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1. Shibata H, Takano H, Ito M, Shioya H, Hirota M, Matsumoto H, Kakudo Y, Ishioka C, Akiyama T, Kanegae Y, Saito I, Noda T: Alpha-catenin is essential in intestinal adenoma formation. Proc Natl Acad Sci U S A; 2007 Nov 13;104(46):18199-204
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  • [Title] Alpha-catenin is essential in intestinal adenoma formation.
  • These data strongly indicate that simultaneous inactivation of alpha-catenin and Apc during tumor initiation suppresses adenoma formation in line19-Apc(580D/+), suggesting that alpha-catenin plays an essential role in the initiation of intestinal adenomas.
  • Although accumulating evidence obtained from human colon tumors with invasive or metastatic potential has established a tumor-suppressive role for alpha-catenin in late-stage tumorigenesis, the role of alpha-catenin in the initiation of intestinal tumorigenesis is not well documented, especially compared with that of beta-catenin.
  • [MeSH-major] Adenoma / pathology. Intestinal Neoplasms / pathology. alpha Catenin / physiology

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  • (PMID = 17989230.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / alpha Catenin
  • [Other-IDs] NLM/ PMC2084320
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2. Bioulac-Sage P, Laumonier H, Laurent C, Zucman-Rossi J, Balabaud C: Hepatocellular adenoma: what is new in 2008. Hepatol Int; 2008 Sep;2(3):316-21
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  • [Title] Hepatocellular adenoma: what is new in 2008.
  • Patients (85%) with hepatocellular adenoma (HCA) are women taking oral contraceptives.
  • An HNF1alpha germline mutation is observed in less than 5% of HCA cases and can be associated with MODY 3 diabetes. (2) An activating beta-catenin mutation was found in 10% of HCA.
  • These beta-catenin activated HCAs are observed in men and women, and specific risk factors, such as male hormone administration or glycogenosis, are associated with their development.
  • Immunohistochemistry studies show that these HCAs overexpress beta-catenin (nuclear and cytoplasmic) and glutamine synthetase.
  • An additional 10% of inflammatory HCAs express beta-catenin, and are also at risk of malignant transformation. (4) Currently, less than 10% of HCAs are unclassified.

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  • (PMID = 19669260.001).
  • [ISSN] 1936-0533
  • [Journal-full-title] Hepatology international
  • [ISO-abbreviation] Hepatol Int
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2716879
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3. 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
MedlinePlus Health Information. consumer health - Liver Cancer.

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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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4. Bioulac-Sage P, Laumonier H, Couchy G, Le Bail B, Sa Cunha A, Rullier A, Laurent C, Blanc JF, Cubel G, Trillaud H, Zucman-Rossi J, Balabaud C, Saric J: Hepatocellular adenoma management and phenotypic classification: the Bordeaux experience. Hepatology; 2009 Aug;50(2):481-9
MedlinePlus Health Information. consumer health - Liver Cancer.

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  • [Title] Hepatocellular adenoma management and phenotypic classification: the Bordeaux experience.
  • We took advantage of the reported genotype/phenotype classification to analyze our surgical series of hepatocellular adenoma (HCA).
  • We identified 46 HNF1alpha-inactivated HCAs (44 women), 63 inflammatory HCAs (IHCA, 53 women) of which nine were also beta-catenin-activated, and seven beta-catenin-activated HCAs (all women); six additional cases had no known phenotypic marker and six others could not be phenotypically analyzed.
  • Six patients of 128 developed hepatocellular carcinoma (HCC) (all were beta-catenin-activated, whether inflammatory or not).
  • CONCLUSION: There were noticeable clinical differences between HNF1alpha-inactivated HCA and IHCA; there was no increased risk of bleeding or HCC related to the number of HCAs; beta-catenin-activated HCAs are at higher risk of HCC.
  • [MeSH-major] Adenoma, Liver Cell / classification. Liver Neoplasms / classification
  • [MeSH-minor] Adult. Aged. C-Reactive Protein / metabolism. Fatty Acid-Binding Proteins / metabolism. Female. Hepatocyte Nuclear Factor 1-alpha / metabolism. Humans. Male. Middle Aged. Phenotype. Serum Amyloid A Protein / metabolism. Young Adult. beta Catenin / metabolism

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  • (PMID = 19585623.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acid-Binding Proteins; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / Serum Amyloid A Protein; 0 / beta Catenin; 9007-41-4 / C-Reactive Protein
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5. Soreide K, Buter TC, Janssen EA, Gudlaugsson E, Skaland I, Körner H, Baak JP: Cell-cycle and apoptosis regulators (p16INK4A, p21CIP1, beta-catenin, survivin, and hTERT) and morphometry-defined MPECs predict metachronous cancer development in colorectal adenoma patients. Cell Oncol; 2007;29(4):301-13
MedlinePlus Health Information. consumer health - Colorectal Cancer.

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  • [Title] Cell-cycle and apoptosis regulators (p16INK4A, p21CIP1, beta-catenin, survivin, and hTERT) and morphometry-defined MPECs predict metachronous cancer development in colorectal adenoma patients.
  • We assessed whether differential expression of cell-cycle and apoptosis-regulating proteins and a monotonous population of elongated cells (MPECs) in colorectal adenomas could predict metachronous CRC.
  • RESULTS: Of 171 patients with colorectal adenoma 86% (n=147) were eligible for study; 10 (7%) developed metachronous CRC.
  • Elevated expression of cell-cycle regulators p16(INK4A), p21(CIP1), and cytoplasmic/nuclear beta-catenin correlated with increased CRC risk (all P<0.0001), as did elevated expression of the anti-apoptosis protein survivin (P<0.0001) and human telomerase reverse transcriptase (hTERT; P<0.001).
  • Survivin, hTERT, and nuclear beta-catenin were the most predictive molecular markers (hazard ratios [HRs]: 6.3, 9.4, and 5.8, respectively).
  • CONCLUSIONS: Among several markers predictive for metachronous CRC development in colorectal adenomas, MPECs, survivin and hTERT may, when validated, provide information superior to conventional histology, with relevance for the clinical management of patients with colorectal adenoma.
  • [MeSH-major] Adenoma / pathology. Apoptosis Regulatory Proteins / metabolism. Cell Cycle Proteins / metabolism. Colorectal Neoplasms / pathology. Neoplasms, Second Primary / pathology
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Demography. Female. Humans. Immunohistochemistry. Inhibitor of Apoptosis Proteins. Kaplan-Meier Estimate. Male. Microtubule-Associated Proteins / metabolism. Middle Aged. Multivariate Analysis. Neoplasm Proteins / metabolism. Proportional Hazards Models. Telomerase / metabolism. beta Catenin / metabolism

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  • (PMID = 17641414.001).
  • [ISSN] 1570-5870
  • [Journal-full-title] Cellular oncology : the official journal of the International Society for Cellular Oncology
  • [ISO-abbreviation] Cell. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / beta Catenin; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC4617994
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6. 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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7. do Prado RF, Consolaro A, Taveira LA: Expression of betacatenin in carcinoma in pleomorphic adenoma, pleomorphic adenoma and normal salivary gland: an immunohistochemical study. Med Oral Patol Oral Cir Bucal; 2006 May;11(3):E247-51
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  • [Title] Expression of betacatenin in carcinoma in pleomorphic adenoma, pleomorphic adenoma and normal salivary gland: an immunohistochemical study.
  • Beta-catenin is a cell adhesion molecule associated with the invasion and metastasis of carcinomas of the head and neck, esophagus.
  • The objective of this study was to detect the expression of beta-catenin in pleomorphic adenomas, carcinomas in pleomorphic adenomas and normal salivary glands to discuss its role in the development of these two lesions.
  • STUDY DESIGN: The expression of beta-catenin (BD Transduction Laboratories) was analyzed by immunohistochemistry in formalin-fixed, paraffin embedded specimens by the avidin-biotin-peroxidase complex method in 16 pleomorphic adenomas (12 from minor salivary glands), 3 carcinomas in pleomorphic adenomas (all from palate) and 10 normal salivary glands as control group (5 from major and 5 from minor salivary glands).
  • Nuclear beta-catenin immunostaining was not observed.
  • Higher beta-catenin index rates were seen mainly in salivary gland ducts and in ductal structures in the adenomas and carcinomas in pleomorphic adenomas.
  • CONCLUSIONS: The present study showed participation of the loss of beta-catenin adhesion molecule in the development of pleomorphic adenoma, and that the cytoplasmic accumulation of the molecule takes part in the malignant transformation of the pleomorphic adenoma into carcinoma in pleomorphic adenoma.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. Carcinoma / metabolism. Neoplasms, Multiple Primary / metabolism. Salivary Gland Neoplasms / metabolism. Salivary Glands / metabolism. beta Catenin / biosynthesis

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  • (PMID = 16648762.001).
  • [ISSN] 1698-6946
  • [Journal-full-title] Medicina oral, patología oral y cirugía bucal
  • [ISO-abbreviation] Med Oral Patol Oral Cir Bucal
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / beta Catenin
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8. 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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9. Kang WY, Chen WT, Wu MT, Chai CY: The expression of CD66a and possible roles in colorectal adenoma and adenocarcinoma. Int J Colorectal Dis; 2007 Aug;22(8):869-74
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  • [Title] The expression of CD66a and possible roles in colorectal adenoma and adenocarcinoma.
  • BACKGROUND: The aim of our study was to analyze the expression and possible role of CD66a in colorectal adenoma and adenocarcinoma and the relationship between its expression and pre-operation serum carcinoembryonic antigen (CEA) level and tumor stage in patients with colorectal adenocarcinomas.
  • Immunohistochemical analysis was performed, and the expression and the location of CD66a were evaluated and were correlated with beta-catenin nuclear expression.
  • Expressions of secreted CD66a were of higher level in adenocarcinoma than in adenoma with high-grade dysplasia and adenoma with low-grade dysplasia (p < 0.0001).
  • CONCLUSIONS: This study implied that CD66a can function both as an epithelial cell adhesion protein or alternatively as secreted CD66a.
  • [MeSH-major] Adenocarcinoma / immunology. Adenoma / immunology. Antigens, CD / analysis. Cell Adhesion Molecules / analysis. Colorectal Neoplasms / immunology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Carcinoembryonic Antigen / blood. Cell Nucleus / chemistry. Female. Humans. Lymph Nodes / pathology. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. beta Catenin / analysis

