuhrer D: Proteomic profiling of cold thyroid nodules. Endocrinology; 2007 Apr;148(4):1754-63
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  • To obtain novel insights into their pathogenesis, protein expression profiling was performed in a series of 27 solitary CTNs (10 follicular adenoma and 20 adenomatous nodules) and surrounding normal thyroid tissues using two-dimensional gel electrophoresis combined with mass spectrometry analysis, Western blotting, and immunohistochemistry.
  • 1) thyroid cell proliferation, 2) turnover of thyroglobulin, and 3) H2O2 detoxification.
  • [MeSH-minor] Adult. Aged. Amyloid beta-Protein Precursor / metabolism. Antioxidants / metabolism. Female. Humans. Male. Middle Aged. Models, Biological. Oxidative Stress / genetics. Protease Nexins. Receptors, Cell Surface / metabolism


19. Halsey MA, Calder KB, Mathew R, Schlauder S, Morgan MB: Expression of alpha-methylacyl-CoA racemase (P504S) in sebaceous neoplasms. J Cutan Pathol; 2010 Apr;37(4):446-51
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  • BACKGROUND: Alpha-methylacyl-CoA racemase (AMACR), also known as P504S, is a protein that plays an important role in mitochondrial and peroxisomal beta-oxidation of branched-chain fatty acid and bile acid intermediates.
  • METHODS: Five samples of normal sebaceous glands as well as five cases each of sebaceous hyperplasia (SH), sebaceous adenoma (SA), basal cell carcinoma (BCC) with sebaceous differentiation and extraocular sebaceous carcinoma (SC) were evaluated for immunohistochemical (IHC) expression of AMACR.
  • [MeSH-major] Adenoma / enzymology. Carcinoma / enzymology. Racemases and Epimerases / metabolism. Sebaceous Gland Neoplasms / enzymology. Sebaceous Glands / enzymology

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  • (PMID = 19638170.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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20. Hahner S, Stuermer A, Kreissl M, Reiners C, Fassnacht M, Haenscheid H, Beuschlein F, Zink M, Lang K, Allolio B, Schirbel A: [123 I]Iodometomidate for molecular imaging of adrenocortical cytochrome P450 family 11B enzymes. J Clin Endocrinol Metab; 2008 Jun;93(6):2358-65
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  • Furthermore, four patients with known adrenal tumors (two metastatic adrenal adenocarcinomas, one bilateral adrenocortical adenoma, and one melanoma metastasis) were investigated with [(123)I]iodometomidate-SPECT.
  • RESULTS: In cell culture experiments, all compounds potently inhibited both Cyp11B1 and Cyp11B2.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis. Cytochrome P-450 CYP11B2 / analysis. Iodine Radioisotopes. Steroid 11-beta-Hydroxylase / analysis

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  • (PMID = 18397978.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 0 / Radioactive Tracers; 5377-20-8 / metomidate; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; Z22628B598 / Etomidate
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21. Montero-Conde C, Martín-Campos JM, Lerma E, Gimenez G, Martínez-Guitarte JL, Combalía N, Montaner D, Matías-Guiu X, Dopazo J, de Leiva A, Robledo M, Mauricio D: Molecular profiling related to poor prognosis in thyroid carcinoma. Combining gene expression data and biological information. Oncogene; 2008 Mar 6;27(11):1554-61
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  • According to known molecular interaction and reaction networks, the products of these genes were mainly clustered in the MAPkinase signaling pathway, the TGF-beta signaling pathway, focal adhesion and cell motility, activation of actin polymerization and cell cycle.
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adolescent. Adult. Aged. Carcinoma / genetics. Carcinoma / metabolism. Carcinoma / pathology. Carcinoma, Papillary / genetics. Carcinoma, Papillary / metabolism. Carcinoma, Papillary / pathology. Cell Differentiation. Female. Humans. Male. Middle Aged. Prognosis. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction


22. Chamorro MN, Schwartz DR, Vonica A, Brivanlou AH, Cho KR, Varmus HE: FGF-20 and DKK1 are transcriptional targets of beta-catenin and FGF-20 is implicated in cancer and development. EMBO J; 2005 Jan 12;24(1):73-84
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  • [Title] FGF-20 and DKK1 are transcriptional targets of beta-catenin and FGF-20 is implicated in cancer and development.
  • beta-catenin is the major effector of the canonical Wnt signaling pathway.
  • Mutations in components of the pathway that stabilize beta-catenin result in augmented gene transcription and play a major role in many human cancers.
  • We employed microarrays to identify transcriptional targets of deregulated beta-catenin in a human epithelial cell line (293) engineered to produce mutant beta-catenin and in ovarian endometrioid adenocarcinomas characterized with respect to mutations affecting the Wnt/beta-catenin pathway.
  • Furthermore, FGF20 and DKK1 appear to be direct targets for beta-catenin/TCF transcriptional regulation via LEF/TCF-binding sites.
  • Finally, by using small inhibitory RNAs specific for FGF20, we show that continued expression of FGF20 is necessary for maintenance of the anchorage-independent growth state in RK3E cells transformed by beta-catenin, implying that FGF-20 may be a critical element in oncogenesis induced by the Wnt signaling pathway.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenoma / genetics. Adenoma / metabolism. Animals. Cell Line. Epithelial Cells / cytology. Epithelial Cells / physiology. Female. Gene Expression Profiling. Gene Expression Regulation. Humans. Intercellular Signaling Peptides and Proteins / metabolism. Intestinal Mucosa / physiology. Mice. Oligonucleotide Array Sequence Analysis. Ovarian Neoplasms / genetics. Ovarian Neoplasms / metabolism. Promoter Regions, Genetic. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Signal Transduction / physiology. Wnt Proteins. Xenopus Proteins. beta Catenin

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  • (PMID = 15592430.001).
  • [ISSN] 0261-4189
  • [Journal-full-title] The EMBO journal
  • [ISO-abbreviation] EMBO J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / CTNNB1 protein, mouse; 0 / Cytoskeletal Proteins; 0 / DKK1 protein, human; 0 / Dkk1 protein, mouse; 0 / FGF20 protein, human; 0 / Fgf20 protein, mouse; 0 / Intercellular Signaling Peptides and Proteins; 0 / Proteins; 0 / RNA, Small Interfering; 0 / Trans-Activators; 0 / Wnt Proteins; 0 / Xenopus Proteins; 0 / beta Catenin; 0 / beta-catenin protein, Xenopus; 0 / dkk1 protein, Xenopus; 62031-54-3 / Fibroblast Growth Factors
  • [Other-IDs] NLM/ PMC544900
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23. Wang Y, Kowalski J, Tsai HL, Marik R, Prasad N, Somervell H, Lo PK, Sangenario LE, Dyrskjot L, Orntoft TF, Westra WH, Meeker AK, Eshleman JR, Umbricht CB, Zeiger MA: Differentiating alternative splice variant patterns of human telomerase reverse transcriptase in thyroid neoplasms. Thyroid; 2008 Oct;18(10):1055-63
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  • RESULTS: Malignant thyroid tumors exhibited a greater proportion of the active full-length hTERT transcript (0.57 +/- 0.15) than inactive splice variants, alpha(-) (0.13 +/- 0.02), or beta(-)/alpha(-)beta(-) deletion transcripts (0.30 +/- 0.11; p < 0.001).
  • The opposite was observed in benign tumors, which exhibited greater proportions of beta(-)/alpha(-)beta(-) deletion transcripts (0.64 +/- 0.08) than either the full-length (0.19 +/- 0.06) or alpha(-) deletion transcripts (0.17 +/- 0.02; p < 0.001).

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  • (PMID = 18816183.001).
  • [ISSN] 1557-9077
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21CA81162
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myc; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC2857449
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24. Gamero AM, Young MR, Mentor-Marcel R, Bobe G, Scarzello AJ, Wise J, Colburn NH: STAT2 contributes to promotion of colorectal and skin carcinogenesis. Cancer Prev Res (Phila); 2010 Apr;3(4):495-504
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  • Signal transducer and activator of transcription 2 (STAT2) is an essential transcription factor in the type I IFN (IFN-alpha/beta) signal transduction pathway and known for its role in mediating antiviral immunity and cell growth inhibition.
  • Contrary to our hypothesis, deletion of STAT2 inhibited azoxymethane/dextran sodium sulfate-induced colorectal carcinogenesis as measured by prolonged survival, lower adenoma incidence, smaller polyps, and less chronic inflammation.

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  • (PMID = 20233899.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R03 CA162545; United States / NCI NIH HHS / CA / K22 CA095326; United States / NCI NIH HHS / CA / CA095326-02; United States / NCI NIH HHS / CA / R01 CA140499; United States / NCI NIH HHS / CA / K22 CA095326-02; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / K22CA095326; United States / NCI NIH HHS / CA / N01CO12400; United States / NCI NIH HHS / CO / N01-CO-12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / STAT2 Transcription Factor
  • [Other-IDs] NLM/ NIHMS181318; NLM/ PMC2851485
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25. Hussaini IM, Trotter C, Zhao Y, Abdel-Fattah R, Amos S, Xiao A, Agi CU, Redpath GT, Fang Z, Leung GK, Lopes MB, Laws ER Jr: Matrix metalloproteinase-9 is differentially expressed in nonfunctioning invasive and noninvasive pituitary adenomas and increases invasion in human pituitary adenoma cell line. Am J Pathol; 2007 Jan;170(1):356-65
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  • [Title] Matrix metalloproteinase-9 is differentially expressed in nonfunctioning invasive and noninvasive pituitary adenomas and increases invasion in human pituitary adenoma cell line.
  • Gene clustering revealed a robust eightfold increase in matrix metalloproteinase (MMP)-9 expression in surgically resected human invasive PAs and in the (nonfunctioning) HP75 human pituitary tumor-derived cell line treated with phorbol-12-myristate-13-acetate; these results were confirmed by real-time polymerase chain reaction, gelatin zymography, reverse transcriptase-polymerase chain reaction, Western blot, immunohistochemistry, and Northern blot analyses.
  • The activation of protein kinase C (PKC) increased both MMP-9 activity and expression, which were blocked by some PKC inhibitors (Gö6976, bisindolylmaleimide, and Rottlerin), PKC-alpha, and PKC-delta small interfering (si)RNAs but not by hispidin (PKC-beta inhibitor).

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  • (PMID = 17200207.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS035122; United States / NCI NIH HHS / CA / R01 CA090851; United States / NINDS NIH HHS / NS / R29 NS035122; United States / NINDS NIH HHS / NS / NS35122; United States / NCI NIH HHS / CA / CA90851
  • [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 / Enzyme Inhibitors; 0 / Pyrones; 0 / RNA, Small Interfering; 56937-68-9 / phorbolol myristate acetate; EC 2.7.11.13 / Protein Kinase C; EC 3.4.24.35 / Matrix Metalloproteinase 9; NI40JAQ945 / Tetradecanoylphorbol Acetate; SSJ18CG55E / hispidin
  • [Other-IDs] NLM/ PMC1762693
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26. Davis JR, McNeilly JR, Norris AJ, Pope C, Wilding M, McDowell G, Holland JP, McNeilly AS: Fetal gonadotrope cell origin of FSH-secreting pituitary adenoma - insight into human pituitary tumour pathogenesis. Clin Endocrinol (Oxf); 2006 Nov;65(5):648-54
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  • [Title] Fetal gonadotrope cell origin of FSH-secreting pituitary adenoma - insight into human pituitary tumour pathogenesis.
  • OBJECTIVE: The pathogenesis of human pituitary adenomas remains unclear, but we report a case of FSH-secreting pituitary adenoma whose monohormonal phenotype suggests it was of fetal origin.
  • Normal components of gonadotrope signalling pathways were expressed, including oestrogen receptor-alpha, activin receptors, secretogranin-II and chromogranin-A. beta-glycan, the putative inhibin coreceptor, was absent.
  • CONCLUSIONS: We propose that this pituitary adenoma represents an indolent tumour of monohormonal fetal gonadotrope cells that originated early in gestation.
  • Pituitary tumours may therefore arise from abnormal persistence of fetal cell types, with extremely slow growth over many years until reaching a size threshold to generate an endocrine syndrome.
  • Understanding fetal pituitary architecture and function may be more informative for new insights into pituitary tumour pathogenesis than classical theories of cancer biology that invoke unrestrained cell proliferation.
  • [MeSH-major] Adenoma / embryology. Gonadotrophs / secretion. Pituitary Neoplasms / embryology

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  • (PMID = 17054468.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 4TI98Z838E / Estradiol; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
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27. Lee CI, Hsu MY, Chou CH, Wang C, Lo YS, Loh JK, Howng SL, Hong YR: CTNNB1 (beta-catenin) mutation is rare in brain tumours but involved as a sporadic event in a brain metastasis. Acta Neurochir (Wien); 2009 Sep;151(9):1107-11
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  • [Title] CTNNB1 (beta-catenin) mutation is rare in brain tumours but involved as a sporadic event in a brain metastasis.
  • Nevertheless, few or no mutations of CTNNB1 (beta-catenin) have so far been described in brain cancer.
  • We therefore examined the prevalence of constitutive activation of the Wnt signaling pathway in brain cancer specimens as well as cancer cell lines.
  • METHOD: We used polymerase chain reaction PCR and direct sequencing methods to investigate whether mutations in the CTNNB1 phosphorylation sites S33, S37, S41 and T45 were present in 68 brain tumours, including meningioma, astrocytoma, pituitary adenoma, neuroblastoma, metastasis to the brain, and cell lines.
  • FINDINGS: CTNNB1 gene mutations were not found in either the original brain tumour specimens or the cell lines.
  • In addition, in vitro functional assay showed that the S33C mutant of beta-catenin did affect transcriptional activity in a TCF-4-luciferase reporter construct.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / metabolism. Genetic Predisposition to Disease / genetics. Mutation / genetics. Neoplasm Metastasis / genetics. beta Catenin / genetics
  • [MeSH-minor] Biomarkers, Tumor / genetics. Carcinoma / secondary. Catalytic Domain / genetics. Cell Line, Tumor. DNA Mutational Analysis. Exons / genetics. Gene Expression Regulation, Neoplastic / genetics. Gene Frequency. Genetic Markers. Genetic Testing. Humans. Lung Neoplasms / pathology. Phosphorylation. Signal Transduction / genetics. Transcriptional Activation / genetics. Wnt Proteins / genetics

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  • (PMID = 19582367.001).
  • [ISSN] 0942-0940
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Genetic Markers; 0 / Wnt Proteins; 0 / beta Catenin
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28. Pannequin J, Delaunay N, Buchert M, Surrel F, Bourgaux JF, Ryan J, Boireau S, Coelho J, Pélegrin A, Singh P, Shulkes A, Yim M, Baldwin GS, Pignodel C, Lambeau G, Jay P, Joubert D, Hollande F: Beta-catenin/Tcf-4 inhibition after progastrin targeting reduces growth and drives differentiation of intestinal tumors. Gastroenterology; 2007 Nov;133(5):1554-68
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  • [Title] Beta-catenin/Tcf-4 inhibition after progastrin targeting reduces growth and drives differentiation of intestinal tumors.
  • BACKGROUND & AIMS: Aberrant activation of the beta-catenin/Tcf-4 transcriptional complex represents an initiating event for colorectal carcinogenesis, shifting the balance from differentiation toward proliferation in colonic crypts.
  • Here, we assessed whether endogenous progastrin, encoded by a target gene of this complex, was in turn able to regulate beta-catenin/Tcf-4 activity in adenomatous polyposis coli (APC)-mutated cells, and we analyzed the impact of topical progastrin depletion on intestinal tumor growth in vivo.
  • RESULTS: Depletion of endogenous progastrin production strongly decreased intestinal tumor growth in vivo through a marked inhibition of constitutive beta-catenin/Tcf-4 activity in tumor cells.
  • This effect was mediated by the de novo expression of the inhibitor of beta-catenin and Tcf-4 (ICAT), resulting from a down-regulation of integrin-linked kinase in progastrin-depleted cells.
  • In APCDelta14 mice, small interfering RNA-mediated progastrin depletion not only reduced intestinal tumor size and numbers, but also increased goblet cell lineage differentiation and cell apoptosis in the remaining adenomas.

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  • (PMID = 17920061.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM065926-05; United States / NIGMS NIH HHS / GM / R01 GM065926; United States / NIGMS NIH HHS / GM / R01 GM065926-05
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Ctnnbip1 protein, mouse; 0 / Gastrins; 0 / Protein Precursors; 0 / RNA, Small Interfering; 0 / Repressor Proteins; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Tcf7l2 protein, mouse; 0 / Transcription Factor 7-Like 2 Protein; 0 / Transcription Factors; 0 / beta Catenin; 53988-98-0 / big gastrin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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29. Preston SL, Leedham SJ, Oukrif D, Deheregoda M, Goodlad RA, Poulsom R, Alison MR, Wright NA, Novelli M: The development of duodenal microadenomas in FAP patients: the human correlate of the Min mouse. J Pathol; 2008 Feb;214(3):294-301
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  • The morphological changes associated with the adenoma-carcinoma sequence are well documented in the colorectum.
  • Small intestinal carcinogenesis is thought to progress through a similar adenoma-to-carcinoma pathway, but there is a relative dearth of studies examining the associated morphological changes.
  • Serial sections of these were stained with haematoxylin and eosin for beta-catenin and its downstream target CD44, for BMPR1a, lysozyme, carbonic anhydrase II, and with MIB-1.
  • [MeSH-major] Adenoma / pathology. Adenomatous Polyposis Coli / pathology. Duodenal Neoplasms / pathology
  • [MeSH-minor] Animals. Antigens, CD44 / analysis. Cell Differentiation. Cell Movement. Gene Expression. Genes, APC. Humans. Immunohistochemistry. Mice. Mice, Mutant Strains. Models, Animal. Mutation. Paneth Cells / pathology. Polymerase Chain Reaction. Precancerous Conditions / pathology. Staining and Labeling. beta Catenin / analysis


30. Dai WB, Ren ZP, Chen WL, DU J, Shi Z, Tang DY: [Expression and significance of APC, beta-catenin, C-myc, and Cyclin D1 proteins in colorectal carcinoma]. Ai Zheng; 2007 Sep;26(9):963-6
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  • [Title] [Expression and significance of APC, beta-catenin, C-myc, and Cyclin D1 proteins in colorectal carcinoma].
  • This study was to examine the expression of adenomatous polyposis coli (APC), beta-catenin, C-myc, and Cyclin D1 in different colorectal tissues, and investigate their possible roles in the carcinogenesis of colorectal carcinoma.
  • METHODS: The expression of APC, beta-catenin, C-myc, and Cyclin D1 in 30 specimens of normal colorectal mucosa, 30 specimens of colorectal adenoma, 10 specimens of colorectal adenoma with malignancy, and 50 specimens of colorectal carcinoma was examined by immunohistochemistry.
  • The expression of beta-catenin on cell membrane was regarded as normal, and its expression in cytoplasm and nuclei was defined as ectopic expression.
  • RESULTS: The positive rate of APC was significantly lower in colorectal carcinoma and colorectal adenoma with malignancy than in colorectal adenoma and normal colorectal mucosa (44.0% and 40.0% vs. 86.7% and 100.0%, P<0.01).
  • The ectopic expression rate of beta-catenin was significantly higher in colorectal carcinoma, colorectal adenoma with malignancy, and colorectal adenoma than in normal colorectal mucosa (62.0%, 50.0%, and 30.0% vs. 0%, P<0.01), and significantly higher in colorectal carcinoma than in colorectal adenoma (P<0.01).
  • The positive rate of C-myc was significantly higher in colorectal carcinoma, colorectal adenoma with malignancy, and colorectal adenoma than in normal colorectal mucosa (56.0%, 60.0%, and 46.7% vs. 0%, P<0.01).
  • The positive rate of Cyclin D1 was significantly higher in colorectal carcinoma, colorectal adenoma with malignancy, and colorectal adenoma than in normal colorectal mucosa (66.0%, 60.0%, and 30.0% vs. 0%,P<0.01), and significantly higher in colorectal carcinoma than in colorectal adenoma (P<0.01).
  • The ectopic expression of beta-catenin was positively correlated to the expression of C-myc and Cyclin D1 (r=0.63,P<0.01; r=0.57, P<0.01), and negatively correlated to the expression of APC (r=-0.39, P<0.05).
  • CONCLUSION: The reduced expression of APC, ectopic expression of beta-catenin, overexpression of C-myc and Cyclin D1 exist in colorectal carcinoma, which may play important roles in the carcinogenesis of colorectal carcinoma.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Colorectal Neoplasms / metabolism. Cyclin D1 / metabolism. Proto-Oncogene Proteins c-myc / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenoma / metabolism. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Intestinal Mucosa / metabolism. Precancerous Conditions / metabolism

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  • (PMID = 17927853.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / CCND1 protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / beta Catenin; 136601-57-5 / Cyclin D1
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31. Pantelis A, Wenghoefer M, Haas S, Merkelbach-Bruse S, Pantelis D, Jepsen S, Bootz F, Winter J: Down regulation and nuclear localization of human beta-defensin-1 in pleomorphic adenomas of salivary glands. Oral Oncol; 2009 Jun;45(6):526-30
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  • [Title] Down regulation and nuclear localization of human beta-defensin-1 in pleomorphic adenomas of salivary glands.
  • Although antimicrobial peptides (AMPs) appear to have diverse functional activities in innate immunity, a few reports suggest a potential role of human beta-defensin (hBD)-1 in tumor suppression.
  • Twenty human salivary gland specimens (five healthy, five chronic sialadenitis, five pleomorphic adenomas and five adenoma adjacent normal tissues (AANTs)) were investigated for mRNA expression levels of hBD-1, -2 and -3 by quantitative real-time RT-PCR.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. Neoplasm Proteins / metabolism. Salivary Gland Neoplasms / metabolism. beta-Defensins / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Cell Nucleus / metabolism. Chronic Disease. Down-Regulation. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction / methods. RNA, Messenger. Sialadenitis / metabolism. Sialadenitis / pathology. Young Adult

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  • (PMID = 18805729.001).
  • [ISSN] 1879-0593
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DEFB1 protein, human; 0 / DEFB4A protein, human; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / beta-Defensins; 0 / beta-defensin 3, human
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32. Das P, Jain D, Vaiphei K, Wig JD: Abberant crypt foci -- importance in colorectal carcinogenesis and expression of p53 and mdm2: a changing concept. Dig Dis Sci; 2008 Aug;53(8):2183-8
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  • Till date, in human ACF, K-ras, beta-catenin, carcinoembryonic antigen (CEA) and adenomatous polyposis coli (APC) protein expression have been investigated, but the expression of late markers of colon carcinogenesis have not been studied in great detail.
  • This results suggests that the conventional adenoma-carcinoma sequence is not completely correct.
  • [MeSH-major] Adenocarcinoma / chemistry. Cell Transformation, Neoplastic / chemistry. Colorectal Neoplasms / chemistry. Precancerous Conditions / chemistry. Proto-Oncogene Proteins c-mdm2 / analysis. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 18080767.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. Ceccarelli C, Canale D, Battisti P, Caglieresi C, Moschini C, Fiore E, Grasso L, Pinchera A, Vitti P: Testicular function after 131I therapy for hyperthyroidism. Clin Endocrinol (Oxf); 2006 Oct;65(4):446-52
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  • Seventeen of the patients had Graves' disease and two had toxic adenoma.
  • The beta dose delivered to the testes was evaluated by the Medical Internal Radiation Dose (MIRD) method.
  • RESULTS: In the dosimetric study, the beta dose absorbed in the testes was 12.5 +/- 8.8 mGy (range 29-15 mGy) and the gamma dose was 15.8 +/- 5.3 mGy (range 24-11 mGy).
  • CONCLUSIONS: After (131)I therapy, germinal epithelium and Leydig cell function undergo only marginal changes, which may have some significance in subjects with a pre-existing fertility impairment.

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  • (PMID = 16984236.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 3XMK78S47O / Testosterone
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34. Sabates-Bellver J, Van der Flier LG, de Palo M, Cattaneo E, Maake C, Rehrauer H, Laczko E, Kurowski MA, Bujnicki JM, Menigatti M, Luz J, Ranalli TV, Gomes V, Pastorelli A, Faggiani R, Anti M, Jiricny J, Clevers H, Marra G: Transcriptome profile of human colorectal adenomas. Mol Cancer Res; 2007 Dec;5(12):1263-75
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  • In normal mucosa, KIAA1199 expression was confined to cells in the lower portion of intestinal crypts, where Wnt signaling is physiologically active, but it was markedly increased in all adenomas, where it was expressed in most of the epithelial cells, and in colon cancer cell lines, it was markedly reduced by inactivation of the beta-catenin/T-cell factor(s) transcription complex, the pivotal mediator of Wnt signaling.
  • [MeSH-major] Adenoma / genetics. Biomarkers, Tumor / genetics. Colorectal Neoplasms / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic
  • [MeSH-minor] Aged. Cell Transformation, Neoplastic / genetics. Female. Genetic Markers. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Phylogeny. RNA, Messenger / metabolism. Transcription, Genetic

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  • (PMID = 18171984.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / RNA, Messenger
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35. Takayama T, Miyanishi K, Hayashi T, Sato Y, Niitsu Y: Colorectal cancer: genetics of development and metastasis. J Gastroenterol; 2006 Mar;41(3):185-92
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  • One is the chromosomal instability pathway (adenoma-carcinoma sequence), which is characterized by allelic losses on chromosome 5q (APC), 17p (p53), and 18q (DCC/SMAD4), and the other is a pathway that involves microsatellite instability.
  • Other routes, including the transforming growth factor-beta/SMAD pathway, the serrated pathway, and the epigenetic pathway, have been reported.
  • In the invasion and metastasis steps of colorectal cancers, many more genes have now been identified as being involved in proteolysis, adhesion, angiogenesis, and cell growth.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma / genetics. Cell Transformation, Neoplastic / genetics. Colorectal Neoplasms / genetics
  • [MeSH-minor] Chromosomal Instability. Epigenesis, Genetic. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Genes, ras. Genetic Predisposition to Disease. Humans. Microsatellite Instability. Signal Transduction / genetics. Smad4 Protein / genetics. Transforming Growth Factor beta / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 16699851.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Smad4 Protein; 0 / Transforming Growth Factor beta; 0 / Tumor Suppressor Proteins
  • [Number-of-references] 98
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36. Kim I, Morimura K, Shah Y, Yang Q, Ward JM, Gonzalez FJ: Spontaneous hepatocarcinogenesis in farnesoid X receptor-null mice. Carcinogenesis; 2007 May;28(5):940-6
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  • Surprisingly, at 12 months of age, male and female Fxr-null mice had a high incidence of degenerative hepatic lesions, altered cell foci and liver tumors including hepatocellular adenoma, carcinoma and hepatocholangiocellular carcinoma, the latter of which is rarely observed in mice.
  • At 3 months, Fxr-null mice had increased expression of the proinflammatory cytokine IL-1beta mRNA and elevated beta-catenin and its target gene c-myc.
  • They also had increased cell proliferation as revealed by increased PCNA mRNA and BrdU incorporation.