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  • (PMID = 17143599.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD66 antigens; 0 / CTNNB1 protein, human; 0 / Carcinoembryonic Antigen; 0 / Cell Adhesion Molecules; 0 / beta Catenin
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10. Koga Y, Yao T, Hirahashi M, Kumashiro Y, Ohji Y, Yamada T, Tanaka M, Tsuneyoshi M: Flat adenoma-carcinoma sequence with high-malignancy potential as demonstrated by CD10 and beta-catenin expression: a different pathway from the polypoid adenoma-carcinoma sequence. Histopathology; 2008 Apr;52(5):569-77
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  • [Title] Flat adenoma-carcinoma sequence with high-malignancy potential as demonstrated by CD10 and beta-catenin expression: a different pathway from the polypoid adenoma-carcinoma sequence.
  • The aim was to examine phenotypic expression in colorectal neoplasia and to elucidate changes in such expression through the adenoma-carcinoma sequence.
  • Nuclear beta-catenin was more frequently expressed in NPG-LGN than in PG-LGN.
  • CONCLUSIONS: From the viewpoint of the expression of CD10 and beta-catenin, it would appear that NPG-LGN differs significantly from PG-LGN, thereby indicating that NPG-LGN is a precursor of CD10+ carcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Colonic Polyps / pathology. Colorectal Neoplasms / pathology. Neprilysin / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Cell Nucleus / metabolism. Cell Nucleus / pathology. Disease Progression. Early Diagnosis. Female. Humans. Immunohistochemistry. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Male. Neoplasm Invasiveness

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  • (PMID = 18370954.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / beta Catenin; EC 3.4.24.11 / Neprilysin
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11. Yang GZ, Li J, Ding HY: [Nipple adenoma: report of 18 cases with review of literatures]. Zhonghua Bing Li Xue Za Zhi; 2009 Sep;38(9):614-6
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  • [Title] [Nipple adenoma: report of 18 cases with review of literatures].
  • OBJECTIVE: To investigate the clinicopathological and immunohistochemical features, diagnosis and differential diagnosis of nipple adenoma of the breast.
  • METHODS: Morphological observation and immunohistochemistry were applied to 18 cases of nipple adenoma with a review of the related literatures.
  • The glandular epithelium showed various type of proliferation, forming thick layers or complex structures such as papillae, micropapillae, tufts, fronds, arcades or bridges accompanying with solid or cribriform cell nests.
  • CONCLUSIONS: Nipple adenoma is an infrequent type of benign breast neoplasm, presenting as sclerosing papilloma, papillomatosis or florid sclerosing adenosis.
  • [MeSH-major] Adenoma / pathology. Breast Neoplasms / pathology. Nipples / pathology

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  • (PMID = 20079190.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CK-34 beta E12; 0 / Keratin-5; 68238-35-7 / Keratins
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12. Zucman-Rossi J, Jeannot E, Nhieu JT, Scoazec JY, Guettier C, Rebouissou S, Bacq Y, Leteurtre E, Paradis V, Michalak S, Wendum D, Chiche L, Fabre M, Mellottee L, Laurent C, Partensky C, Castaing D, Zafrani ES, Laurent-Puig P, Balabaud C, Bioulac-Sage P: Genotype-phenotype correlation in hepatocellular adenoma: new classification and relationship with HCC. Hepatology; 2006 Mar;43(3):515-24
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  • [Title] Genotype-phenotype correlation in hepatocellular adenoma: new classification and relationship with HCC.
  • A multicentric series of 96 liver tumors with a firm or possible diagnosis of hepatocellular adenoma was reviewed by liver pathologists.
  • In all cases, the genes coding for hepatocyte nuclear factor 1alpha (HNF1alpha) and beta-catenin were sequenced.
  • No tumors were mutated in both HNF1alpha and beta-catenin enabling tumors to be classified into 3 groups, according to genotype.
  • In contrast, the group of tumors defined by beta-catenin activation included 13 lesions with frequent cytological abnormalities and pseudo-glandular formation (P < 10(-5)).
  • In this classification, hepatocellular carcinoma associated with adenoma or borderline lesions between carcinoma and adenoma is found in 46% of the beta-catenin-mutated tumors whereas they are never observed in inflammatory lesions and are rarely found in HNF1alpha mutated tumors (P = .004).
  • In conclusion, the molecular and pathological classification of hepatocellular adenomas permits the identification of strong genotype-phenotype correlations and suggests that adenomas with beta-catenin activation have a higher risk of malignant transformation.
  • [MeSH-major] Adenoma, Liver Cell / genetics. Carcinoma, Hepatocellular / genetics. Hepatocyte Nuclear Factor 1-alpha / genetics. Liver Neoplasms / genetics. beta Catenin / genetics

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  • [CommentIn] Hepatology. 2006 Mar;43(3):401-4 [16496344.001]
  • [CommentIn] Histopathology. 2007 Dec;51(6):855-6 [17903198.001]
  • (PMID = 16496320.001).
  • [ISSN] 0270-9139
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / beta Catenin
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13. Yoshida A, Sen C, Asa SL, Rosenblum MK: Composite pituitary adenoma and craniopharyngioma?: an unusual sellar neoplasm with divergent differentiation. Am J Surg Pathol; 2008 Nov;32(11):1736-41
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  • [Title] Composite pituitary adenoma and craniopharyngioma?: an unusual sellar neoplasm with divergent differentiation.
  • At transsphenoidal surgery, a tumor consisting of a pituitary adenoma and adamantinomatous craniopharyngiomalike components was resected.
  • Immunohistochemically, the adenoma was not only positive for beta-thyroid stimulating hormone, alpha subunit, and pituitary transcription factor 1, but also stained for beta-follicle stimulating hormone, steroidogenic factor-1, adrenocorticotropic hormone, and pituitary-restricted transcription factor (Tpit), exhibiting an unusual plurihormonal profile.
  • Alternatively, it may be viewed as a pituitary adenoma showing metaplastic change analogous to the development of squamous cell nests of the pars tuberalis from adenohypophyseal endocrine cells.
  • [MeSH-major] Adenoma / pathology. Craniopharyngioma / pathology. Neoplasms, Multiple Primary / pathology. Pituitary Neoplasms / pathology

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  • (PMID = 18769335.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-71-5 / Thyrotropin
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14. 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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15. Cavallaro G, Cucina A, Coluccia P, Petramala L, Cotesta D, Polistena A, Zinnamosca L, Letizia C, Rosato L, Cavallaro A, De Toma G: Role of growth factors on human parathyroid adenoma cell proliferation. World J Surg; 2010 Jan;34(1):48-54

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of growth factors on human parathyroid adenoma cell proliferation.
  • INTRODUCTION: Primary hyperparathyroidism (pHPT) is caused by a single monoclonal adenoma in more than 80% of patients.
  • Among the latter, insulin-like growth factor 1 (IGF-1), basic fibroblastic growth factor (bFGF), vascular endothelial growth factor (VEGF), and transforming growth factor beta 1 (TGF-beta1) and their effects have been extensively evaluated in different kinds of endocrine disease.
  • METHODS: Parathyroid cell cultures were prepared from six human adenomatous parathyroid glands that were surgically removed.
  • Then, after 48-hour incubation, cell count was performed by a particle count and size analyzer, and prevalence of cell cycle was analyzed by using a flow cytometer.
  • RESULTS: Cell count (x10000) in the control group was 3.73 +/- 0.32.
  • CONCLUSIONS: Growth factors seem to play an important role in parathyroid adenoma cell proliferation; IGF-1, bFGF, VEGF, and low-dose TGF-beta1 promote cell proliferation, whereas high-dose TGF-beta1 inhibits these phenomena.
  • [MeSH-major] Adenoma / pathology. Cell Proliferation / drug effects. Fibroblast Growth Factor 2 / pharmacology. Insulin-Like Growth Factor I / pharmacology. Parathyroid Neoplasms / pathology. Transforming Growth Factor beta1 / pharmacology. Vascular Endothelial Growth Factor A / pharmacology

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  • (PMID = 20020293.001).
  • [ISSN] 1432-2323
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta1; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2; 67763-96-6 / Insulin-Like Growth Factor I
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16. Araújo VC, Demasi AP, Furuse C, Altemani A, Alves VA, Freitas LL, Araújo NS: Collagen type I may influence the expression of E-cadherin and beta-catenin in carcinoma ex-pleomorphic adenoma. Appl Immunohistochem Mol Morphol; 2009 Jul;17(4):312-8
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  • [Title] Collagen type I may influence the expression of E-cadherin and beta-catenin in carcinoma ex-pleomorphic adenoma.
  • Carcinoma ex-pleomorphic adenoma (CXPA) is an aggressive salivary gland malignancy, usually derived from a long-standing or a recurrent benign tumor, the pleomorphic adenoma (PA).
  • In the context of dynamic reciprocity, changes in the composition and structure of extracellular matrix proteins and cell surface receptors have been frequently associated with dysfunctional adhesion and invasive behavior of tumor cells.
  • In this study, different progression stages of CXPA were investigated regarding the expression of the major extracellular matrix proteins, collagen type I, and of E-cadherin and beta-catenin, the components of adherens junctions.
  • By immunohistochemical analysis, we have demonstrated that direct contact of tumor cells with fibrillar type I collagen, particularly near the invasive front and in invasive areas prevailing small nests of CXPA cells, could be associated with reduced expression of the E-cadherin and beta-catenin adhesion molecules and with invasive behavior of epithelial, but not of CXPA with myoepithelial component.