37. Usui T, Izawa S, Sano T, Tagami T, Nagata D, Shimatsu A, Takahashi JA, Naruse M: Clinical and molecular features of a TSH-secreting pituitary microadenoma. Pituitary; 2005;8(2):127-34
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  • There was no thyroid hormone receptor (TR) beta gene mutation.
  • The patient was diagnosed with a TSH-secreting pituitary adenoma, and trans-sphenoid surgery was performed.
  • The histologic features and immunophenotype were consistent with a TSH-secreting pituitary adenoma.
  • The tumor expressed TSH, growth hormone, prolactin, alpha-subunit, pituitary transcription factor-1 (pit-1) but not proopiomelanocortin (POMC), prophet of pit-1 (prop-1) and pituitary cell-restricted T box factor (Tpit).
  • [MeSH-major] Adenoma / physiopathology. Pituitary Neoplasms / physiopathology. Thyrotropin / secretion
  • [MeSH-minor] Female. Humans. Middle Aged. Polymerase Chain Reaction. Thyroid Hormone Receptors beta / biosynthesis. Thyrotropin-Releasing Hormone. Triiodothyronine

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  • (PMID = 16379036.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Thyroid Hormone Receptors beta; 06LU7C9H1V / Triiodothyronine; 5Y5F15120W / Thyrotropin-Releasing Hormone; 9002-71-5 / Thyrotropin
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38. Declercq J, Van Dyck F, Van Damme B, Van de Ven WJ: Upregulation of Igf and Wnt signalling associated genes in pleomorphic adenomas of the salivary glands in PLAG1 transgenic mice. Int J Oncol; 2008 May;32(5):1041-7
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  • The Pleomorphic adenoma gene 1 (PLAG1) is involved in various human neoplasias, including pleomorphic adenomas of the salivary glands.
  • Further studies revealed that several genes such as H19, Dlk1, Gtl2, Igfbp2, Igfbp3 and genes involved in Wnt signalling, such as Wnt6, Cyclin D1 and beta-catenin are upregulated in P1-MCre mice in which Igf2 is inactivated.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Neoplastic. Insulin-Like Growth Factor II / metabolism. Salivary Gland Neoplasms / metabolism. Signal Transduction / genetics. Wnt Proteins / metabolism
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Mice. Mice, Knockout. Mice, Transgenic. Time Factors

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  • (PMID = 18425330.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / IGF2 protein, mouse; 0 / Plag1 protein, mouse; 0 / Wnt Proteins; 67763-97-7 / Insulin-Like Growth Factor II
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39. Rojas A, Meherem S, Kim YH, Washington MK, Willis JE, Markowitz SD, Grady WM: The aberrant methylation of TSP1 suppresses TGF-beta1 activation in colorectal cancer. Int J Cancer; 2008 Jul 1;123(1):14-21
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  • Such alterations often deregulate signaling pathways that affect the formation of colon cancer, such as the Wnt, RAS-MAPK and TGF-beta pathways.
  • The tumor promoting effects of mutations in genes, such as APC, have been demonstrated in cancer cell lines and in mouse models of intestinal cancer; however, the biological effects of most epigenetic events identified in colorectal cancer remain unknown.
  • Consequently, we assessed whether the aberrant methylation of TSP1, the gene for thrombospondin 1, a regulator of TGF-beta ligand activation, is an epigenetic mechanism for inhibiting the TGF-beta signaling pathway.
  • We found methylated TSP1 occurs in colon cancer cell lines (33%), colon adenomas (14%) and colon adenocarcinomas (21%).
  • In primary colorectal cancers, loss of TSP1 expression correlated with impaired TGF-beta signaling as indicated by decreased Smad2 phosphorylation and nuclear localization.
  • Furthermore, methylation-induced silencing of TSP1 expression reduced the concentration of secreted active TGF-beta1 and attenuated TGF-beta signaling.
  • Reversal of TSP1 methylation resulted in increased TSP1 mediated activation of the latent LAP:TGF-beta complex and subsequent TGF-beta receptor activation.
  • Our results demonstrate that the aberrant methylation of TSP1 has biological consequences and provide evidence that the aberrant methylation of TSP1 is a novel epigenetic mechanism for suppressing TGF-beta signaling in colorectal cancer.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
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  • (PMID = 18425817.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA115513-01A2; United States / NCI NIH HHS / CA / R01 CA115513; United States / NCI NIH HHS / CA / R01 CA115513-01A2
  • [Publication-type] Journal Article; 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 / RNA, Small Interfering; 0 / SMAD2 protein, human; 0 / Smad2 Protein; 0 / Thrombospondin 1; 0 / Transforming Growth Factor beta1
  • [Other-IDs] NLM/ NIHMS156274; NLM/ PMC2777657
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40. Savas B, Ensari A, Percinel S, Kuzu I, Kuzu MA, Bektas M, Cetinkaya H, Kursun N: The significance of beta-catenin, E-cadherin, and P-cadherin expressions in neoplastic progression of colorectal mucosa: an immunohistochemical study. Acta Gastroenterol Belg; 2007 Oct-Dec;70(4):339-44
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  • [Title] The significance of beta-catenin, E-cadherin, and P-cadherin expressions in neoplastic progression of colorectal mucosa: an immunohistochemical study.
  • BACKGROUND AND STUDY AIMS: The purpose of the current study was to investigate the role of beta-catenin, E-cadherin and P-cadherin in colorectal carcinogenesis using tissue array method.
  • PATIENTS AND METHODS: Core tissue biopsies were taken from paraffin-embedded tissue blocks of 167 cases including 26 normal mucosae (NM), 99 colorectal polyps (10 hyperplastic polyps (HP), 8 traditional serrated (TSA), 17 tubular (TA), 37 tubulovillous (TVA), and 27 villous adenomas (VA)), 14 adenomas with intramucosal carcinoma (ACA), and 28 colorectal cancers (CCA).
  • Immunohistochemistry was performed using antibodies to beta-catenin, E-cadherin, and P-cadherin.
  • RESULTS: beta-catenin expression was cytoplasmic, membranous, and nuclear.
  • Membranous expression of beta-catenin significantly decreased in CCA (p < 0.01).
  • Nuclear beta-catenin expression significantly increased in close correlation with neoplastic sequence reaching its highest expression in ACA and CCA (p < 0.001).
  • Polyps with intraepithelial neoplasia (IEN) showed significantly higher nuclear beta-catenin expression in parallel with increasing grades of IEN (p < 0.001).
  • CONCLUSIONS: Nuclear beta-catenin expression correlating with the grade of IEN in polyps and carcinomas supports its role in colorectal carcinogenesis.
  • E-cadherin and P-cadherin expressions in adenomas suggest that these molecules might have role in adenoma formation though not necessarily be involved in neoplastic progression.
  • [MeSH-major] Cadherins / analysis. Colonic Neoplasms / pathology. Intestinal Mucosa / pathology. Rectal Neoplasms / pathology. beta Catenin / analysis
  • [MeSH-minor] Adenoma / pathology. Adenoma, Villous / pathology. Adult. Aged. Aged, 80 and over. Carcinoma / pathology. Carcinoma in Situ / pathology. Cell Membrane / ultrastructure. Cell Nucleus / ultrastructure. Cytoplasm / ultrastructure. Disease Progression. Female. Humans. Hyperplasia. Immunohistochemistry. Intestinal Polyps / pathology. Male. Middle Aged. Tissue Array Analysis


41. Adsay NV: Cystic neoplasia of the pancreas: pathology and biology. J Gastrointest Surg; 2008 Mar;12(3):401-4
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  • SPT holds a distinctive place among pancreatic neoplasia because of its highly peculiar characteristics, undetermined cell lineage, occurrence almost exclusively in young females, association with beta-catenin pathway, and also by being a very low-grade curable malignancy.
  • [MeSH-major] Adenoma / pathology. Carcinoma in Situ / pathology. Neoplasms, Cystic, Mucinous, and Serous / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology. Precancerous Conditions / pathology

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  • (PMID = 17957438.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 19
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42. Hsu HH, Cheng SF, Wu CC, Chu CH, Weng YJ, Lin CS, Lee SD, Wu HC, Huang CY, Kuo WW: Apoptotic effects of over-expressed estrogen receptor-beta on LoVo colon cancer cell is mediated by p53 signalings in a ligand-dependent manner. Chin J Physiol; 2006 Apr 30;49(2):110-6
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  • [Title] Apoptotic effects of over-expressed estrogen receptor-beta on LoVo colon cancer cell is mediated by p53 signalings in a ligand-dependent manner.
  • Patients that received E2 replacement therapy were found to have a reduction in the incidence of colon adenoma and carcinoma.
  • LoVo cells were transient transfected to overexpress ER-beta, DNA fragmentation and caspase activity assay were performed to evaluate apoptotic effects.
  • Our data clearly demonstrated that E2 and ER-beta alone could upregulate p21 and p27 proteins, which further activate caspase-8 and caspase-9 to induce apoptosis in LoVo cell, and the ER-beta. effects were enhanced by E2.
  • However, overexpressed ER-beta did not influence the expression and promoter activity of TNF-alpha.
  • In addition, E2 and overexpressed ER-beta downregulated the beta-catenin proteins which cause the downregulation of its target genes, cyclin D1 and Rb, to inhibit the cell cycle and cell proliferation.
  • The results indicate that overexpressed ER-beta may induce LoVo cell apoptosis and anti-proliferation by increasing p53 signaling in a ligand-dependent manner, and without hTNF-alpha involvement.
  • Efforts aiming at enhancing ER-beta expression and/or activity may prove to be an attractive alternative therapy against colorectal cancer.
  • [MeSH-major] Apoptosis. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Estrogen Receptor beta / metabolism. Signal Transduction. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. Ligands. Recombinant Proteins / metabolism. Up-Regulation

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  • [ErratumIn] Chin J Physiol. 2006 Jun 30;49(3):167
  • (PMID = 16830793.001).
  • [ISSN] 0304-4920
  • [Journal-full-title] The Chinese journal of physiology
  • [ISO-abbreviation] Chin J Physiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / Estrogen Receptor beta; 0 / Ligands; 0 / Recombinant Proteins; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
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43. Fan XS, Wu HY, Yu HP, Zhou Q, Zhang YF, Huang Q: Expression of Lgr5 in human colorectal carcinogenesis and its potential correlation with beta-catenin. Int J Colorectal Dis; 2010 May;25(5):583-90
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  • [Title] Expression of Lgr5 in human colorectal carcinogenesis and its potential correlation with beta-catenin.
  • BACKGROUNDS AND AIMS: Lgr5 is a member of the G protein receptor super-family and was shown recently to be a stem cell marker for cells with intestinal differentiation.
  • Its over-expression has been demonstrated in hepatocellular, basal cell carcinoma, and ovarian cancers but the underlying mechanisms are poorly understood.
  • The aim of this study was to investigate if Lgr5 over-expression was correlated with human colorectal carcinogenesis and its potential correlation with beta-catenin.
  • METHODS: The study was carried out on a tissue microarray that consisted of 102 colorectal carcinomas (CRC; M:F = 55:47), 18 colon adenoma, and 12 colon normal mucosa cases.
  • Immunostains were performed with the standard EnVision method with primary antibodies against Lgr5, beta-catenin, and p53 antigens.
  • In normal mucosa, adenoma, and CRC, beta-catenin expression was seen in 25% (three out of 12), 27% (five out of 18), and 81% (83/102) cases, respectively, in contrast to 0, 0, and 40% (41/102) for p53 expression, respectively.
  • In CRC, Lgr5 expression was more intense in women than men (p < 0.0001), and positively correlated with beta-catenin expression (p < 0.001), but not with patients' ages, tumor sizes, nodal status, TNM stages, and p53 expression.
  • CONCLUSIONS: The results suggest that up-regulation of Lgr5 expression, especially in female patients, may play an important role in colorectal carcinogenesis, probably through the WNT/beta-catenin pathway, but not involve the progression of the CRC.
  • [MeSH-major] Colorectal Neoplasms / metabolism. Colorectal Neoplasms / pathology. Receptors, G-Protein-Coupled / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Male. Middle Aged. Neoplasm Invasiveness. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 20195621.001).
  • [ISSN] 1432-1262
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / LGR5 protein, human; 0 / Receptors, G-Protein-Coupled; 0 / Tumor Suppressor Protein p53; 0 / beta Catenin
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44. Obrador-Hevia A, Chin SF, González S, Rees J, Vilardell F, Greenson JK, Cordero D, Moreno V, Caldas C, Capellá G: Oncogenic KRAS is not necessary for Wnt signalling activation in APC-associated FAP adenomas. J Pathol; 2010 May;221(1):57-67
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  • Recent studies have suggested that APC loss alone may be insufficient to promote aberrant Wnt/beta-catenin signalling.
  • Somatic APC and KRAS mutations, beta-catenin immunostaining, and qRT-PCR of APC, MYC, AXIN2 and SFRP1 were analysed.
  • Array-comparative genomic hybridization (aCGH) was also assessed in 26 FAP adenomas and 24 paired adenoma-carcinoma samples.
  • Increased cytoplasmic and/or nuclear beta-catenin staining was seen in 94% and 80% of the adenomas. beta-Catenin nuclear staining was strongly associated with MYC levels (p value 0.03) but not with KRAS mutations.
  • Based on beta-catenin staining and Wnt pathway target genes alterations the Wnt pathway appears to be constitutively activated in all APC-FAP tumours, with alterations occurring both upstream and downstream of APC.
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / biosynthesis. Adenomatous Polyposis Coli Protein / genetics. Adult. Cell Nucleus / metabolism. Comparative Genomic Hybridization. Female. Gene Expression Regulation, Neoplastic. Genetic Predisposition to Disease. Germ-Line Mutation. Humans. Loss of Heterozygosity. Male. Signal Transduction / physiology. Young Adult. beta Catenin / metabolism

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  • [Copyright] Copyright (c) 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • [CommentIn] J Pathol. 2010 Jul;221(3):239-41 [20527017.001]
  • (PMID = 20196079.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Wnt Proteins; 0 / beta Catenin; EC 3.6.5.2 / ras Proteins
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45. Arzt E, Chesnokova V, Stalla GK, Melmed S: Pituitary adenoma growth: a model for cellular senescence and cytokine action. Cell Cycle; 2009 Mar 1;8(5):677-8
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  • [Title] Pituitary adenoma growth: a model for cellular senescence and cytokine action.