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  • (PMID = 19276972.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / Collagen Type I; 0 / Neoplasm Proteins; 0 / beta Catenin
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17. Sillars-Hardebol AH, Carvalho B, de Wit M, Postma C, Delis-van Diemen PM, Mongera S, Ylstra B, van de Wiel MA, Meijer GA, Fijneman RJ: Identification of key genes for carcinogenic pathways associated with colorectal adenoma-to-carcinoma progression. Tumour Biol; 2010 Apr;31(2):89-96
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  • [Title] Identification of key genes for carcinogenic pathways associated with colorectal adenoma-to-carcinoma progression.
  • Only 5% of adenomas progress into adenocarcinomas, indicating that malignant transformation requires other biological alterations than those involved in adenoma formation.
  • The present study aimed to explore which cancer-related biological processes are affected during colorectal adenoma-to-carcinoma progression and to identify key genes within these pathways that can serve as tumor markers for malignant transformation.
  • [MeSH-major] Adenoma / genetics. Carcinoma / genetics. Colorectal Neoplasms / genetics
  • [MeSH-minor] Aurora Kinase A. Aurora Kinases. Cell Cycle Proteins / analysis. Cell Transformation, Neoplastic. Disease Progression. Humans. Immunohistochemistry. Protein-Serine-Threonine Kinases / analysis. Proto-Oncogene Proteins / analysis. Receptor, Platelet-Derived Growth Factor beta / analysis

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  • (PMID = 20358421.001).
  • [ISSN] 1423-0380
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.11.1 / AURKA protein, human; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / polo-like kinase 1
  • [Other-IDs] NLM/ PMC2848338
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18. Foley PJ, Scheri RP, Smolock CJ, Pippin J, Green DW, Drebin JA: Targeted suppression of beta-catenin blocks intestinal adenoma formation in APC Min mice. J Gastrointest Surg; 2008 Aug;12(8):1452-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted suppression of beta-catenin blocks intestinal adenoma formation in APC Min mice.
  • INTRODUCTION: Mutations involving the adenomatous polyposis coli (APC) tumor suppressor gene leading to activation of beta-catenin have been identified in the majority of sporadic colonic adenocarcinomas and in essentially all colonic tumors from patients with Familial Adenomatous Polyposis.
  • The C57BL/6J-APC(min) (Min) mouse, which carries a germ line mutation in the murine homolog of the APC gene is a useful model for intestinal adenoma formation linked to loss of APC activity.
  • One of the critical downstream molecules regulated by APC is beta-catenin; molecular targeting of beta-catenin is, thus, an attractive chemopreventative strategy in colon cancer.
  • Antisense oligodeoxynucleotides (AODNs) capable of downregulating murine beta-catenin have been identified.
  • ANALYSIS OF beta-CATENIN PROTEIN EXPRESSION IN LIVER TISSUE AND INTESTINAL ADENOMAS: Adenomas harvested from mice treated for 7 days with beta-catenin AODNs demonstrated clear downregulation of beta-catenin expression, which was accompanied by a significant reduction in proliferation.
  • Min mice treated systemically with beta-catenin AODNs over a 6-week period had a statistically significant reduction in the number of intestinal adenomas.
  • These studies provide direct evidence that targeted suppression of beta-catenin inhibits the formation of intestinal adenomas in APC-mutant mice.
  • Furthermore, these studies suggest that molecular targeting of beta-catenin holds significant promise as a chemopreventative strategy in colon cancer.
  • [MeSH-major] Adenomatous Polyposis Coli / therapy. Colonic Neoplasms / therapy. Gene Expression Regulation, Neoplastic. Gene Targeting / methods. RNA, Neoplasm / genetics. beta Catenin / genetics
  • [MeSH-minor] Animals. Blotting, Northern. Blotting, Western. Cell Proliferation. Disease Progression. Female. Immunohistochemistry. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Neoplasms, Experimental. Treatment Outcome

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  • (PMID = 18521697.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100189
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, mouse; 0 / RNA, Neoplasm; 0 / beta Catenin
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19. 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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20. Wani Y, Notohara K, Fujisawa M: Aberrant expression of an "intestinal marker" Cdx2 in pyloric gland adenoma of the gallbladder. Virchows Arch; 2008 Nov;453(5):521-7
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  • [Title] Aberrant expression of an "intestinal marker" Cdx2 in pyloric gland adenoma of the gallbladder.
  • The aim of this study was to survey Cdx2 expression in pyloric gland adenoma (PGA) of the gallbladder.
  • The immunostaining for Cdx2, beta-catenin, MUC5AC, MUC2, MUC6, and M-GGMC-1 was performed and scored (0 = negative, 1+ = <10%, 2+ = 10% to <30%, 3+ = 30% to <50%, 4+ = 50% to <70%, 5+ = 70-100%).
  • Furthermore, the p value of scores between Cdx2 and beta-catenin was 0.051, and both mean labeling indices (LIs) were correlated (r = 0.736).
  • Finally, we concluded that aberrant Cdx2 expression in PGAs is closely associated with nuclear beta-catenin expression and SM in contrast with IM.
  • [MeSH-major] Adenoma / metabolism. Gallbladder Neoplasms / metabolism. Gastric Mucosa / metabolism. Homeodomain Proteins / metabolism
  • [MeSH-minor] Cell Differentiation. Gene Expression Regulation, Neoplastic. Humans. Retrospective Studies. beta Catenin / metabolism

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  • (PMID = 18843504.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / beta Catenin
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21. Miyai S, Yoshimura S, Iwasaki Y, Takekoshi S, Lloyd RV, Osamura RY: Induction of GH, PRL, and TSH beta mRNA by transfection of Pit-1 in a human pituitary adenoma-derived cell line. Cell Tissue Res; 2005 Nov;322(2):269-77
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  • [Title] Induction of GH, PRL, and TSH beta mRNA by transfection of Pit-1 in a human pituitary adenoma-derived cell line.
  • Pituitary-specific transcription factor-1 (Pit-1) is required for the expression of growth hormone (GH), prolactin (PRL), and the thyroid-stimulating hormone beta subunit (TSH beta) and acts synergistically with the estrogen receptor (ER) and GATA-binding protein 2 (GATA-2) to induce PRL and TSH beta expression, respectively.
  • These findings have led to the suggestion that the expression of Pit-1 in cells of the alpha SU-based gonadotropin cell lineage might also lead to the expression of GH.
  • In this study, we transfected HP 75 cells (derived from a human non-functioning pituitary adenoma that expressed alpha SU and LH beta) with Pit-1 by using an adenovirus FLAG-Pit-1 construct.
  • Most of the transfected cells expressed GH mRNA, with fewer cells expressing PRL and TSH beta mRNA.
  • The HP 75 cells expressed the genes for ER and GATA-2, thus allowing their expression of GH, PRL, and TSH beta mRNA in response to Pit-1.
  • These results support the hypothesis that GH can be induced in cells that possess an active alpha SU gene and shed light on the basic molecular mechanism that drives the development of GH, PRL, and TSH beta expression in the alpha SU-based gonadotroph lineage.
  • [MeSH-major] Adenoma / metabolism. Human Growth Hormone / metabolism. Pituitary Neoplasms / metabolism. Prolactin / metabolism. RNA, Messenger / metabolism. Thyrotropin, beta Subunit / metabolism. Transcription Factor Pit-1 / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Lineage. GATA2 Transcription Factor / genetics. GATA2 Transcription Factor / metabolism. Glycoprotein Hormones, alpha Subunit / genetics. Glycoprotein Hormones, alpha Subunit / metabolism. Humans. Pituitary Gland / cytology. Pituitary Gland / growth & development. Pituitary Gland / metabolism. Receptors, Estrogen / genetics. Receptors, Estrogen / metabolism. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism

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  • (PMID = 16133148.001).
  • [ISSN] 0302-766X
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / GATA2 Transcription Factor; 0 / Glycoprotein Hormones, alpha Subunit; 0 / RNA, Messenger; 0 / Receptors, Estrogen; 0 / Recombinant Fusion Proteins; 0 / Thyrotropin, beta Subunit; 0 / Transcription Factor Pit-1; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
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22. Sornmayura P, Siripornpitak S, Leela-udomlipi S, Bunyaratvej S: Hepatocellular adenoma: a case report. J Med Assoc Thai; 2010 Mar;93(3):393-7
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  • [Title] Hepatocellular adenoma: a case report.
  • A case of hepatocellular adenoma (HCA) was described in a 26-year-old woman, who was a potential kidney donor for her father and denied taking the oral contraceptive pill.
  • Molecular biological studies disclosed three variants of HCAs, i.e., I) with mutation of HNF 1-alpha gene, II) with mutation of beta-catenin gene, and III) no mutation of the two genes.
  • [MeSH-major] Adenoma, Liver Cell / diagnosis. Liver Neoplasms / diagnosis

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  • (PMID = 20420118.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Thailand
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23. Schulenburg A, Cech P, Herbacek I, Marian B, Wrba F, Valent P, Ulrich-Pur H: CD44-positive colorectal adenoma cells express the potential stem cell markers musashi antigen (msi1) and ephrin B2 receptor (EphB2). J Pathol; 2007 Oct;213(2):152-60
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  • [Title] CD44-positive colorectal adenoma cells express the potential stem cell markers musashi antigen (msi1) and ephrin B2 receptor (EphB2).
  • As wnt signalling preserves stem cell functions, it would be expected that stem cells would be enriched in adenomas.
  • We have shown expression of the wnt target gene CD44, which may characterize the expanded stem cell compartment, in colorectal tumours.
  • To investigate this possibility, we performed an immunohistological survey of CD44 expression in relation to the proliferation marker Ki67 and apoptosis in colorectal tumour tissue, and have isolated a CD44-positive subpopulation of the human colorectal adenoma cell line LT97 for cell biological analysis.
  • In comparison to unsorted growing LT97 cells, the CD44-positive cells had shifted beta-catenin into the nucleus and expressed beta-catenin target genes, such as ephrin B receptor (ephB2) and musashi antigen (msi1).
  • By contrast, CD44-negative cultures contained no cells with nuclear beta-catenin.
  • [MeSH-major] Adenoma / metabolism. Biomarkers, Tumor / metabolism. Colorectal Neoplasms / metabolism. Nerve Tissue Proteins / metabolism. RNA-Binding Proteins / metabolism. Receptor, EphB2 / metabolism
  • [MeSH-minor] Antigens, CD44 / metabolism. Apoptosis. Cell Proliferation. Cell Survival. Flow Cytometry. Humans. Neoplasm Proteins / metabolism. Neoplastic Stem Cells / metabolism. Polymerase Chain Reaction / methods. Tumor Cells, Cultured. beta Catenin / metabolism

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  • (PMID = 17708598.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / MSI1 protein, human; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / RNA-Binding Proteins; 0 / beta Catenin; EC 2.7.10.1 / Receptor, EphB2
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24. Doviner V, Maly B, Kaplan V, Gingis-Velitski S, Ilan N, Vlodavsky I, Sherman Y: Spatial and temporal heparanase expression in colon mucosa throughout the adenoma-carcinoma sequence. Mod Pathol; 2006 Jun;19(6):878-88
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  • [Title] Spatial and temporal heparanase expression in colon mucosa throughout the adenoma-carcinoma sequence.
  • Heparanase is a mammalian endo-beta-D-glucuronidase that cleaves heparan sulfate side chains at a limited number of sites.
  • Such enzymatic activity is thought to participate in degradation and remodeling of the extracellular matrix and to facilitate cell invasion associated with tumor metastasis, angiogenesis and inflammation.
  • Traditionally, heparanase activity was well correlated with the metastatic potential of a large number of tumor-derived cell types.
  • Here, we employed anti-heparanase 733 polyclonal antibody that preferentially recognizes the 50 kDa active heparanase subunit over the 65 kDa proenzyme, as well as anti-heparanase 92.4 monoclonal antibody that recognizes both the latent and the active enzyme, to follow heparanase expression, processing and localization throughout the adenoma-carcinoma transition of the colon epithelium.
  • These results suggest that heparanase expression is induced during colon carcinogenesis, and that its processing, conformation and localization are tightly regulated during the course of colon adenoma-carcinoma progression.
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Cell Line, Tumor / enzymology. Cell Line, Tumor / pathology. Disease Progression. Female. Fluorescent Antibody Technique, Indirect. Humans. Immunoenzyme Techniques. Mice. Mice, SCID. Neoplasm Transplantation. Transfection

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  • (PMID = 16607375.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106456
  • [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 / Biomarkers, Tumor; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
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25. Furuse C, Miguita L, Rosa AC, Soares AB, Martinez EF, Altemani A, de Araújo VC: Study of growth factors and receptors in carcinoma ex pleomorphic adenoma. J Oral Pathol Med; 2010 Aug 1;39(7):540-7
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  • [Title] Study of growth factors and receptors in carcinoma ex pleomorphic adenoma.
  • Carcinoma ex pleomorphic adenoma (CXPA) is a rare malignant salivary gland tumor derived from a pre-existing pleomorphic adenoma.
  • Malignant epithelial cells starting with in situ areas showed stronger expression than luminal cells of pleomorphic adenoma for all antibodies.
  • Altogether this data infers that these factors may contribute to cell proliferation during initial phases of the tumor.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma, Pleomorphic / pathology. Intercellular Signaling Peptides and Proteins / analysis. Parotid Neoplasms / pathology. Receptors, Growth Factor / analysis
  • [MeSH-minor] Adult. Aged. Carcinoma in Situ / pathology. Cell Proliferation. Coloring Agents. Disease Progression. Epithelial Cells / pathology. Female. Fibroblast Growth Factors / analysis. Hepatocyte Growth Factor / analysis. Humans. Male. Middle Aged. Neoplasm Invasiveness. Protein-Serine-Threonine Kinases / analysis. Proto-Oncogene Proteins c-met / analysis. Receptor, Epidermal Growth Factor / analysis. Receptor, Fibroblast Growth Factor, Type 1 / analysis. Receptor, Fibroblast Growth Factor, Type 2 / analysis. Receptor, IGF Type 1 / analysis. Receptors, Transforming Growth Factor beta / analysis. Submandibular Gland Neoplasms / pathology. Transforming Growth Factor beta1 / analysis

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  • (PMID = 20149060.001).
  • [ISSN] 1600-0714
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / Intercellular Signaling Peptides and Proteins; 0 / Receptors, Growth Factor; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 62031-54-3 / Fibroblast Growth Factors; 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / FGFR2 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 2; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
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26. Harper J, Burns JL, Foulstone EJ, Pignatelli M, Zaina S, Hassan AB: Soluble IGF2 receptor rescues Apc(Min/+) intestinal adenoma progression induced by Igf2 loss of imprinting. Cancer Res; 2006 Feb 15;66(4):1940-8
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  • [Title] Soluble IGF2 receptor rescues Apc(Min/+) intestinal adenoma progression induced by Igf2 loss of imprinting.
  • Increased expression of the normally monoallelic (paternally expressed) mouse (Igf2) and human (IGF2) genes modify progression of intestinal adenoma in the Apc(Min/+) mouse and correlate with a high relative risk of human colorectal cancer susceptibility, respectively.
  • We examined the functional consequence of Igf2 allelic dosage (null, monoallelic, and biallelic) on intestinal adenoma development in the Apc(Min/+) by breeding with mice with either disruption of Igf2 paternal allele or H19 maternal allele and used these models to evaluate an IGF-II-specific therapeutic intervention.
  • Increased allelic Igf2 expression led to elongation of intestinal crypts, increased adenoma growth independent of systemic growth, and increased adenoma nuclear beta-catenin staining.
  • By introducing a transgene expressing a soluble form of the full-length IGF-II/mannose 6-phosphate receptor (sIGF2R) in the intestine, which acts as a specific inhibitor of IGF-II ligand bioavailability (ligand trap), we show rescue of the Igf2-dependent intestinal and adenoma phenotype.
  • [MeSH-minor] Alleles. Animals. Cell Growth Processes / genetics. Crosses, Genetic. Disease Progression. Female. Gene Dosage. Genomic Imprinting. Ligands. Male. Mice. Mice, Inbred C57BL. Transgenes. beta Catenin / metabolism

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  • (PMID = 16488992.001).
  • [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 / Ligands; 0 / Receptor, IGF Type 2; 0 / beta Catenin; 67763-97-7 / Insulin-Like Growth Factor II
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27. Herbst A, Bommer GT, Kriegl L, Jung A, Behrens A, Csanadi E, Gerhard M, Bolz C, Riesenberg R, Zimmermann W, Dietmaier W, Wolf I, Brabletz T, Göke B, Kolligs FT: ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition. Gastroenterology; 2009 Aug;137(2):639-48, 648.e1-9
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  • [Title] ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition.
  • BACKGROUND & AIMS: The ubiquitously expressed basic helix-loop-helix transcription factor ITF-2B has an important role in differentiation processes, and its transcription is regulated by beta-catenin.
  • ITF-2B induces cell cycle arrest and regulates the expression of p21(Cip1) via newly identified E-boxes in the CDKN1A gene, independently of p53.
  • This finding, along with the fact that ITF-2B is a regulator of the key cell cycle inhibitor p21(Cip1), indicates that ITF-2B is a tumor suppressor that has an important function at the adenoma to carcinoma transition.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyposis Coli / genetics. Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 18 / genetics. Colorectal Neoplasms / genetics. DNA-Binding Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Basic Helix-Loop-Helix Leucine Zipper Transcription Factors. Cell Line, Tumor. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Genetic Predisposition to Disease. Humans. Immunohistochemistry. Loss of Heterozygosity. Mutation. Neoplasm Proteins / genetics. Precancerous Conditions / genetics. Precancerous Conditions / pathology

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  • (PMID = 19394332.001).
  • [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 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / TCF3 protein, human; 0 / TCF4 protein, human; 0 / Transcription Factors
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28. 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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29. Jeannot E, Wendum D, Paye F, Mourra N, de Toma C, Fléjou JF, Zucman-Rossi J: Hepatocellular adenoma displaying a HNF1alpha inactivation in a patient with familial adenomatous polyposis coli. J Hepatol; 2006 Dec;45(6):883-6
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  • [Title] Hepatocellular adenoma displaying a HNF1alpha inactivation in a patient with familial adenomatous polyposis coli.
  • Patients with familial adenomatous polyposis coli (FAP) may rarely develop hepatocellular adenoma.
  • Here we report the case of a 37-year-old FAP woman presenting a hepatocellular adenoma after oestroprogestative oral contraception use.
  • In this steatotic adenoma, we identified an inactivating biallelic mutation of HNF1alpha.
  • In addition to the known germline APC mutation Q1062fs, we did not find an inactivation of the second APC allele nor an activation of the beta-catenin target genes GLUL and GPR49.
  • Our findings contrast with two hepatocellular adenoma cases related to FAP, for which a biallelic inactivation of the APC gene was previously described.
  • Altogether, these results suggest that benign hepatocellular carcinogenesis may be dependent on or independent of the Wnt/beta-catenin pathway in patients with FAP.

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  • [Cites] Gastroenterology. 2001 Jun;120(7):1763-73 [11375957.001]
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  • (PMID = 17049664.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha
  • [Other-IDs] NLM/ HALMS130312; NLM/ PMC2121664
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30. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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31. Bioulac-Sage P, Rebouissou S, Thomas C, Blanc JF, Saric J, Sa Cunha A, Rullier A, Cubel G, Couchy G, Imbeaud S, Balabaud C, Zucman-Rossi J: Hepatocellular adenoma subtype classification using molecular markers and immunohistochemistry. Hepatology; 2007 Sep;46(3):740-8
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  • [Title] Hepatocellular adenoma subtype classification using molecular markers and immunohistochemistry.
  • Hepatocellular adenomas (HCA) with activated beta-catenin present a high risk of malignant transformation.
  • We analyzed the expression of candidate genes by quantitative reverse transcription polymerase chain reaction QRT-PCR followed by immunohistochemistry to validate their specificity and sensitivity according to hepatocyte nuclear factor 1 alpha (HNF1alpha) and beta-catenin mutations as well as inflammatory phenotype.
  • Quantitative RT-PCR showed that FABP1 (liver fatty acid binding protein) and UGT2B7 were downregulated in HNF1alpha-inactivated HCA (P <or= 0.0002); GLUL (glutamine synthetase) and GPR49 overexpression were associated with beta-catenin-activating mutations (P <or= 0.0005), and SAA2 (serum amyloid A2) and CRP (C-reactive protein) were upregulated in inflammatory HCA (P = 0.0001).
  • Immunohistochemistry validation confirmed that the absence of liver-fatty acid binding protein (L-FABP) expression rightly indicated HNF1alpha mutation (100% sensitivity and specificity), the combination of glutamine synthetase overexpression and nuclear beta-catenin staining were excellent predictors of beta-catenin-activating mutation (85% sensitivity, 100% specificity), and SAA hepatocytic staining was ideal to classify inflammatory HCA (91% sensitivity and specificity).
  • Previously described associations were confirmed and in particular the significant association between beta-catenin-activated HCA and hepatocellular carcinomas (HCC) at diagnosis or during follow-up (P < 10(-5)).
  • [MeSH-major] Adenoma, Liver Cell / classification. Adenoma, Liver Cell / pathology. Biomarkers, Tumor / analysis. Liver Neoplasms / classification. Liver Neoplasms / pathology
  • [MeSH-minor] Adult. Fatty Acid-Binding Proteins / analysis. Fatty Acid-Binding Proteins / genetics. Fatty Acid-Binding Proteins / metabolism. Female. Glucuronosyltransferase / analysis. Glucuronosyltransferase / genetics. Glucuronosyltransferase / metabolism. Glutamate-Ammonia Ligase / analysis. Glutamate-Ammonia Ligase / genetics. Glutamate-Ammonia Ligase / metabolism. Hepatocyte Nuclear Factor 1-alpha / analysis. Hepatocyte Nuclear Factor 1-alpha / genetics. Hepatocyte Nuclear Factor 1-alpha / metabolism. Humans. Immunohistochemistry / methods. Male. beta Catenin / metabolism