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  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA075979-10; United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / R01 CA075979-10
  • [Publication-type] Editorial
  • [Publication-country] United States
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46. Carothers AM, Davids JS, Damas BC, Bertagnolli MM: Persistent cyclooxygenase-2 inhibition downregulates NF-{kappa}B, resulting in chronic intestinal inflammation in the min/+ mouse model of colon tumorigenesis. Cancer Res; 2010 Jun 1;70(11):4433-42
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  • Cyclooxygenase-2 (COX-2) inhibition prevents adenoma formation in humans and mouse models of colon cancer.
  • The selective COX-2 inhibitor celecoxib reduces COX-2 and prostaglandin E(2) (PGE(2)) expression and adenomas in the intestine of Min/+ mice after treatment for several weeks, but prolonged treatment increases PGE(2) production, resulting in drug-resistant tumor formation and transforming growth factor beta (TGFbeta)-dependent intestinal fibrosis.
  • This effect was associated with inhibition of TGFbeta-associated kinase-1 and IkappaB kinase alpha/beta activities and reduced expression of the Toll-like receptor (TLR) 2 and TLR4 that enhance colonic barrier function.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Colitis / metabolism. Colonic Neoplasms / metabolism. Cyclooxygenase 2 / metabolism. Cyclooxygenase 2 Inhibitors / pharmacology. NF-kappa B / metabolism

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  • [Copyright] Copyright 2010 AACR.
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  • (PMID = 20484034.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K05 CA131504; United States / NCI NIH HHS / CA / K05 CA131504-04
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Cyclooxygenase 2 Inhibitors; 0 / Interleukin-1beta; 0 / NF-kappa B; 0 / Pyrazoles; 0 / Sulfonamides; 0 / Toll-Like Receptors; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / MAP kinase kinase kinase 7; JCX84Q7J1L / Celecoxib
  • [Other-IDs] NLM/ NIHMS196066; NLM/ PMC3242378
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47. Jiao YF, Nakamura S, Sugai T, Yamada N, Habano W: Serrated adenoma of the colorectum undergoes a proliferation versus differentiation process: new conceptual interpretation of morphogenesis. Oncology; 2008;74(3-4):127-34
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  • [Title] Serrated adenoma of the colorectum undergoes a proliferation versus differentiation process: new conceptual interpretation of morphogenesis.
  • OBJECTIVE: Serrated adenoma (SA) consists of glands both with intraluminal projection of tall columnar cells, which resemble the terminally differentiated cells in the surface epithelium, and with concave short cells, which resemble progenitor crypt cells of the colon.
  • METHODS: The expressions of both terminally differentiated markers, such as p21, cytokeratin 20 and carbonic anhydrase I, and progenitor/proliferative markers, such as beta-catenin, CD44 and Ki-67, were immunohistochemically examined in 43 SAs and 20 tubular adenomas.
  • Cytokeratin 20 and carbonic anhydrase I expressions were confined to the tall cells, while nuclear beta-catenin and CD44 were expressed in the short cells in SAs.
  • [MeSH-major] Adenoma / pathology. Adenomatous Polyps / pathology. Cell Differentiation. Colonic Polyps / pathology. Colorectal Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD44 / metabolism. Carbonic Anhydrase I / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Female. Humans. Immunoenzyme Techniques. Keratin-20 / metabolism. Ki-67 Antigen / metabolism. Male. Middle Aged. Morphogenesis. beta Catenin / metabolism

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18708730.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / CD44 protein, human; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Keratin-20; 0 / Ki-67 Antigen; 0 / beta Catenin; EC 4.2.1.- / Carbonic Anhydrase I
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48. Andreu P, Colnot S, Godard C, Laurent-Puig P, Lamarque D, Kahn A, Perret C, Romagnolo B: Identification of the IFITM family as a new molecular marker in human colorectal tumors. Cancer Res; 2006 Feb 15;66(4):1949-55
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  • We identified 18 candidate genes having increased expression levels in the adenoma.
  • Subsequent Northern blotting, real-time reverse transcription-PCR, and in situ hybridization analysis confirmed their induction in beta-catenin-activated epithelial cells of murine adenomas.
  • Using a conditional mouse model of Apc inactivation and a human colon carcinoma cell line, we showed that IFITM gene expression is rapidly induced after activation of the beta-catenin signaling.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenoma / genetics. Adenoma / metabolism. Animals. Antigens, Differentiation. Gene Expression Regulation, Neoplastic. Humans. Intestinal Neoplasms / genetics. Intestinal Neoplasms / metabolism. Male. Mice. RNA-Binding Proteins / biosynthesis. RNA-Binding Proteins / genetics. Up-Regulation. Wnt Proteins / metabolism. beta Catenin / metabolism

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  • (PMID = 16488993.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Biomarkers, Tumor; 0 / IFITM2 protein, human; 0 / IFITM3 protein, human; 0 / Membrane Proteins; 0 / RNA-Binding Proteins; 0 / Wnt Proteins; 0 / beta Catenin; 0 / leu-13 antigen
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49. Than TH, Swethadri GK, Wong J, Ahmad T, Jamil D, Maganlal RK, Hamdi MM, Abdullah MS: Expression of Galectin-3 and Galectin-7 in thyroid malignancy as potential diagnostic indicators. Singapore Med J; 2008 Apr;49(4):333-8
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  • Galectins are beta-galactoside-binding proteins with Gal-3 being a redundant pre-mRNA splicing factor.
  • They are supposed to be p53-related regulators in cell growth and apoptosis, being either anti-apoptotic or pro-apoptotic.
  • [MeSH-minor] Adenocarcinoma, Follicular / diagnosis. Adenocarcinoma, Follicular / metabolism. Adenoma / diagnosis. Adenoma / metabolism. Carcinoma, Papillary / diagnosis. Humans. Immunohistochemistry

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  • (PMID = 18418527.001).
  • [ISSN] 0037-5675
  • [Journal-full-title] Singapore medical journal
  • [ISO-abbreviation] Singapore Med J
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 3; 0 / Galectins; 0 / LGALS7 protein, human
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50. van der Weyden L, Arends MJ, Dovey OM, Harrison HL, Lefebvre G, Conte N, Gergely FV, Bradley A, Adams DJ: Loss of Rassf1a cooperates with Apc(Min) to accelerate intestinal tumourigenesis. Oncogene; 2008 Jul 24;27(32):4503-8
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  • RASSF1A has been implicated in an array of pivotal cellular processes, including regulation of the cell cycle, apoptosis, microtubule stability and most recently in the beta-catenin signalling pathway.
  • Immunohistochemical analysis of adenomas revealed increased nuclear beta-catenin accumulation in adenomas from Rassf1a(-/-); Apc(+/Min) mice, compared to those from Rassf1a(+/+); Apc(+/Min) mice, but no differences in proliferation marker (Ki67) staining patterns.
  • Collectively these data demonstrate cooperation between inactivation of Rassf1a and Apc resulting in accelerated intestinal tumourigenesis, with adenomas showing increased nuclear accumulation of beta-catenin, supporting a mechanistic link via loss of the known interaction of Rassf1 with beta-TrCP that usually mediates degradation of beta-catenin.
  • [MeSH-minor] Adenoma / etiology. Adenoma / genetics. Aneuploidy. Animals. Cell Nucleus / metabolism. Chromosomal Instability. Humans. Ki-67 Antigen / analysis. Mice. Mice, Inbred C57BL. Signal Transduction. beta Catenin / metabolism

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  • (PMID = 18391979.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 079643; United Kingdom / Cancer Research UK / / A8449; United Kingdom / Cancer Research UK / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Mki67 protein, mouse; 0 / RASSF1 protein, mouse; 0 / Tumor Suppressor Proteins; 0 / beta Catenin
  • [Other-IDs] NLM/ EMS52273; NLM/ PMC3706934
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51. do Prado RF, Cardoso CL, Consolaro A, de Assis Taveira LA: Nuclear beta-catenin in basal cell adenomas. Int J Surg Pathol; 2007 Apr;15(2):219-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nuclear beta-catenin in basal cell adenomas.
  • [MeSH-major] Adenoma / metabolism. Adenoma, Pleomorphic / metabolism. Cell Nucleus / metabolism. Parotid Neoplasms / metabolism. beta Catenin / metabolism

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  • [CommentOn] Int J Surg Pathol. 2006 Jul;14(3):212-7 [16959701.001]
  • (PMID = 17478787.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / beta Catenin
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52. Femia AP, Dolara P, Giannini A, Salvadori M, Biggeri A, Caderni G: Frequent mutation of Apc gene in rat colon tumors and mucin-depleted foci, preneoplastic lesions in experimental colon carcinogenesis. Cancer Res; 2007 Jan 15;67(2):445-9
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  • Most MDF show Wnt pathway activation, whereas only a subset shows mutations in the Ctnnb1 gene, coding for beta-catenin.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenoma / genetics. Adenoma / metabolism. Animals. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Male. Rats. Rats, Inbred F344

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  • (PMID = 17234750.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mucins
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53. Chen YT, Tu JJ, Kao J, Zhou XK, Mazumdar M: Messenger RNA expression ratios among four genes predict subtypes of renal cell carcinoma and distinguish oncocytoma from carcinoma. Clin Cancer Res; 2005 Sep 15;11(18):6558-66
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  • [Title] Messenger RNA expression ratios among four genes predict subtypes of renal cell carcinoma and distinguish oncocytoma from carcinoma.
  • PURPOSE: Morphologic distinction among clear cell, papillary, and chromophobe types of renal cell carcinoma (RCC) can be difficult, as is the differential diagnosis between oncocytoma and RCC.
  • RESULTS: CA9 expression was highest in clear cell carcinoma and lowest in chromophobe RCC and in oncocytoma.
  • PVALB was highest in chromophobe RCC, variable in oncocytoma, and low in clear cell and papillary types.
  • This algorithm accurately classified the 31 fresh-frozen tumors into 14 clear cell, 5 papillary, 6 chromophobe, and 6 oncocytomas.
  • In the formalin-fixed group, the molecular criteria accurately classified the cases into 15 clear cell, 16 papillary, and 32 in the chromophobe/oncocytoma group but could only separate some, but not all, oncocytomas from chromophobe RCC.
  • [MeSH-minor] Adenocarcinoma, Clear Cell / genetics. Adenocarcinoma, Clear Cell / pathology. Adenoma, Oxyphilic / genetics. Adenoma, Oxyphilic / pathology. Algorithms. Anion Transport Proteins / genetics. Antigens, Neoplasm / genetics. Carbonic Anhydrases / genetics. Carcinoma, Renal Cell / genetics. Carcinoma, Renal Cell / pathology. Chloride Channels / genetics. Diagnosis, Differential. Humans. Membrane Proteins / genetics. Racemases and Epimerases / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. beta-Defensins / genetics

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  • (PMID = 16166433.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anion Transport Proteins; 0 / Antigens, Neoplasm; 0 / CLCNKB protein, human; 0 / Chloride Channels; 0 / DEFB1 protein, human; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / beta-Defensins; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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54. Zhu L, Gibson P, Currle DS, Tong Y, Richardson RJ, Bayazitov IT, Poppleton H, Zakharenko S, Ellison DW, Gilbertson RJ: Prominin 1 marks intestinal stem cells that are susceptible to neoplastic transformation. Nature; 2009 Jan 29;457(7229):603-7
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  • What remains unclear is whether cancer stem cells are the direct progeny of mutated stem cells or more mature cells that reacquire stem cell properties during tumour formation.
  • 2), generate the entire intestinal epithelium, and are therefore the small intestinal stem cell.
  • Activation of endogenous Wnt signalling in Prom1(+/C-L) mice containing a Cre-dependent mutant allele of beta-catenin (Ctnnb1(lox(ex3))) resulted in a gross disruption of crypt architecture and a disproportionate expansion of Prom1(+) cells at the crypt base.
  • Lineage tracing demonstrated that the progeny of these cells replaced the mucosa of the entire small intestine with neoplastic tissue that was characterized by focal high-grade intraepithelial neoplasia and crypt adenoma formation.

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  • (PMID = 19092805.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA129541; United States / NIMH NIH HHS / MH / R01 MH079079-03; United States / NCI NIH HHS / CA / R01CA129541; United States / NCI NIH HHS / CA / P01 CA096832-01A10003; United States / NCI NIH HHS / CA / P01CA96832; United States / NCI NIH HHS / CA / R01 CA129541-02; United States / NCI NIH HHS / CA / P30CA021765; United States / NIMH NIH HHS / MH / R01 MH079079-05; United States / NCI NIH HHS / CA / R01 CA129541-01; United States / NCI NIH HHS / CA / P30 CA021765; United States / NIMH NIH HHS / MH / R01 MH079079; United States / NIMH NIH HHS / MH / R01 MH079079-02; United States / NIMH NIH HHS / MH / R01 MH079079-01A2; United States / NCI NIH HHS / CA / P01 CA096832; United States / NCI NIH HHS / CA / CA096832-01A10003; United States / NIMH NIH HHS / MH / R01 MH079079-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Biomarkers; 0 / CTNNB1 protein, mouse; 0 / Glycoproteins; 0 / Lgr5 protein, mouse; 0 / Peptides; 0 / Receptors, G-Protein-Coupled; 0 / Wnt Proteins; 0 / beta Catenin
  • [Other-IDs] NLM/ NIHMS75275; NLM/ PMC2633030
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55. Bioulac-Sage P, Balabaud C, Zucman-Rossi J: [Benign liver cell tumors: recent results, from molecular biology to diagnosis]. Gastroenterol Clin Biol; 2008 Mar;32(3):296-303; quiz 293, 314
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  • [Title] [Benign liver cell tumors: recent results, from molecular biology to diagnosis].
  • [MeSH-major] Adenoma / pathology. Focal Nodular Hyperplasia / pathology. Liver Neoplasms / pathology
  • [MeSH-minor] Biomarkers. Hepatocyte Nuclear Factor 1-alpha / genetics. Humans. Immunohistochemistry. Mutation. beta Catenin / genetics

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  • [CommentIn] Gastroenterol Clin Biol. 2008 Mar;32(3):294-5 [18367360.001]
  • (PMID = 18367358.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / beta Catenin
  • [Number-of-references] 43
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56. Kress E, Skah S, Sirakov M, Nadjar J, Gadot N, Scoazec JY, Samarut J, Plateroti M: Cooperation between the thyroid hormone receptor TRalpha1 and the WNT pathway in the induction of intestinal tumorigenesis. Gastroenterology; 2010 May;138(5):1863-74
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  • More precisely, TRalpha1 directly enhances the transcription of several components of this pathway, allowing increased expression of beta-catenin/Tcf4 target genes and stimulation of cell proliferation.
  • RESULTS: The intestine of vil-TRalpha1 mice presents aberrant intestinal mucosal architecture and increased cell proliferation and develops adenoma at a low rate.
  • [MeSH-major] Adenoma / metabolism. Cell Transformation, Neoplastic / metabolism. Intestinal Mucosa / metabolism. Intestinal Neoplasms / metabolism. Signal Transduction. Thyroid Hormone Receptors alpha / metabolism. Wnt Proteins / metabolism
  • [MeSH-minor] Animals. Cell Proliferation. Disease Models, Animal. Gene Expression Regulation, Neoplastic. Genes, APC. Genotype. Mice. Mice, Inbred C57BL. Mice, Transgenic. Phenotype. Time Factors. beta Catenin / metabolism

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  • [Copyright] Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20114049.001).
  • [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 / CTNNB1 protein, mouse; 0 / Thyroid Hormone Receptors alpha; 0 / Wnt Proteins; 0 / beta Catenin
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57. Luciani P, Gelmini S, Ferrante E, Lania A, Benvenuti S, Baglioni S, Mantovani G, Cellai I, Ammannati F, Spada A, Serio M, Peri A: Expression of the antiapoptotic gene seladin-1 and octreotide-induced apoptosis in growth hormone-secreting and nonfunctioning pituitary adenomas. J Clin Endocrinol Metab; 2005 Nov;90(11):6156-61
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  • Seladin-1 effectively protects neurons against beta-amyloid-mediated toxicity and prevents apoptosis via inhibition of the activation of caspase-3, a key mediator of the apoptotic cascade.
  • Although the amount of activated caspase-3 did not differ between the two groups of tumors, in primary cell cultures, octreotide was able to increase apoptosis, evaluated by the level of cleaved cytokeratin 18 and the presence of apoptotic nuclei, in GH-secreting adenomas, but not in NFPA.
  • [MeSH-major] Adenoma / metabolism. Apoptosis / drug effects. Human Growth Hormone / secretion. Nerve Tissue Proteins / genetics. Octreotide / pharmacology. Oxidoreductases Acting on CH-CH Group Donors / genetics. Pituitary Neoplasms / metabolism

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  • (PMID = 16091489.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 12629-01-5 / Human Growth Hormone; EC 1.3.- / Oxidoreductases Acting on CH-CH Group Donors; EC 1.3.1.- / DHCR24 protein, human; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; RWM8CCW8GP / Octreotide
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58. Park S, Kim SW, Lee BL, Jung EJ, Kim WH: Expression of E-cadherin and beta-catenin in the adenoma-carcinoma sequence of ampulla of Vater cancer. Hepatogastroenterology; 2006 Jan-Feb;53(67):28-32
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  • [Title] Expression of E-cadherin and beta-catenin in the adenoma-carcinoma sequence of ampulla of Vater cancer.
  • BACKGROUND/AIMS: Ampullary carcinoma is uncommon but provides a good model for adenoma-carcinoma sequence.
  • During the adenoma-carcinoma transition, the tumor cells should acquire the ability to invade.
  • The E-cadherin-catenin complex connects the adjacent epithelial cells at the zona adherens, and this adhesion interferes with the tumor cell invasion.
  • METHODOLOGY: 111 cases of ampullary carcinoma were investigated with E-cadherin and beta-catenin expression with immunohistochemistry and the result was compared with their clinicopathologic and survival results.
  • RESULTS: Expressional loss of E-cadherin was detected in 3 (6.1%) adenomas and 73 (65.8%) carcinomas, and the expressional loss was significantly associated with tumor cell differentiation (p<0.05) and survival (p<0.05) in carcinoma.
  • In beta-catenin immunostaining, 4 (8.2%) adenomas and 45 (40.5%) carcinomas showed abnormal staining patterns either as nuclear staining or as a loss of membrane staining.
  • The cases with membranous loss of beta-catenin expression were correlated with poor survival rate.
  • CONCLUSIONS: Alteration of E-cadherin and beta-catenin is a late event during the adenoma-carcinoma sequence in ampullary neoplasms, and the loss of membranous expression of both E-cadherin and beta-catenin is closely correlated with less differentiated histology and poor prognosis.
  • [MeSH-major] Adenoma / metabolism. Adenoma / pathology. Ampulla of Vater. Cadherins / biosynthesis. Carcinoma / metabolism. Carcinoma / pathology. Common Bile Duct Neoplasms / metabolism. Common Bile Duct Neoplasms / pathology. beta Catenin / biosynthesis

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  • (PMID = 16506371.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cadherins; 0 / beta Catenin
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59. Van der Flier LG, Sabates-Bellver J, Oving I, Haegebarth A, De Palo M, Anti M, Van Gijn ME, Suijkerbuijk S, Van de Wetering M, Marra G, Clevers H: The Intestinal Wnt/TCF Signature. Gastroenterology; 2007 Feb;132(2):628-32
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  • METHODS: We have now performed an exhaustive array-based analysis of this target gene program in colorectal cancer cell lines carrying an inducible block of the Wnt cascade.
  • RESULTS: Expression analyses of approximately 80 genes common between these data sets were performed in a murine adenoma model.
  • A module of 17 genes was specifically expressed at the position of the crypt stem cell.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Gene Expression Regulation, Neoplastic. Intestinal Mucosa / metabolism. Signal Transduction. TCF Transcription Factors / metabolism. Wnt Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenoma / genetics. Adenoma / metabolism. Animals. Cell Line, Tumor. Colorectal Neoplasms / genetics. Colorectal Neoplasms / metabolism. Gene Expression Profiling. Humans. Mice. Oligonucleotide Array Sequence Analysis. Paneth Cells / metabolism. RNA, Messenger / metabolism. T Cell Transcription Factor 1 / metabolism. Time Factors. Transcription Factor 7-Like 2 Protein. Transfection. beta Catenin / metabolism

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  • (PMID = 17320548.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / T Cell Transcription Factor 1; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Tcf7l2 protein, mouse; 0 / Transcription Factor 7-Like 2 Protein; 0 / Wnt Proteins; 0 / beta Catenin
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60. McDonald SA, Preston SL, Lovell MJ, Wright NA, Jankowski JA: Mechanisms of disease: from stem cells to colorectal cancer. Nat Clin Pract Gastroenterol Hepatol; 2006 May;3(5):267-74
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  • Over the past decade, the advances in our understanding of stem cell biology and the role of stem cells in diseases, such as colorectal cancer, have been remarkable.
  • In particular, discoveries related to the control of stem cell proliferation and how dysregulation of proliferation leads to oncogenesis have been foremost.
  • For intestinal stem cells, the WNT family of growth factors, and events such as the regulation of the nuclear localization of beta-catenin, seem to be central to normal homeostasis, and mutations in the components of these pathways seem to lead to the development of colorectal cancer.
  • A paradigm of abnormal stem cell biology is illustrated by patients with familial adenomatous polyposis, who have mutations in the adenomatous polyposis coli gene.
  • The wild-type protein encoded by this gene is important for the prevention of mass beta-catenin accumulation in the nucleus and the subsequent overtranscription of cell cycle proteins.
  • This review discusses the basic mechanisms behind stem cell regulation in the gut and follows their role in the natural history of tumor progression.
  • [MeSH-minor] Adenoma / genetics. Animals. Cell Differentiation / physiology. Cell Division / physiology. Epithelial Cells / physiology. Humans. Mutagenesis / genetics. Transcription, Genetic / physiology. Wnt Proteins / physiology. beta Catenin / physiology

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  • (PMID = 16673006.001).
  • [ISSN] 1743-4378
  • [Journal-full-title] Nature clinical practice. Gastroenterology & hepatology
  • [ISO-abbreviation] Nat Clin Pract Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Wnt Proteins; 0 / beta Catenin
  • [Number-of-references] 74
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61. Ahtiainen P, Rulli SB, Shariatmadari R, Pelliniemi LJ, Toppari J, Poutanen M, Huhtaniemi IT: Fetal but not adult Leydig cells are susceptible to adenoma formation in response to persistently high hCG level: a study on hCG overexpressing transgenic mice. Oncogene; 2005 Nov 10;24(49):7301-9
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  • [Title] Fetal but not adult Leydig cells are susceptible to adenoma formation in response to persistently high hCG level: a study on hCG overexpressing transgenic mice.
  • Leydig cell (LC) adenomas were found in prepubertal mice, most prominently at the age of 10 days, but not in adult age.
  • The temporal expression patterns of the fetal LC marker gene, thrombospondin 2, and those of adult LCs, hydroxysteroid dehydrogenase-6, delta5-3-beta and prostaglandin D synthase, were similar in wild-type and hCG+ males.
  • [MeSH-major] Adenoma / etiology. Chorionic Gonadotropin, beta Subunit, Human / metabolism. Gene Expression Regulation, Developmental. Glycoprotein Hormones, alpha Subunit / metabolism. Leydig Cells / metabolism

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  • (PMID = 16007123.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / Glycoprotein Hormones, alpha Subunit; 0 / Lipocalins; 0 / Thrombospondins; 0 / thrombospondin 2; EC 1.1.- / 3-Hydroxysteroid Dehydrogenases; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.99.2 / prostaglandin R2 D-isomerase
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62. Sobczak I, Galabova-Kovacs G, Sadzak I, Kren A, Christofori G, Baccarini M: B-Raf is required for ERK activation and tumor progression in a mouse model of pancreatic beta-cell carcinogenesis. Oncogene; 2008 Aug 14;27(35):4779-87
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  • [Title] B-Raf is required for ERK activation and tumor progression in a mouse model of pancreatic beta-cell carcinogenesis.
  • The extracellular signal-regulated kinase (ERK) pathway is required for the proliferation of cancer cell lines harboring activating BRAF or, to a lesser extent, activating RAS mutations.
  • The progression from adenoma to carcinoma is also significantly impaired.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Extracellular Signal-Regulated MAP Kinases / metabolism. Islets of Langerhans / pathology. Pancreatic Neoplasms / pathology. Proto-Oncogene Proteins B-raf / physiology
  • [MeSH-minor] Animals. Base Sequence. DNA Primers. Disease Models, Animal. Disease Progression. Enzyme Activation. Immunohistochemistry. Mice. Mice, Knockout. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor beta / metabolism. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism


63. Tward AD, Jones KD, Yant S, Cheung ST, Fan ST, Chen X, Kay MA, Wang R, Bishop JM: Distinct pathways of genomic progression to benign and malignant tumors of the liver. Proc Natl Acad Sci U S A; 2007 Sep 11;104(37):14771-6
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  • We used several of the genetic lesions commonly associated with human liver tumors to reconstruct genetic progression to hepatocellular carcinoma and adenoma in mouse models.
  • Hepatocellular carcinoma in both instances arose from cooperation between MET and constitutively active versions of beta-catenin.
  • Prompted by these findings, we uncovered a coincidence between activation of the protein-tyrosine kinase encoded by MET and activating mutations of beta-catenin in a subset of human hepatocellular carcinomas.
  • Inactivation of MET transgenes led to regression of hepatocellular carcinomas despite the persistence of activated beta-catenin.
  • The tumors eventually recurred in the absence of MET expression, however, presumably after the occurrence of one or more events that cooperated with activated beta-catenin in lieu of MET.