32. Rebouissou S, Bioulac-Sage P, Zucman-Rossi J: Molecular pathogenesis of focal nodular hyperplasia and hepatocellular adenoma. J Hepatol; 2008 Jan;48(1):163-70
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  • [Title] Molecular pathogenesis of focal nodular hyperplasia and hepatocellular adenoma.
  • In contrast, HCAs are consistently monoclonal tumors, which have been divided up into three subtypes of tumors depending on the molecular alteration detected in the tumors: HNF1alpha inactivation, beta-catenin activation and/or an acute inflammatory response in the tumor.
  • These molecular features are closely related to clinical and pathological characteristics, and one of the most critical correlations is the higher risk of malignant transformation for beta-catenin activated HCA cases.
  • [MeSH-major] Adenoma, Liver Cell / genetics. Adenoma, Liver Cell / pathology. Focal Nodular Hyperplasia / genetics. Focal Nodular Hyperplasia / pathology. Liver Neoplasms / genetics. Liver Neoplasms / pathology

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  • (PMID = 17997499.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 110
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33. Yoshida D, Koketshu K, Nomura R, Teramoto A: The CXCR4 antagonist AMD3100 suppresses hypoxia-mediated growth hormone production in GH3 rat pituitary adenoma cells. J Neurooncol; 2010 Oct;100(1):51-64
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  • [Title] The CXCR4 antagonist AMD3100 suppresses hypoxia-mediated growth hormone production in GH3 rat pituitary adenoma cells.
  • Pituitary adenomas produce the chemokine stromal cell-derived factor (SDF-1α/CXCL12) and its receptor, CXCR4.
  • CXCR4 expression in pituitary adenoma tissues was determined by a tissue microarray analysis of 62 pituitary adenoma samples.
  • The relative expression of genes/gene categories that were modulated by up-regulated CXCL12/CXCR4 signaling was determined by a comparative transcriptome analysis of wild-type and CXCR4-knockdown cells in normoxia and hypoxia using the rat GH-producing and prolactin-producing pituitary adenoma cell line, GH3.
  • [MeSH-major] Cell Hypoxia / drug effects. Cell Hypoxia / physiology. Growth Hormone / metabolism. Heterocyclic Compounds / pharmacology. Receptors, CXCR4 / antagonists & inhibitors
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Animals. Cell Line, Tumor. Chemokine CXCL12 / metabolism. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay / methods. Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic / drug effects. Humans. Middle Aged. Oligonucleotide Array Sequence Analysis / methods. Pituitary Neoplasms / genetics. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Rats. Statistics as Topic. beta Carotene / metabolism

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  • (PMID = 20309720.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokine CXCL12; 0 / Heterocyclic Compounds; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, CXCR4; 01YAE03M7J / beta Carotene; 155148-31-5 / JM 3100; 9002-72-6 / Growth Hormone
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34. Moran AE, Carothers AM, Weyant MJ, Redston M, Bertagnolli MM: Carnosol inhibits beta-catenin tyrosine phosphorylation and prevents adenoma formation in the C57BL/6J/Min/+ (Min/+) mouse. Cancer Res; 2005 Feb 1;65(3):1097-104
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  • [Title] Carnosol inhibits beta-catenin tyrosine phosphorylation and prevents adenoma formation in the C57BL/6J/Min/+ (Min/+) mouse.
  • Previous studies showed that tumor formation in the Min/+ mouse was associated with alterations in the adherens junctions, including an increased expression of tyrosine-phosphorylated beta-catenin, dissociation of beta-catenin from E-cadherin, and strongly reduced amounts of E-cadherin located at lateral plasma membranes of histologically normal enterocytes.
  • Here, we confirm these findings and show that treatment of Min/+ intestinal tissue with carnosol restored both E-cadherin and beta-catenin to these enterocyte membranes, yielding a phenotype similar to that of the Apc(+/+) wild-type (WT) littermate.
  • Moreover, treatment of WT intestine with the phosphatase inhibitor, pervanadate, removed E-cadherin and beta-catenin from the lateral membranes of enterocytes, mimicking the appearance of the Min/+ tissue.
  • Pretreatment of WT tissue with carnosol inhibited the pervanadate-inducible expression of tyrosine-phosphorylated beta-catenin.
  • Thus, the Apc(Min) allele produces adhesion defects that involve up-regulated expression of tyrosine-phosphorylated proteins, including beta-catenin.
  • Moreover, these data suggest that carnosol prevents Apc-associated intestinal tumorigenesis, potentially via its ability to enhance E-cadherin-mediated adhesion and suppress beta-catenin tyrosine phosphorylation.
  • [MeSH-major] Adenoma / prevention & control. Colonic Neoplasms / prevention & control. Cytoskeletal Proteins / metabolism. Diterpenes, Abietane / pharmacology. Phenanthrenes / pharmacology. Trans-Activators / metabolism
  • [MeSH-minor] Animals. Cadherins / metabolism. Cell Adhesion / drug effects. Cell Membrane / drug effects. Cell Membrane / metabolism. Enterocytes / drug effects. Enterocytes / metabolism. Female. Intestine, Small / cytology. Intestine, Small / drug effects. Intestine, Small / metabolism. Mice. Mice, Inbred C57BL. Phosphorylation / drug effects. Rosmarinus / chemistry. Tyrosine / metabolism. Vanadates / antagonists & inhibitors. Vanadates / pharmacology. beta Catenin

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  • (PMID = 15705912.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R29 CA 74162; United States / NCI NIH HHS / CA / T32 CA 68971
  • [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 / Cadherins; 0 / Cytoskeletal Proteins; 0 / Diterpenes, Abietane; 0 / Phenanthrenes; 0 / Trans-Activators; 0 / beta Catenin; 0 / pervanadate; 3WHH0066W5 / Vanadates; 42HK56048U / Tyrosine; 5957-80-2 / carnosol
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35. Igreja S, Chahal HS, King P, Bolger GB, Srirangalingam U, Guasti L, Chapple JP, Trivellin G, Gueorguiev M, Guegan K, Stals K, Khoo B, Kumar AV, Ellard S, Grossman AB, Korbonits M, International FIPA Consortium: Characterization of aryl hydrocarbon receptor interacting protein (AIP) mutations in familial isolated pituitary adenoma families. Hum Mutat; 2010 Aug;31(8):950-60
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  • [Title] Characterization of aryl hydrocarbon receptor interacting protein (AIP) mutations in familial isolated pituitary adenoma families.
  • Familial isolated pituitary adenoma (FIPA) is an autosomal dominant condition with variable genetic background and incomplete penetrance.
  • We describe a large cohort of FIPA families and characterize missense and silent mutations using minigene constructs, luciferase and beta-galactosidase assays, as well as in silico predictions.

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  • (PMID = 20506337.001).
  • [ISSN] 1098-1004
  • [Journal-full-title] Human mutation
  • [ISO-abbreviation] Hum. Mutat.
  • [Language] ENG
  • [Grant] United Kingdom / Medical Research Council / / G0701307; United Kingdom / Medical Research Council / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Mutant Proteins; 0 / RNA Splice Sites; 0 / RNA, Messenger; 0 / aryl hydrocarbon receptor-interacting protein; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Other-IDs] NLM/ PMC3065644
  • [Investigator] Akker S; Atkinson B; Aylwin S; Baldeweg S; Bevan J; Cheetham T; Chew S; Choudry K; Clayton R; Damjanovic S; Darzy K; Dattani M; Davis J; Drake W; Dzeranova L; Eden B; Eguchi K; Fica S; Flanagan D; Frohman L; Gadelha M; Gallego P; Gla E; Goldman J; Goldstone T; Howlett T; Inder W; Iwata T; Kaplan F; Karavitaki N; Laws E; Lechan R; Levy M; Matsuno A; Miljic D; Modenesi S; Molitch M; Musat M; Orme S; Patocs A; Popovic V; Powell M; Quinton R; Randeva H; Ribeiro de Oliveira J R A; Schofl C; Soares B; Spada A; Strasburger C; Swords F; Tsagarakis S; Vaks V; Wass JA; Widell H; Yarman S; Yoshimoto K
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36. Phelps RA, Chidester S, Dehghanizadeh S, Phelps J, Sandoval IT, Rai K, Broadbent T, Sarkar S, Burt RW, Jones DA: A two-step model for colon adenoma initiation and progression caused by APC loss. Cell; 2009 May 15;137(4):623-34
ZFIN. ZFIN .

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  • [Title] A two-step model for colon adenoma initiation and progression caused by APC loss.
  • Aberrant Wnt/beta-catenin signaling following loss of the tumor suppressor adenomatous polyposis coli (APC) is thought to initiate colon adenoma formation.
  • Using zebrafish and human cells, we show that homozygous loss of APC causes failed intestinal cell differentiation but that this occurs in the absence of nuclear beta-catenin and increased intestinal cell proliferation.
  • Therefore, loss of APC is insufficient for causing beta-catenin nuclear localization.
  • APC mutation-induced intestinal differentiation defects instead depend on the transcriptional corepressor C-terminal binding protein-1 (CtBP1), whereas proliferation defects and nuclear accumulation of beta-catenin require the additional activation of KRAS.
  • These findings suggest that, following APC loss, CtBP1 contributes to adenoma initiation as a first step, whereas KRAS activation and beta-catenin nuclear localization promote adenoma progression to carcinomas as a second step.
  • Consistent with this model, human FAP adenomas showed robust upregulation of CtBP1 in the absence of detectable nuclear beta-catenin, whereas nuclear beta-catenin was detected in carcinomas.