64. Akiyama T, Kawasaki Y: Wnt signalling and the actin cytoskeleton. Oncogene; 2006 Dec 4;25(57):7538-44
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  • APC binds to beta-catenin, a key component of the Wnt signalling pathway, and induces its degradation.
  • IQGAP1 mediates association of APC with cortical actin in the leading edge of migrating cell and both proteins are required for cell polarization and directional migration.
  • APC interacts with Asef and stimulates its activity, thereby regulating the actin cytoskeletal network, cell morphology, adhesion and migration.
  • Truncated mutant APCs present in colorectal tumour cells activate Asef constitutively and contribute to their aberrant migratory properties, which may be important for adenoma formation as well as tumour progression to invasive malignancy.
  • [MeSH-minor] Animals. Astrocytes / metabolism. Cell Membrane / metabolism. Genes, Tumor Suppressor. Humans. Kinesin / metabolism. Microtubules / metabolism. Models, Biological. Mutation. Signal Transduction

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  • (PMID = 17143298.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / KIF2A protein, human; 0 / Wnt Proteins; EC 3.6.1.- / Kinesin
  • [Number-of-references] 45
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65. Misikangas M, Tanayama H, Rajakangas J, Lindén J, Pajari AM, Mutanen M: Inulin results in increased levels of beta-catenin and cyclin D1 as the adenomas increase in size from small to large in the Min/+ mouse. Br J Nutr; 2008 May;99(5):963-70
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  • [Title] Inulin results in increased levels of beta-catenin and cyclin D1 as the adenomas increase in size from small to large in the Min/+ mouse.
  • To address this issue we fed Min/+ mice with two diets known to lead to different adenoma outcomes: a high-fat control diet (n 15) or a high-fat inulin-enriched (10 % w/w) diet (n 13).
  • To study the effect of diet on cell signalling during adenoma growth, the adenomas of each Min/+ mouse were divided into three size-categories, and the levels of beta-catenin, E-cadherin, cyclin D1 and matrix metalloproteinase-9, which are known to be involved in colon tumorigenesis, were determined.
  • The inulin diet increased the expression of nuclear beta-catenin (P = 0.004) and its target cyclin D1 (P = 0.017) as the adenomas increased in size from small to large, indicating the presence of an accelerated cancerous process.
  • Neither phenomenon was seen in the control group during adenoma growth.
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Cyclin D1 / metabolism. Diet. Inulin / pharmacology. beta Catenin / metabolism


66. Anderson CE, Graham C, Herriot MM, Kamel HM, Salter DM: CD98 expression is decreased in papillary carcinoma of the thyroid and Hashimoto's thyroiditis. Histopathology; 2009 Dec;55(6):683-6
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  • AIMS: CD98 is a component of the large neutral amino acid transporter (LAT), which is a cell surface amino acid transporter.
  • CD98 also binds to and activates beta(1)-integrin, promoting anchorage-independent growth.
  • METHODS AND RESULTS: One hundred and forty thyroid cases were selected from the archives of the Department of Pathology, including normal controls, neoplasms (follicular adenoma, follicular carcinoma and papillary carcinoma) and non-neoplastic conditions (multinodular goitre, Graves' disease and Hashimoto's thyroiditis).
  • In normal thyroid, there was moderately strong expression of CD98 in the lateral cell membranes of follicular cells.
  • A similar pattern of expression was seen in follicular adenoma, minimally invasive follicular carcinoma, multinodular goitre and Graves' disease.
  • [MeSH-minor] Adenocarcinoma, Follicular / metabolism. Adenoma / metabolism. Down-Regulation. Graves Disease / metabolism. Humans. Immunohistochemistry. Prognosis

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  • (PMID = 19922591.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD98
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67. Labbé E, Lock L, Letamendia A, Gorska AE, Gryfe R, Gallinger S, Moses HL, Attisano L: Transcriptional cooperation between the transforming growth factor-beta and Wnt pathways in mammary and intestinal tumorigenesis. Cancer Res; 2007 Jan 1;67(1):75-84
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  • [Title] Transcriptional cooperation between the transforming growth factor-beta and Wnt pathways in mammary and intestinal tumorigenesis.
  • Transforming growth factor-beta (TGF-beta) and Wnt ligands function in numerous developmental processes, and alterations of both signaling pathways are associated with common pathologic conditions, including cancer.
  • To obtain insight into the extent of interdependence of the two signaling cascades in regulating biological responses, we used an oligonucleotide microarray approach to identify Wnt and TGF-beta target genes using normal murine mammary gland epithelial cells as a model.
  • Combination treatment of TGF-beta and Wnt revealed a novel transcriptional program that could not have been predicted from single ligand treatments and included a cohort of genes that were cooperatively induced by both pathways.
  • These included both novel and known components or modulators of TGF-beta and Wnt pathways, suggesting that mutual feedback is a feature of the coordinated activities of the ligands.
  • Reduction of TGF-beta signaling by expression of a dominant-negative TGF-beta type II receptor in bigenic MMTV-Wnt1/DNIIR mice increased mammary tumor latency and was correlated with a decrease in expression of Gpc1, Inhba, and Robo1, three of the TGF-beta/Wnt cooperative targets.
  • Our results indicate that the TGF-beta and Wnt/beta-catenin pathways are firmly intertwined and generate a unique gene expression pattern that can contribute to tumor progression.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Intestinal Neoplasms / genetics. Mammary Neoplasms, Experimental / genetics. Transforming Growth Factor beta / genetics. Wnt Proteins / genetics
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Animals. Female. Gene Expression Regulation, Neoplastic. Humans. L Cells (Cell Line). Mice. Mice, Inbred C57BL. Mice, Transgenic. Signal Transduction. Transcription, Genetic. Wnt3 Protein

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  • (PMID = 17210685.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 085492; United States / NCI NIH HHS / CA / CA 102162
  • [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 / Transforming Growth Factor beta; 0 / Wnt Proteins; 0 / Wnt3 Protein
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68. van den Broek FJ, de Graaf EJ, Dijkgraaf MG, Reitsma JB, Haringsma J, Timmer R, Weusten BL, Gerhards MF, Consten EC, Schwartz MP, Boom MJ, Derksen EJ, Bijnen AB, Davids PH, Hoff C, van Dullemen HM, Heine GD, van der Linde K, Jansen JM, Mallant-Hent RC, Breumelhof R, Geldof H, Hardwick JC, Doornebosch PG, Depla AC, Ernst MF, van Munster IP, de Hingh IH, Schoon EJ, Bemelman WA, Fockens P, Dekker E: Transanal endoscopic microsurgery versus endoscopic mucosal resection for large rectal adenomas (TREND-study). BMC Surg; 2009;9:4
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  • Patients with a rectal adenoma > or = 3 cm, located between 1-15 cm ab ano, will be randomized to a TEM- or EMR-treatment strategy.
  • Residual adenoma that is visible during the first surveillance endoscopy at 3 months will be removed endoscopically in both treatment strategies and is considered as part of the primary treatment.
  • Based on comparable recurrence rates for TEM and EMR of 3.3% and considering an upper-limit of 10% for EMR to be non-inferior (beta-error 0.2 and one-sided alpha-error 0.05), 89 patients are needed per group.
  • [MeSH-major] Adenoma / surgery. Endoscopy / economics. Rectal Neoplasms / surgery

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  • (PMID = 19284647.001).
  • [ISSN] 1471-2482
  • [Journal-full-title] BMC surgery
  • [ISO-abbreviation] BMC Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2664790
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69. Rebouissou S, Vasiliu V, Thomas C, Bellanné-Chantelot C, Bui H, Chrétien Y, Timsit J, Rosty C, Laurent-Puig P, Chauveau D, Zucman-Rossi J: Germline hepatocyte nuclear factor 1alpha and 1beta mutations in renal cell carcinomas. Hum Mol Genet; 2005 Mar 1;14(5):603-14
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  • [Title] Germline hepatocyte nuclear factor 1alpha and 1beta mutations in renal cell carcinomas.
  • Moreover, previous identification of biallelic inactivation of HNF1alpha in hepatocellular adenoma identified its tumor suppressor function in hepatocarcinogenesis.
  • The seminal observation of an ovarian carcinoma in a MODY5 patient who subsequently developed a chromophobe renal cell carcinoma, prompted us to screen for HNF1beta and HNF1alpha inactivation in a series of 20 ovarian and 35 renal neoplasms.
  • Interestingly, in two of 13 clear cell renal carcinomas, we found a monoallelic germline mutation of HNF1alpha with no associated suppression of target mRNA expression.
  • Furthermore, we suggest that HNF1beta functions as a tumor suppressor gene in chromophobe renal cell carcinogenesis through a PKHD1 expression control.
  • [MeSH-major] Carcinoma, Renal Cell / genetics. DNA-Binding Proteins / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adult. Aged. DNA Mutational Analysis. Female. Hepatocyte Nuclear Factor 1. Hepatocyte Nuclear Factor 1-alpha. Hepatocyte Nuclear Factor 1-beta. Humans. Male. Middle Aged. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15649945.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / HNF1A protein, human; 0 / HNF1B protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 126548-29-6 / Hepatocyte Nuclear Factor 1; 138674-15-4 / Hepatocyte Nuclear Factor 1-beta
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70. Shibata H, Yamakoshi H, Sato A, Ohori H, Kakudo Y, Kudo C, Takahashi Y, Watanabe M, Takano H, Ishioka C, Noda T, Iwabuchi Y: Newly synthesized curcumin analog has improved potential to prevent colorectal carcinogenesis in vivo. Cancer Sci; 2009 May;100(5):956-60
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  • Degradation of accumulated beta-catenin with curcumin is one of the major mechanisms of chemoprevention in colorectal carcinogenesis.
  • It was demonstrated that the number of beta-catenin-positive adenoma cells in Apc(580D/+) mice fed GO-Y030 was reduced.
  • [MeSH-major] Benzene Derivatives / chemical synthesis. Benzene Derivatives / pharmacology. Cell Transformation, Neoplastic / pathology. Colorectal Neoplasms / pathology. Colorectal Neoplasms / prevention & control. Curcumin / chemical synthesis. Curcumin / pharmacology. Ketones / chemical synthesis. Ketones / pharmacology
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Animals. Disease Models, Animal. Genetic Predisposition to Disease. Mice. Molecular Structure. Survival Rate. beta Catenin / metabolism

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  • (PMID = 19445025.001).
  • [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 / 1,5-bis(3,5-bis(methoxymethoxy)phenyl)penta-1,4-dien-3-one; 0 / Benzene Derivatives; 0 / Ketones; 0 / beta Catenin; IT942ZTH98 / Curcumin
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71. Aoki K, Aoki M, Sugai M, Harada N, Miyoshi H, Tsukamoto T, Mizoshita T, Tatematsu M, Seno H, Chiba T, Oshima M, Hsieh CL, Taketo MM: Chromosomal instability by beta-catenin/TCF transcription in APC or beta-catenin mutant cells. Oncogene; 2007 May 24;26(24):3511-20
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  • [Title] Chromosomal instability by beta-catenin/TCF transcription in APC or beta-catenin mutant cells.
  • Adenomatous polyposis coli (APC/Apc) gene encodes a key tumor suppressor whose mutations activate beta-catenin/T-cell factor (TCF)-mediated transcription (canonical Wnt signaling).
  • As an indicator of CIN, we scored anaphase bridge index (ABI) in mouse polyps and ES cells where Wnt signaling was activated by Apc or beta-catenin mutations.
  • In human gastric cancer tissues with nuclear beta-catenin, ABI was significantly higher than in those without.
  • These results collectively indicate that beta-catenin/TCF-mediated transcription itself increases CIN through dysregulation of G2/M progression.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Chromosomal Instability. Mutation. TCF Transcription Factors / genetics. beta Catenin / genetics
  • [MeSH-minor] Adenoma / genetics. Animals. Cell Division / genetics. Cell Survival / genetics. Cells, Cultured. Chromosome Aberrations. Colonic Neoplasms / genetics. Colonic Neoplasms / metabolism. Embryonic Stem Cells. G2 Phase / genetics. Humans. Intestinal Neoplasms / genetics. Intestinal Polyps / genetics. Mice. Microtubules / metabolism. Signal Transduction. Transcription, Genetic. Wnt Proteins / metabolism

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  • (PMID = 17160019.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / TCF Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin
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72. Jin L, Riss D, Ruebel K, Kajita S, Scheithauer BW, Horvath E, Kovacs K, Lloyd RV: Galectin-3 Expression in Functioning and Silent ACTH-Producing Adenomas. Endocr Pathol; 2005;16(2):107-14
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  • Galectin-3 (Gal-3), a beta galactoside-binding protein, has been implicated in a variety of biological functions including cell growth, differentiation, tumor cell adhesion, angiogenesis, tumor progression, and metastasis.
  • We recently reported that Gal-3 was expressed in a subset of normal pituitary cells and tumors including PRL, ACTH, and in folliculo-stellate (FS) cells and tumors and that Gal-3 had an important regulatory role in pituitary cell proliferation.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Adrenocorticotropic Hormone / secretion. Galectin 3 / biosynthesis. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism

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  • (PMID = 16199895.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA90249
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Galectin 3; 0 / RNA, Messenger; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
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73. Shan L, Yu M, Snyderwine EG: Global gene expression profiling of chemically induced rat mammary gland carcinomas and adenomas. Toxicol Pathol; 2005;33(7):768-75
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  • Carcinomas showed relatively high expression of several genes associated with mammary epithelial cell growth and proliferation (e.g., cyclin D1, PDGFalpha) and relatively low expression of differentiation marker genes (e.g., beta -casein, whey acidic protein, transferrin).
  • Other categories of genes showing differential expression between carcinomas and adenomas were associated with protein homeostasis, cytoskeleton, extracellular matrix, and cell metabolism (fatty acid metabolism, oxidative phosphorylation, and glycolysis).
  • [MeSH-major] Adenoma / chemically induced. Adenoma / genetics. Carcinoma / chemically induced. Carcinoma / genetics. Gene Expression Regulation, Neoplastic / genetics. Mammary Neoplasms, Experimental / chemically induced. Mammary Neoplasms, Experimental / genetics


74. Ciznadija D, Tothill R, Waterman ML, Zhao L, Huynh D, Yu RM, Ernst M, Ishii S, Mantamadiotis T, Gonda TJ, Ramsay RG, Malaterre J: Intestinal adenoma formation and MYC activation are regulated by cooperation between MYB and Wnt signaling. Cell Death Differ; 2009 Nov;16(11):1530-8
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  • [Title] Intestinal adenoma formation and MYC activation are regulated by cooperation between MYB and Wnt signaling.
  • Aberrant Wnt signaling mediated by mutations affecting APC (adenomatous polyposis coli) or beta-catenin initiates the majority of human colorectal cancers (CRC) and drives tumorigenesis through the activation of specific genes such as MYC.
  • We report here a novel association whereby another oncogenic transcription factor, MYB/c-Myb, is necessary for intestinal adenoma development directed by activated Wnt signaling.
  • APC(Min/+) mice in which c-myb is haploinsufficient survive longer than wild-type APC(Min/+) animals due to a delay in adenoma formation.
  • We explored the relationship between activated Wnt signaling and MYB in regulating MYC and found activated beta-catenin in combination with MYB induces robust upregulation of MYC promoter activity, as well as endogenous MYC mRNA and protein expression, in human cells.
  • This cooperation occurred through independent binding of MYB and beta-catenin to the MYC promoter.
  • [MeSH-major] Adenoma / metabolism. Colorectal Neoplasms / metabolism. Proto-Oncogene Proteins c-myb / metabolism. Proto-Oncogene Proteins c-myc / metabolism. Wnt Proteins / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Alleles. Animals. Cell Line. Humans. Mice. Mice, Inbred C57BL. Mice, Knockout. RNA Interference. RNA, Messenger / metabolism. RNA, Small Interfering / metabolism. Signal Transduction. Up-Regulation. beta Catenin / metabolism

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  • (PMID = 19609274.001).
  • [ISSN] 1476-5403
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Wnt Proteins; 0 / beta Catenin
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75. Yen TH, Chen Y, Fu JF, Weng CH, Tian YC, Hung CC, Lin JL, Yang CW: Proliferation of myofibroblasts in the stroma of renal oncocytoma. Cell Prolif; 2010 Jun;43(3):287-96
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  • Wnt/beta-catenin signalling was not implicated in this neoplasm, as there was no loss of E-cadherin membranous localization or expression of intranuclear beta-catenin in the cells.
  • [MeSH-major] Adenoma, Oxyphilic / pathology. Fibroblasts / pathology. Kidney Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Cell Proliferation. Extracellular Matrix / metabolism. Extracellular Matrix / pathology. Extracellular Matrix Proteins / metabolism. Female. Humans. Male. Middle Aged. Myoblasts / metabolism. Myoblasts / pathology. Neoplasm Invasiveness / pathology. Neoplasm Invasiveness / physiopathology. Stromal Cells / metabolism. Stromal Cells / pathology

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  • (PMID = 20412129.001).
  • [ISSN] 1365-2184
  • [Journal-full-title] Cell proliferation
  • [ISO-abbreviation] Cell Prolif.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Extracellular Matrix Proteins
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76. Giles RH, Lolkema MP, Snijckers CM, Belderbos M, van der Groep P, Mans DA, van Beest M, van Noort M, Goldschmeding R, van Diest PJ, Clevers H, Voest EE: Interplay between VHL/HIF1alpha and Wnt/beta-catenin pathways during colorectal tumorigenesis. Oncogene; 2006 May 18;25(21):3065-70
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  • [Title] Interplay between VHL/HIF1alpha and Wnt/beta-catenin pathways during colorectal tumorigenesis.
  • [MeSH-major] Adenocarcinoma / etiology. Cell Transformation, Neoplastic / genetics. Colorectal Neoplasms / etiology. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Nerve Tissue Proteins / physiology. TCF Transcription Factors / physiology. Von Hippel-Lindau Tumor Suppressor Protein / physiology. Wnt Proteins / physiology. beta Catenin / physiology
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Adenomatous Polyposis Coli / pathology. Animals. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors. Cell Line. Colon / cytology. Colon / metabolism. Colon / pathology. Colonic Polyps / genetics. Colonic Polyps / metabolism. Colonic Polyps / pathology. Disease Progression. Epithelial Cells / metabolism. Erythropoietin / genetics. Gene Expression Regulation, Neoplastic. Genes, Reporter. Humans. Intestinal Mucosa / cytology. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Kidney. L Cells (Cell Line). Mice. Mice, Knockout. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Promoter Regions, Genetic. Recombinant Fusion Proteins / biosynthesis. Recombinant Fusion Proteins / genetics. Signal Transduction / physiology. Transcription Factor 7-Like 2 Protein. Wnt3 Protein

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  • (PMID = 16407833.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / CTNNB1 protein, human; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Nerve Tissue Proteins; 0 / Recombinant Fusion Proteins; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Tcf4 protein, mouse; 0 / Tcf7l2 protein, mouse; 0 / Transcription Factor 7-Like 2 Protein; 0 / Wnt Proteins; 0 / Wnt3 Protein; 0 / beta Catenin; 11096-26-7 / Erythropoietin; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Vhlh protein, mouse; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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77. Paulsen JE, Knutsen H, Ølstørn HB, Løberg EM, Alexander J: Identification of flat dysplastic aberrant crypt foci in the colon of azoxymethane-treated A/J mice. Int J Cancer; 2006 Feb 1;118(3):540-6
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  • Flat ACF and nascent tumors displayed a uniform picture of severe dysplasia, compressed pit pattern, overexpression of cytoplasmic/nuclear beta-catenin and nuclear overexpression of cyclin D1.
  • They infrequently (1/20) possessed severe dysplasia, overexpression of cytoplasmic/nuclear beta-catenin, or nuclear overexpression of cyclin D1, and they did not have compressed crypt openings.
  • In conclusion, our data indicate a development from flat ACF to adenoma characterized by aberrant activation of the Wnt signaling pathway and fast crypt multiplication.
  • [MeSH-minor] Animals. Cell Nucleus / metabolism. Cyclin D1 / metabolism. Female. Male. Mice. Mice, Inbred A. beta Catenin / metabolism

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16094649.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / beta Catenin; 136601-57-5 / Cyclin D1; MO0N1J0SEN / Azoxymethane
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78. Chen G, A J, Wang M, Farley S, Lee LY, Lee LC, Sawicki MP: Menin promotes the Wnt signaling pathway in pancreatic endocrine cells. Mol Cancer Res; 2008 Dec;6(12):1894-907
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  • We show that menin is essential for canonical Wnt/beta-catenin signaling in cultured rodent islet tumor cells.
  • In these cells, overexpression of menin significantly enhances TCF gene assay reporter activity in response to beta-catenin activation.
  • We show that menin physically interacts with proteins involved in the canonical Wnt signaling pathway, including beta-catenin, TCF3 (TCFL1), and weakly with TCF4 (TCFL2).
  • Menin overexpression increases expression of the Wnt/beta-catenin downstream target gene Axin2, which is associated with increased H3K4 trimethylation of the Axin2 gene promoter.
  • Based on these studies, we hypothesized that Wnt signaling could inhibit islet cell proliferation because loss of menin function is thought to increase endocrine tumor cell proliferation.
  • TGP61 rodent islet tumor cells treated with a glycogen synthase kinase 3beta inhibitor that increases Wnt pathway signaling had decreased cell proliferation compared with vehicle-treated cells.
  • Collectively, these data suggest that menin has an essential role in Wnt/beta-catenin signaling through a mechanism that eventually affects histone trimethylation of the downstream target gene Axin2, and activation of Wnt/beta-catenin signaling inhibits islet tumor cell proliferation.
  • [MeSH-major] Adenoma, Islet Cell / metabolism. Multiple Endocrine Neoplasia Type 1 / metabolism. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins / metabolism. Wnt Proteins / metabolism
  • [MeSH-minor] Animals. Axin Protein. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors. Basic Helix-Loop-Helix Transcription Factors / genetics. Cricetinae. Cytoskeletal Proteins / genetics. Cytoskeletal Proteins / metabolism. DNA-Binding Proteins / genetics. Histones / metabolism. Humans. Kidney / cytology. Methylation. Mice. Mice, Knockout. Mutation, Missense. Promoter Regions, Genetic / physiology. Protein Structure, Tertiary. RNA, Small Interfering. Signal Transduction / physiology. Transcription Factors / genetics. beta Catenin / metabolism

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  • (PMID = 19074834.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 095148
  • [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 / AXIN2 protein, human; 0 / Axin Protein; 0 / Axin2 protein, mouse; 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Histones; 0 / MEN1 protein, human; 0 / Men1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / TCF3 protein, human; 0 / TCF4 protein, human; 0 / Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin
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79. Carlin RW, Sedlacek RL, Quesnell RR, Pierucci-Alves F, Grieger DM, Schultz BD: PVD9902, a porcine vas deferens epithelial cell line that exhibits neurotransmitter-stimulated anion secretion and expresses numerous HCO3(-) transporters. Am J Physiol Cell Physiol; 2006 Jun;290(6):C1560-71
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  • [Title] PVD9902, a porcine vas deferens epithelial cell line that exhibits neurotransmitter-stimulated anion secretion and expresses numerous HCO3(-) transporters.
  • Continuous cell lines that could be used to define ion transport mechanisms in this tissue are not readily available.
  • In the present study, porcine vas deferens epithelial cells were isolated by standard techniques, and the cells spontaneously immortalized to form a porcine vas deferens epithelial cell line that we have titled PVD9902.
  • When seeded on permeable supports, PVD9902 cells grew as electrically tight (>6,000 ohms x cm2), confluent monolayers that responded to forskolin with an increase in short-circuit current (I(sc); 8 +/- 1 microA/cm2) that required Cl-, HCO3(-), and Na+, and was partially sensitive to bumetanide. mRNA was expressed for a number of anion transporters, including CFTR, electrogenic Na+-HCO3(-) cotransporter 1b (NBCe1b), downregulated in adenoma, pendrin, and Cl-/formate exchanger.
  • In addition, PVD9902 cell monolayers responded to physiological (i.e., adenosine, norepinephrine) and pharmacological [i.e., 5'-(N-ethylcarboxamido)adenosine, isoproterenol] agonists with increases in I(sc).
  • RT-PCR analysis revealed the presence of both glucocorticoid and mineralocorticoid receptor mRNA as well as mRNA for the alpha- and gamma-subunits of the epithelia Na+ channels (alpha- and gamma-ENaC), but not beta-ENaC.
  • [MeSH-major] Anions / metabolism. Cell Line / physiology. Epithelium / metabolism. Sodium-Bicarbonate Symporters / metabolism. Vas Deferens / cytology