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  • (PMID = 19450512.001).
  • [ISSN] 1097-4172
  • [Journal-full-title] Cell
  • [ISO-abbreviation] Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA073992; United States / NCI NIH HHS / CA / CA116468-03; United States / NCI NIH HHS / CA / CA073992-06A10003; United States / NCI NIH HHS / CA / R01 CA116468-03; United States / NCI NIH HHS / CA / CA96934; United States / NCI NIH HHS / CA / P01 CA073992-06A10003; United States / NCI NIH HHS / CA / R01 CA116468; United States / NCI NIH HHS / CA / P01 CA073992; United States / NCI NIH HHS / CA / CA116468-04; United States / NCI NIH HHS / CA / CA042014; United States / NCI NIH HHS / CA / P30 CA042014; United States / NCI NIH HHS / CA / R01 CA116468-04
  • [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 / Adenomatous Polyposis Coli Protein; 0 / DNA-Binding Proteins; 0 / Peptide Fragments; 0 / Rac1 GTP-binding protein (17-32); 0 / beta Catenin; EC 1.1.- / Alcohol Oxidoreductases; EC 1.1.1.- / C-terminal binding protein; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf; EC 3.6.5.2 / rac1 GTP-Binding Protein; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS102940; NLM/ PMC2706149
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37. Oh K, Redston M, Odze RD: Support for hMLH1 and MGMT silencing as a mechanism of tumorigenesis in the hyperplastic-adenoma-carcinoma (serrated) carcinogenic pathway in the colon. Hum Pathol; 2005 Jan;36(1):101-11
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  • [Title] Support for hMLH1 and MGMT silencing as a mechanism of tumorigenesis in the hyperplastic-adenoma-carcinoma (serrated) carcinogenic pathway in the colon.
  • This mechanism has also recently been implicated in the newly postulated hyperplastic polyp-serrated adenoma-carcinoma ("serrated") pathway of carcinogenesis, although this has never been investigated thoroughly.
  • The aim of this study was to evaluate hMLH1, hMSH2, MGMT, as well as MIB-1, p53, and beta-catenin immunoexpression in an uncommon cohort of mixed colonic polyps that contain a combination of hyperplastic and adenomatous features (n = 21), and in some (n = 7), carcinoma as well.
  • DESIGN: The clinical, pathological, and immunophenotypic (hMLH1, hMSH2, MGMT, MIB-1, p53, and beta-catenin) properties of 28 mixed hyperplastic and adenomatous polyps of the colon (7 of which also contained carcinoma within the same lesion) were evaluated for the above immunopeptides in each of the different morphologic areas of the polyps, and the results were compared to traditional hyperplastic polyps, serrated adenomas, and conventional (nonserrated) adenomas.
  • However, hMSH2 loss was only present in the adenoma component and never in the hyperplastic or carcinomatous areas of these polyps.
  • However, conventional adenomas showed significantly higher rates of nuclear beta -catenin staining (100%) in comparison to the adenomatous component of mixed polyps (60%).
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Colonic Neoplasms / genetics. Colonic Polyps / genetics. Gene Silencing. Neoplasm Proteins / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adult. Aged. Aged, 80 and over. Carcinoma / genetics. Carcinoma / metabolism. Carcinoma / pathology. Carrier Proteins. Cytoskeletal Proteins / metabolism. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Female. Humans. Hyperplasia / genetics. Hyperplasia / metabolism. Hyperplasia / pathology. Immunohistochemistry. Ki-67 Antigen / metabolism. Male. Middle Aged. MutS Homolog 2 Protein. Nuclear Proteins. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Trans-Activators / metabolism. Tumor Suppressor Protein p53 / metabolism. beta Catenin

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  • (PMID = 15712188.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / CTNNB1 protein, human; 0 / Carrier Proteins; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / MLH1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / Tumor Suppressor Protein p53; 0 / beta Catenin; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein
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38. Lourenço SV, Lima DM: Pleomorphic adenoma and adenoid cystic carcinoma: in vitro study of the impact of TGFbeta1 on the expression of integrins and cytoskeleton markers of cell differentiation. Int J Exp Pathol; 2007 Jun;88(3):191-8
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  • [Title] Pleomorphic adenoma and adenoid cystic carcinoma: in vitro study of the impact of TGFbeta1 on the expression of integrins and cytoskeleton markers of cell differentiation.
  • Pleomorphic adenoma (PA) and adenoid cystic carcinoma (ACC) are the commonest benign and malignant salivary gland tumours respectively.
  • Our study investigated the effects of TGFbeta1 on the expression of integrin beta subunits in vitro and on the expression of cytoskeletal proteins of cells derived from PA and ACC.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. Carcinoma, Adenoid Cystic / metabolism. Integrins / metabolism. Parotid Neoplasms / metabolism. Transforming Growth Factor beta1 / pharmacology
  • [MeSH-minor] Adult. Antigens, CD29 / analysis. Antigens, CD29 / metabolism. Antigens, Differentiation / analysis. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Cytoskeleton / metabolism. Enzyme-Linked Immunosorbent Assay / methods. Female. Fluorescent Antibody Technique. Humans. Integrin beta3 / analysis. Integrin beta3 / metabolism. Integrin beta4 / analysis. Integrin beta4 / metabolism. Middle Aged. Stimulation, Chemical. Tumor Cells, Cultured

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  • (PMID = 17504449.001).
  • [ISSN] 0959-9673
  • [Journal-full-title] International journal of experimental pathology
  • [ISO-abbreviation] Int J Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD29; 0 / Antigens, Differentiation; 0 / Integrin beta3; 0 / Integrin beta4; 0 / Integrins; 0 / Transforming Growth Factor beta1
  • [Other-IDs] NLM/ PMC2517303
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39. May R, Riehl TE, Hunt C, Sureban SM, Anant S, Houchen CW: Identification of a novel putative gastrointestinal stem cell and adenoma stem cell marker, doublecortin and CaM kinase-like-1, following radiation injury and in adenomatous polyposis coli/multiple intestinal neoplasia mice. Stem Cells; 2008 Mar;26(3):630-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of a novel putative gastrointestinal stem cell and adenoma stem cell marker, doublecortin and CaM kinase-like-1, following radiation injury and in adenomatous polyposis coli/multiple intestinal neoplasia mice.
  • Here, we used the putative stem cell marker doublecortin and CaM kinase-like-1 (DCAMKL-1) to examine radiation-induced stem cell apoptosis and adenomatous polyposis coli (APC)/multiple intestinal neoplasia (min) mice to determine the effects of APC mutation on DCAMKL-1 expression.
  • Immunoreactive DCAMKL-1 staining was demonstrated in the intestinal stem cell zone.
  • We also observed stem cell apoptosis and mitotic DCAMKL-1-expressing cells 24 hours after irradiation.
  • Moreover, in APC/min mice, DCAMKL-1-expressing cells were negative for proliferating cell nuclear antigen and nuclear beta-catenin in normal-appearing intestine.
  • However, beta-catenin was nuclear in DCAMKL-1-positive cells in adenomas.
  • Thus, nuclear translocation of beta-catenin distinguishes normal and adenoma stem cells.
  • [MeSH-minor] Animals. Intestines / cytology. Intestines / metabolism. Intestines / pathology. Intestines / radiation effects. Mice. Nerve Tissue Proteins / metabolism. Protein Transport / radiation effects. RNA-Binding Proteins / metabolism. Radiation, Ionizing. Regeneration / radiation effects. beta Catenin / metabolism

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  • (PMID = 18055444.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-002822; United States / NIDDK NIH HHS / DK / DK-066161; United States / NIDDK NIH HHS / DK / P30 DK-52574
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Msi1h protein, mouse; 0 / Nerve Tissue Proteins; 0 / RNA-Binding Proteins; 0 / beta Catenin; EC 2.7.1.- / Dcamkl1 protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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40. Haynie LS, Benghuzzi H, Tucci M, England B: Pathophysiological changes associated with the exposure of sustained delivery of glucocorticoids on pituitary adenoma cell line. Biomed Sci Instrum; 2006;42:78-83
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  • [Title] Pathophysiological changes associated with the exposure of sustained delivery of glucocorticoids on pituitary adenoma cell line.
  • Glucocorticoid receptor rich tissues such as pituitary cells express tissue specific 11 beta hydroxysteroid type 1 enzyme, which causes cortisol to act as an autocrine, anti-proliferative, pro-differentiation stimulus in normal tissue.
  • In pituitary tumor cells there is a strong correlation indicating a shift from 11 beta hydroxysteroid type 1 enzyme activity to 11 beta hydroxysteroid type 2 enzyme activity.
  • Overall, the results indicated a decreased in cell number for both acute and chronic administration over a 96 hour period without inducing cellular damage (MDA), reactive nitric intermediates (nitric oxide) or reducing cellular antioxidant status (glutathione).
  • Cortisol administration cause an increase in the number of hyperchromic nuclei suggesting cell cycle regulation.
  • [MeSH-major] Adenoma / pathology. Adenoma / physiopathology. Delayed-Action Preparations / administration & dosage. Glucocorticoids / administration & dosage. Pituitary Neoplasms / pathology. Pituitary Neoplasms / physiopathology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Rats

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  • (PMID = 16817589.001).
  • [ISSN] 0067-8856
  • [Journal-full-title] Biomedical sciences instrumentation
  • [ISO-abbreviation] Biomed Sci Instrum
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Delayed-Action Preparations; 0 / Glucocorticoids
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41. Marsh V, Winton DJ, Williams GT, Dubois N, Trumpp A, Sansom OJ, Clarke AR: Epithelial Pten is dispensable for intestinal homeostasis but suppresses adenoma development and progression after Apc mutation. Nat Genet; 2008 Dec;40(12):1436-44
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  • [Title] Epithelial Pten is dispensable for intestinal homeostasis but suppresses adenoma development and progression after Apc mutation.
  • We show that Pten loss specifically within the adult or embryonic epithelial cell population does not affect the normal architecture or homeostasis of the epithelium.