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  • (PMID = 16421205.001).
  • [ISSN] 0363-6143
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR-017686
  • [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 / Anions; 0 / Neurotransmitter Agents; 0 / Sodium-Bicarbonate Symporters; 1F7A44V6OU / Colforsin
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80. Mayor R, Casadomé L, Azuara D, Moreno V, Clark SJ, Capellà G, Peinado MA: Long-range epigenetic silencing at 2q14.2 affects most human colorectal cancers and may have application as a non-invasive biomarker of disease. Br J Cancer; 2009 May 19;100(10):1534-9
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  • [MeSH-major] Adenoma / pathology. Biomarkers, Tumor / genetics. Carcinoma / diagnosis. Chromosomes, Human, Pair 2. Colorectal Neoplasms / diagnosis. Epigenesis, Genetic / physiology
  • [MeSH-minor] CpG Islands / genetics. DNA Methylation. Feces / chemistry. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Gene Silencing / physiology. Homeodomain Proteins / genetics. Humans. Inhibin-beta Subunits / genetics. Molecular Diagnostic Techniques / methods. Neoplasm Staging. Prognosis. Survival Analysis

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  • (PMID = 19384295.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / EN1 protein, human; 0 / Homeodomain Proteins; 0 / INHBB protein, human; 93443-12-0 / Inhibin-beta Subunits
  • [Other-IDs] NLM/ PMC2696749
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81. Huang L, Shitashige M, Satow R, Honda K, Ono M, Yun J, Tomida A, Tsuruo T, Hirohashi S, Yamada T: Functional interaction of DNA topoisomerase IIalpha with the beta-catenin and T-cell factor-4 complex. Gastroenterology; 2007 Nov;133(5):1569-78
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional interaction of DNA topoisomerase IIalpha with the beta-catenin and T-cell factor-4 complex.
  • DNA topoisomerase IIalpha (Topo IIalpha) is a component of the beta-catenin/T-cell factor-4 (TCF-4) nuclear complex.
  • METHODS: The physical and functional interaction between Topo IIalpha and the beta-catenin/TCF-4 nuclear complex was evaluated by immunoprecipitation, immunofluorescence microscopy, 2-hybrid assay, and luciferase reporter assay.
  • RESULTS: Amino acids 951-1301 of Topo IIalpha were necessary for binding to beta-catenin.
  • The Topo II inhibitors, merbarone and etoposide, suppressed the beta-catenin-mediated TCF/lymphoid enhancer factor transcriptional activity.
  • The catalytic activity of Topo II was augmented by overexpression of beta-catenin as measured by the decatenation of kinetoplast DNA.
  • Topo IIalpha was highly expressed and colocalized with beta-catenin in tumor cells of patients with familial adenomatous polyposis syndrome and patients with sporadic colorectal cancer.
  • CONCLUSIONS: Topo IIalpha interacts with beta-catenin as a novel transcriptional co-activator.
  • A new drug targeting the interaction of Topo IIalpha with beta-catenin as well as its catalytic activity might be more effective for suppressing aberrant Wnt signaling and proliferation of colorectal cancer cells than the current Topo II inhibitors.
  • [MeSH-major] Adenoma / metabolism. Antigens, Neoplasm / metabolism. Colorectal Neoplasms / metabolism. DNA Topoisomerases, Type II / metabolism. DNA-Binding Proteins / metabolism. TCF Transcription Factors / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Enzyme Inhibitors / pharmacology. Etoposide / pharmacology. Gene Expression Regulation, Neoplastic. Humans. RNA, Small Interfering / pharmacology. Signal Transduction / physiology. Thiobarbiturates / pharmacology. Topoisomerase II Inhibitors. Transcription Factor 7-Like 2 Protein. Wnt Proteins / physiology

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  • (PMID = 17983804.001).
  • [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 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / RNA, Small Interfering; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Thiobarbiturates; 0 / Topoisomerase II Inhibitors; 0 / Transcription Factor 7-Like 2 Protein; 0 / Wnt Proteins; 0 / beta Catenin; 6PLQ3CP4P3 / Etoposide; 97534-21-9 / merbarone; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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82. Joo M, Shahsafaei A, Odze RD: Paneth cell differentiation in colonic epithelial neoplasms: evidence for the role of the Apc/beta-catenin/Tcf pathway. Hum Pathol; 2009 Jun;40(6):872-80
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  • [Title] Paneth cell differentiation in colonic epithelial neoplasms: evidence for the role of the Apc/beta-catenin/Tcf pathway.
  • Paneth cell differentiation may occur in colonic epithelial neoplasms.
  • Human defensin 5 is a specific marker of Paneth cells and has been shown to represent one of the target genes of the Apc/beta-catenin/Tcf pathway.
  • The aim of this study was to evaluate the frequency of Paneth cell differentiation in a variety of colonic neoplasms, and to investigate the role of human defensin 5 and beta-catenin in this process.
  • The clinical and pathologic findings, including histologic evidence of Paneth cell differentiation and immunostaining for human defensin 5 and beta-catenin, were evaluated in 29 samples of nonneoplastic colonic mucosa, 18 hyperplastic polyps, 10 sessile serrated adenomas, 12 traditional serrated adenomas, 21 mixed polyps, 39 conventional adenomas, and 40 adenocarcinomas.
  • Human defensin-5 and beta-catenin expression were evaluated for the location and degree of staining in all cell types (dysplastic and nondysplastic) and correlated with histologic areas of Paneth cell differentiation in all types of polyps.
  • Histologic evidence of Paneth cell differentiation was observed in 15 conventional adenomas (38.5%) and 1 adenocarcinoma (2.5%) but not in other types of polyps.
  • Human defensin-5 immunostaining was positive in the cytoplasm of all nonneoplastic Paneth cells and all neoplastic cells with Paneth cell differentiation.
  • Seventeen (53.1%) of 32 human defensin 5 positive conventional adenomas, 6 (86%) of 7 of human defensin 5 positive adenocarcinomas, and all human defensin 5-positive sessile serrated adenomas, traditional serrated adenomas, and mixed polyps did not show histologic evidence of Paneth cell differentiation.
  • Of the 31 conventional adenomas with nuclear beta-catenin staining, 15 (48.4%) revealed histologic evidence of Paneth cell differentiation, and all of the neoplastic cells with Paneth cell differentiation showed nuclear beta-catenin staining, whereas nonneoplastic Paneth cells consistently showed a normal pattern of membranous beta-catenin staining.
  • A strong topographical correlation was noted between human defensin 5 expression and nuclear beta-catenin expression in conventional adenomas and in conventional dysplastic epithelium of mixed polyps.
  • Paneth cell differentiation is common in early colonic neoplasms that develop via the conventional adenoma-carcinoma carcinogenic pathway.
  • Activation of Apc/beta-catenin/Tcf pathway may play a role in Paneth cell differentiation in human colonic neoplasms.
  • [MeSH-major] Adenoma / pathology. Adenoma / physiopathology. Colonic Neoplasms / pathology. Colonic Neoplasms / physiopathology. Defensins / physiology. Paneth Cells / pathology. beta Catenin / physiology
  • [MeSH-minor] Aged. Cell Differentiation. Female. Humans. Male. Middle Aged. Retrospective Studies

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  • (PMID = 19269007.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Defensins; 0 / beta Catenin
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83. Giacchetti G, Ronconi V, Turchi F, Agostinelli L, Mantero F, Rilli S, Boscaro M: Aldosterone as a key mediator of the cardiometabolic syndrome in primary aldosteronism: an observational study. J Hypertens; 2007 Jan;25(1):177-86
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  • METHODS: We prospectively re-examined 61 patients: 25 with aldosterone-producing adenoma (APA), after surgery, and 36 patients with idiopathic hyperaldosteronism (IHA) on pharmacological treatment.
  • Multiple regression analysis at diagnosis showed a positive correlation between homeostasis model assessment (HOMA) insulin resistance index and HOMA beta cell and serum aldosterone levels in both APA and IHA.
  • [MeSH-minor] Adenoma / blood. Adenoma / complications. Adenoma / surgery. Adrenal Gland Neoplasms / blood. Adrenal Gland Neoplasms / complications. Adrenal Gland Neoplasms / surgery. Adrenalectomy. Antihypertensive Agents / therapeutic use. Blood Glucose / drug effects. Blood Pressure / drug effects. Female. Follow-Up Studies. Humans. Hypertension / blood. Hypertension / drug therapy. Hypertension / etiology. Insulin / blood. Insulin Resistance. Linear Models. Longitudinal Studies. Male. Middle Aged. Prospective Studies. Renin-Angiotensin System / drug effects. Time Factors. Ventricular Function, Left / drug effects

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  • (PMID = 17143190.001).
  • [ISSN] 0263-6352
  • [Journal-full-title] Journal of hypertension
  • [ISO-abbreviation] J. Hypertens.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antihypertensive Agents; 0 / Blood Glucose; 0 / Insulin; 0 / Mineralocorticoid Receptor Antagonists; 4964P6T9RB / Aldosterone
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84. Yoon SO, Kim BH, Lee HS, Kang GH, Kim WH, Kim YA, Kim JE, Chang MS: Differential protein immunoexpression profiles in appendiceal mucinous neoplasms: a special reference to classification and predictive factors. Mod Pathol; 2009 Aug;22(8):1102-12
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  • We histologically classified 70 appendiceal mucinous neoplasms into three categories: 32 mucinous adenoma, 23 mucinous neoplasm of uncertain malignant potential, and 15 mucinous adenocarcinomas.
  • Immunohistochemistry was performed for 24 proteins in different functional categories, specifically, oncogenic proteins (bcl-2, beta-catenin, CEA, C-erbB2, c-kit, Cox-2, Cyclin D1, EGFR, Ki-67, NF-kappaB, VEGF), tumor suppressors (E-cadherin, FHIT, hMLH1, p53, p63, smad4), cell-cycle regulators (p21, p27, p16), and mucin proteins (MUC1, MUC2, MUC5AC, MUC6).
  • Our data showed that 9 out of the 24 proteins were more frequently altered in the mucinous adenocarcinoma group than in the mucinous adenoma group (P<0.05), including beta-catenin (13% in mucinous adenoma vs 60% in mucinous adenocarcinoma), CyclinD1 (44 vs 87%), Ki-67 (high labeling index: 31 vs 67%), NF-kappaB (19 vs 60%), VEGF (16 vs 87%), E-cadherin (0 vs 47%), p53 (6 vs 40%), MUC2 (9 vs 67%), and MUC5AC (3 vs 40%).
  • The distinct immunoexpression profile of mucinous neoplasm of uncertain malignant potential was placed between those of mucinous adenoma and mucinous adenocarcinoma (P<0.05).
  • Moreover, the mucinous adenoma, mucinous neoplasm of uncertain malignant potential, and mucinous adenocarcinoma categories displayed differences in terms of the number of altered markers among the nine proteins (P<0.05; mean 1.4 vs 2.6 vs 5.5, respectively).
  • NF-kappaB status and the number of altered protein markers made statistically marginal impacts on disease-free survival; also beta-catenin loss, on overall survival of patients.
  • In our study, the three tumor categories of mucinous adenoma, mucinous neoplasm of uncertain malignant potential, and mucinous adenocarcinoma exhibited distinct immunoexpression profiles.
  • Five and more altered protein markers, p53 overexpression, NF-kappaB positivity, and beta-catenin loss were predictive factors of adverse clinical outcomes in appendiceal mucinous adenocarcinomas.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Disease-Free Survival. Female. Gene Expression. Gene Expression Profiling. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. NF-kappa B / biosynthesis. NF-kappa B / genetics. Prognosis. Tissue Array Analysis. Tumor Suppressor Protein p53 / biosynthesis. Tumor Suppressor Protein p53 / genetics. Young Adult. beta Catenin / biosynthesis. beta Catenin / genetics


85. Zoghbi S, Drouin E, Claustre J, Bara J, Scoazec JY, Plaisancié P: Intestinal MUC2 and gastric M1/MUC5AC in preneoplastic lesions induced by 1,2-dimethylhydrazine in rat: a sequential analysis. Int J Oncol; 2007 Feb;30(2):489-97
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  • The expression of MUC2 and of MUC5AC was studied by immunohistochemistry in preneoplastic lesions classified in two categories: histologically altered foci (HAF) and beta-catenin accumulated crypts (BCAC).
  • [MeSH-minor] Adenoma / metabolism. Animals. Carcinoma / metabolism. Cell Line, Tumor. Colon / metabolism. Humans. Male. Mucin 5AC. Mucin-2. Precancerous Conditions. Rats. Rats, Inbred F344. beta Catenin / metabolism

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  • (PMID = 17203232.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Carcinogens; 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / Muc2 protein, rat; 0 / Muc5ac protein, rat; 0 / Mucin 5AC; 0 / Mucin-2; 0 / Mucins; 0 / beta Catenin; IX068S9745 / 1,2-Dimethylhydrazine
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86. Minhajat R, Mori D, Yamasaki F, Sugita Y, Satoh T, Tokunaga O: Endoglin (CD105) expression in angiogenesis of colon cancer: analysis using tissue microarrays and comparison with other endothelial markers. Virchows Arch; 2006 Feb;448(2):127-34
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  • We immunohistochemically analyzed the expression of the colon adenoma-carcinoma sequence by endothelial cells using a panel of eight endothelial markers.
  • We examined sections from endoscopic mucosal resection and surgical resection of tubular adenoma (n=31), carcinoma in adenoma (n=11), and adenocarcinoma (n=34).
  • CD31 (PECAM-1) was universally expressed in the blood vessels of adenoma-carcinoma lesions as well as in normal mucosal vessels (80-95%), with no significant differ