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  • (PMID = 19011632.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / 9590; United Kingdom / Medical Research Council / / G0301154; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 094ZI81Y45 / Tamoxifen; 6051-87-2 / beta-Naphthoflavone; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
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42. 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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43. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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44. Meier JJ, Menge BA, Breuer TG, Müller CA, Tannapfel A, Uhl W, Schmidt WE, Schrader H: Functional assessment of pancreatic beta-cell area in humans. Diabetes; 2009 Jul;58(7):1595-603
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional assessment of pancreatic beta-cell area in humans.
  • OBJECTIVE: beta-Cell mass declines progressively during the course of diabetes, and various antidiabetic treatment regimens have been suggested to modulate beta-cell mass.
  • However, imaging methods allowing the monitoring of changes in beta-cell mass in vivo have not yet become available.
  • We address whether pancreatic beta-cell area can be assessed by functional test of insulin secretion in humans.
  • Indexes of insulin secretion were calculated and compared with the fractional beta-cell area of the pancreas.
  • RESULTS: beta-Cell area was related to fasting glucose concentrations in an inverse linear fashion (r = -0.53, P = 0.0014) and to 120-min postchallenge glycemia in an inverse exponential fashion (r = -0.89).
  • beta-Cell area was best predicted by a C-peptide-to-glucose ratio determined 15 min after the glucose drink (r = 0.72, P < 0.0001).
  • Homeostasis model assessment (HOMA) beta-cell function was unrelated to beta-cell area.
  • CONCLUSIONS: Glucose control is closely related to pancreatic beta-cell area in humans.
  • A C-peptide-to-glucose ratio after oral glucose ingestion appears to better predict beta-cell area than fasting measures, such as the HOMA index.
  • [MeSH-major] Adenoma / pathology. Insulin-Secreting Cells / physiology. Pancreatic Neoplasms / pathology. Pancreatitis, Chronic / pathology

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
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  • (PMID = 19509022.001).
  • [ISSN] 1939-327X
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / C-Peptide; 0 / Insulin
  • [Other-IDs] NLM/ PMC2699865
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45. Tadjine M, Lampron A, Ouadi L, Bourdeau I: Frequent mutations of beta-catenin gene in sporadic secreting adrenocortical adenomas. Clin Endocrinol (Oxf); 2008 Feb;68(2):264-70

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent mutations of beta-catenin gene in sporadic secreting adrenocortical adenomas.
  • In our previous work, we demonstrated the differential expression of several Wnt/beta-catenin signalling-related genes implicated in ACTH-independent macronodular adrenal hyperplasias (AIMAH).
  • To better understand the role of Wnt/beta-catenin signalling in adrenocortical tumours, we performed mutational analysis of the beta-catenin gene.
  • METHODS: We studied 53 human adrenocortical samples (33 adenomas, 4 carcinomas, 13 AIMAH, 3 ACTH-dependent adrenal hyperplasias) and the human adrenocortical cancer cell line NCI-H295R.
  • All samples were screened for somatic mutations in exons 3 and 5 of the beta-catenin gene.
  • Eleven and six samples were analysed for beta-catenin protein expression by Western blotting and immunohistochemistry, respectively.
  • Genetic alterations were found in 5 (15%) out of 33 adenomas: three cortisol-secreting adenomas, one aldosterone-secreting adenoma and one nonfunctional adenoma.
  • Western blot analysis of samples with 55- and 271-bp deletions showed an additional shorter and more intense band representing an accumulation of the mutated form of beta-catenin protein.
  • In addition, cytoplasmic and/or nuclear accumulation of beta-catenin was observed in mutated adenomas by immunohistochemistry.
  • CONCLUSIONS: Activating mutations of exon 3 of the beta-catenin gene are frequent in adrenocortical adenomas, and further characterization of the Wnt/beta-catenin signalling pathway should lead to a better understanding of adrenal tumourigenesis.
  • [MeSH-major] Adrenocortical Adenoma / genetics. Adrenocortical Adenoma / metabolism. beta Catenin / genetics. beta Catenin / metabolism

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  • (PMID = 17854394.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / beta Catenin
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46. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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47. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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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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48. Miguita L, Martinez EF, de Araújo NS, de Araújo VC: FGF-2, TGFbeta-1, PDGF-A and respective receptors expression in pleomorphic adenoma myoepithelial cells: an in vivo and in vitro study. J Appl Oral Sci; 2010 Jan-Feb;18(1):83-91
MedlinePlus Health Information. consumer health - Salivary Gland Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FGF-2, TGFbeta-1, PDGF-A and respective receptors expression in pleomorphic adenoma myoepithelial cells: an in vivo and in vitro study.
  • OBJECTIVES: This study evaluated the expression of fibroblast growth factor-2 (FGF-2), transforming growth factor beta-1 (TGFbeta-1), platelet-derived growth factor-A (PDGF-A) and their respective receptors (FGFR-1, FGFR-2, TGFbetaR-II and PDGFR-alpha) in myoepithelial cells from pleomorphic adenomas (PA) by in vivo and in vitro experiments.
  • Immunohistochemistry, cell culture and immunofluorescence assays were used to evaluate growth factor expression.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Fibroblast Growth Factor 2 / analysis. Platelet-Derived Growth Factor / analysis. Protein-Serine-Threonine Kinases / analysis. Receptor, Fibroblast Growth Factor, Type 1 / analysis. Receptor, Fibroblast Growth Factor, Type 2 / analysis. Receptor, Platelet-Derived Growth Factor alpha / analysis. Receptors, Transforming Growth Factor beta / analysis. Salivary Gland Neoplasms / pathology. Transforming Growth Factor beta1 / analysis
  • [MeSH-minor] Actins / analysis. Adult. Calcium-Binding Proteins / analysis. Cell Nucleus / ultrastructure. Cells, Cultured. Cytoplasm / ultrastructure. Epithelial Cells / pathology. Female. Fluorescent Antibody Technique. Humans. Immunohistochemistry. Keratin-7 / analysis. Lip Neoplasms / pathology. Male. Microfilament Proteins / analysis. Muscle Cells / pathology. Muscle Proteins / analysis. Muscle, Smooth / pathology. Palatal Neoplasms / pathology. Vimentin / analysis. Young Adult

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  • (PMID = 20379686.001).
  • [ISSN] 1678-7765
  • [Journal-full-title] Journal of applied oral science : revista FOB
  • [ISO-abbreviation] J Appl Oral Sci
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Actins; 0 / Calcium-Binding Proteins; 0 / Keratin-7; 0 / Microfilament Proteins; 0 / Muscle Proteins; 0 / Platelet-Derived Growth Factor; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Vimentin; 0 / calponin; 0 / platelet-derived growth factor A; 103107-01-3 / Fibroblast Growth Factor 2; EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / FGFR2 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 2; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
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49. Manoranjan B, Salehi F, Scheithauer BW, Rotondo F, Kovacs K, Cusimano MD: Estrogen receptors alpha and beta immunohistochemical expression: clinicopathological correlations in pituitary adenomas. Anticancer Res; 2010 Jul;30(7):2897-904
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  • [Title] Estrogen receptors alpha and beta immunohistochemical expression: clinicopathological correlations in pituitary adenomas.
  • AIM: We investigated the immunohistochemical expression of estrogen receptors alpha (ERalpha) and beta (ERbeta) in pituitary adenoma subtypes combined with clinicopathological factors.
  • RESULTS: Nuclear immunoreactivity for both receptors was highest among PRL, FSH/LH, null cell, and GH adenomas.
  • ACTH adenomas expressed significantly less ERalpha than FSH-LH, GH, and null cell adenomas.
  • CONCLUSION: ERalpha and ERbeta are differentially expressed in the various pituitary adenoma subtypes suggesting a cell-specific function for these receptors.
  • [MeSH-major] Adenoma / metabolism. Adenoma / pathology. Estrogen Receptor alpha / biosynthesis. Estrogen Receptor beta / biosynthesis. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology
  • [MeSH-minor] Cell Nucleus / metabolism. Cytoplasm / metabolism. Female. Humans. Immunohistochemistry. Male. Neoplasm Invasiveness

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  • (PMID = 20683030.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta
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50. Herzig M, Savarese F, Novatchkova M, Semb H, Christofori G: Tumor progression induced by the loss of E-cadherin independent of beta-catenin/Tcf-mediated Wnt signaling. Oncogene; 2007 Apr 5;26(16):2290-8
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  • [Title] Tumor progression induced by the loss of E-cadherin independent of beta-catenin/Tcf-mediated Wnt signaling.
  • E-cadherin-mediated cell-cell adhesion is frequently lost during the development of malignant epithelial cancers.
  • Employing a transgenic mouse model of beta-cell carcinogenesis (Rip1Tag2) we have previously shown that the loss of E-cadherin is a rate-limiting step in the progression from adenoma to carcinoma.
  • However, the mere loss of cell adhesion may not be sufficient and additional signals are required to cause tumor cells to permeate the basal membrane and to invade surrounding tissue.
  • Besides being an important component of the E-cadherin cell-adhesion complex, beta-catenin plays a critical role in canonical Wnt signaling.
  • We report here that beta-catenin-mediated Wnt signaling does not contribute to tumor progression in Rip1Tag2 mice.
  • E-cadherin downregulates beta-catenin/Tcf-mediated transcriptional activity by sequestrating beta-catenin into E-cadherin cell-adhesion complexes even in the presence of activated Wnt signaling.
  • Upon loss of E-cadherin expression, beta-catenin is degraded and Tcf/beta-catenin-mediated transcriptional activity is not induced.
  • Moreover, forced expression of constitutive-active beta-catenin or genetic ablation of Tcf/beta-catenin transcriptional activity in tumor cells of Rip1Tag2 transgenic mice does not affect tumor progression.
  • Together, the data indicate that signals other than beta-catenin/Tcf-mediated Wnt signaling are induced by the loss of E-cadherin during tumor progression in Rip1Tag2 transgenic mice.
  • [MeSH-major] Adenoma / pathology. Cadherins / genetics. Lymphoma / pathology. TCF Transcription Factors / physiology. Wnt Proteins / physiology. beta Catenin / physiology

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  • (PMID = 17043652.001).
  • [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 / Cadherins; 0 / DNA Primers; 0 / TCF Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin
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51. Wu JM, Montgomery EA, Iacobuzio-Donahue CA: Frequent beta-catenin nuclear labeling in sessile serrated polyps of the colorectum with neoplastic potential. Am J Clin Pathol; 2008 Mar;129(3):416-23
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  • [Title] Frequent beta-catenin nuclear labeling in sessile serrated polyps of the colorectum with neoplastic potential.
  • We obtained 22 sessile serrated adenomas (SSAs) and 19 hyperplastic polyps (HPs) and performed immunolabeling for cytokeratins (CKs) 7 and 20, CDX2, beta-catenin, and p53 to determine the role of these markers in aiding distinction of lesions with neoplastic potential.
  • Patients with SSAs more frequently had a prior or coexistent tubular adenoma (P = .004) that was right-sided (P = .00001) and larger (P = .03).
  • Surprisingly, aberrant nuclear labeling for beta-catenin was found in 9 (41%) of the SSAs but in none of the HPs (P < .002).
  • We propose that beta-catenin and/or CDX2 immunolabeling may have diagnostic usefulness in the evaluation of serrated polyps.
  • [MeSH-major] Adenoma / metabolism. Biomarkers, Tumor / analysis. Colonic Polyps / metabolism. Colorectal Neoplasms / metabolism. Precancerous Conditions / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Cell Nucleus / metabolism. Female. Homeodomain Proteins / metabolism. Humans. Immunohistochemistry. Keratin-20 / metabolism. Keratin-7 / metabolism. Male. Middle Aged. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 18285264.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA106610
  • [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 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Keratin-20; 0 / Keratin-7; 0 / Tumor Suppressor Protein p53; 0 / beta Catenin
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52. 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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53. Enders GA: Cyclooxygenase-2 overexpression abrogates the antiproliferative effects of TGF-beta. Br J Cancer; 2007 Nov 19;97(10):1388-92
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  • [Title] Cyclooxygenase-2 overexpression abrogates the antiproliferative effects of TGF-beta.
  • An escape of proliferating cells from the regulatory influence of TGF-beta for example in the intestine has been discussed as well as a preponderance or prolongation of growth factor stimulation.
  • The experiments presented here demonstrated that COX-2 transfection of a TGF-beta-sensitive cell line abrogates the growth inhibitory effects of TGF-beta.
  • However, analysis of the TGF-beta/Smad-signalling pathway clearly revealed that COX-2 overexpression did not interfere with that.
  • In addition, a TGF-beta reporter assay revealed no difference between controls and COX-2-transfected cells.
  • Therefore, inhibiting both COX-2 as well as the PPAR and TGF/EGF pathway could be effective in the inhibition of adenoma or even carcinoma development in the intestine.
  • [MeSH-major] Cyclooxygenase 2 / biosynthesis. Cyclooxygenase 2 / genetics. Gene Expression Regulation, Enzymologic / genetics. Transforming Growth Factor beta / pharmacology
  • [MeSH-minor] Animals. Blotting, Western. Cell Proliferation / drug effects. Cells, Cultured. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay / methods. Epidermal Growth Factor / pharmacology. Humans. Mink. Mitogen-Activated Protein Kinase 1 / drug effects. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / drug effects. Mitogen-Activated Protein Kinase 3 / metabolism. Phorbol Esters / pharmacology. Phosphorylation. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 17955050.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Phorbol Esters; 0 / Transforming Growth Factor beta; 62229-50-9 / Epidermal Growth Factor; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ PMC2360247
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54. 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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55. 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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56. 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

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  • (PMID = 18330089.001).
  • [ISSN] 1784-3227
  • [Journal-full-title] Acta gastro-enterologica Belgica
  • [ISO-abbreviation] Acta Gastroenterol. Belg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Cadherins; 0 / beta Catenin
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57. Lebrun JJ: Activin, TGF-beta and menin in pituitary tumorigenesis. Adv Exp Med Biol; 2009;668:69-78
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  • [Title] Activin, TGF-beta and menin in pituitary tumorigenesis.
  • Recent studies indicated that the activin/TGF-beta family of growth factors plays a prominent role in regulating pituitary tumor growth and prolactin secretion from anterior pituitary lactotrope cells.
  • Alterations in the activin/TGF-beta downstream signaling pathways are critical steps towards tumor formation and progression.
  • This chapter will review the role and intracellular molecular mechanisms of action by which activin, TGF-beta, Smads and menin act in concert to prevent pituitary tumor cell growth and control hormonal synthesis by the anterior pituitary.
  • [MeSH-major] Activins / metabolism. Adenoma / metabolism. Pituitary Neoplasms / metabolism. Proto-Oncogene Proteins / metabolism. Transforming Growth Factor beta / metabolism

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  • (PMID = 20175454.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP-53141
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Smad Proteins; 0 / Transforming Growth Factor beta; 104625-48-1 / Activins; 9002-62-4 / Prolactin
  • [Number-of-references] 85
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58. Goralczyk R, Wertz K, Lenz B, Riss G, Buchwald Hunziker P, Geatrix B, Aebischer CP, Bachmann H: Beta-carotene interaction with NNK in the AJ-mouse model: effects on cell proliferation, tumor formation and retinoic acid responsive genes. Biochim Biophys Acta; 2005 May 30;1740(2):179-88
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  • [Title] Beta-carotene interaction with NNK in the AJ-mouse model: effects on cell proliferation, tumor formation and retinoic acid responsive genes.
  • We studied the influence of beta-carotene on the tobacco smoke carcinogen 4-(N-Methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumor development in the A/J-mouse model.
  • The normally low beta-carotene absorption was facilitated with a diet enriched in fat and bile salt, resulting in plasma and lung tissue levels similar to humans. beta-Carotene enhanced NNK-induced early bronchial cell proliferation, however, this effect was not predictive for later tumor development.
  • Tumor multiplicity was not significantly affected by beta-carotene, neither in carcinogen-initiated nor in uninitiated mice, and regardless of dose and time point of supplementation during tumor development.
  • RARbeta isoform and CYP26 gene expression levels analyzed by quantitative RT-PCR were weakly, but significantly, inversely correlated and showed evidence for altered retinoid signaling and catabolism in the lungs of NNK-initiated, beta-carotene supplemented mice.
  • [MeSH-major] Adenoma / pathology. Carcinogens. Lung / drug effects. Lung Neoplasms / pathology. Nitrosamines. beta Carotene / pharmacology

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  • (PMID = 15949685.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrosamines; 0 / Protein Isoforms; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor beta; 01YAE03M7J / beta Carotene; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.14.1 / retinoic acid 4-hydroxylase
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59. Miyakoshi T, Takei M, Kajiya H, Egashira N, Takekoshi S, Teramoto A, Osamura RY: Expression of Wnt4 in human pituitary adenomas regulates activation of the beta-catenin-independent pathway. Endocr Pathol; 2008;19(4):261-73
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  • [Title] Expression of Wnt4 in human pituitary adenomas regulates activation of the beta-catenin-independent pathway.
  • A member of the Wnt family of genes, Wnt4, has been known to regulate proliferation of anterior pituitary cell types in the mouse during embryonic development.
  • The canonical Wnt/beta-catenin signaling pathway was analyzed by beta-catenin immunohistochemistry. beta-Catenin was localized at the cell membrane in all pituitary adenomas, but not in the nuclei.
  • These results suggested that activation of Wnt4/Fzd6 signaling through a "beta-catenin-independent" pathway played a role in proliferation and survival of the pituitary adenoma cells.
  • [MeSH-major] Adenoma / metabolism. Biomarkers, Tumor / metabolism. Pituitary Neoplasms / metabolism. Wnt Proteins / metabolism. beta Catenin / metabolism

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  • (PMID = 19034702.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / FZD6 protein, human; 0 / Frizzled Receptors; 0 / Receptors, G-Protein-Coupled; 0 / WNT4 protein, human; 0 / Wnt Proteins; 0 / Wnt4 Protein; 0 / Wnt4 protein, mouse; 0 / beta Catenin
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60. 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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  • [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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61. Glading AJ, Ginsberg MH: Rap1 and its effector KRIT1/CCM1 regulate beta-catenin signaling. Dis Model Mech; 2010 Jan-Feb;3(1-2):73-83
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  • [Title] Rap1 and its effector KRIT1/CCM1 regulate beta-catenin signaling.
  • KRIT1 mediates the stabilization of beta-catenin-containing endothelial cell-cell junctions downstream of the Rap1 GTPase.
  • Here, we report that Rap1 and KRIT1 are negative regulators of canonical beta-catenin signaling in mice and that hemizygous Krit1 deficiency exacerbates beta-catenin-driven pathologies.
  • Depletion of endothelial KRIT1 caused beta-catenin to dissociate from vascular endothelial (VE)-cadherin and to accumulate in the nucleus with consequent increases in beta-catenin-dependent transcription.
  • Activation of Rap1 inhibited beta-catenin-dependent transcription in confluent endothelial cells; this effect required the presence of intact cell-cell junctions and KRIT1.
  • These effects of KRIT1 were not limited to endothelial cells; the KRIT1 protein was expressed widely and its depletion increased beta-catenin signaling in epithelial cells.
  • Moreover, a reduction in KRIT1 expression also increased beta-catenin signaling in vivo.
  • Hemizygous deficiency of Krit1 resulted in a ~1.5-fold increase in intestinal polyps in the Apc(Min/+) mouse, which was associated with increased beta-catenin-driven transcription.
  • Thus, KRIT1 regulates beta-catenin signaling, and Krit1(+/-) mice are more susceptible to beta-catenin-driven intestinal adenomas.

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  • (PMID = 20007487.001).
  • [ISSN] 1754-8411
  • [Journal-full-title] Disease models & mechanisms
  • [ISO-abbreviation] Dis Model Mech
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL31950; United States / NIAMS NIH HHS / AR / R01 AR027214; United States / NIAMS NIH HHS / AR / AR27214; United States / NHLBI NIH HHS / HL / P01 HL031950; United States / NIAMS NIH HHS / AR / R37 AR027214; United States / NHLBI NIH HHS / HL / P01 HL078784; United States / NHLBI NIH HHS / HL / HL078784
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cadherins; 0 / Krit1 protein, mouse; 0 / Microtubule-Associated Proteins; 0 / Proto-Oncogene Proteins; 0 / beta Catenin; EC 3.6.5.2 / rap1 GTP-Binding Proteins
  • [Other-IDs] NLM/ PMC2806902
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62. Andreu P, Peignon G, Slomianny C, Taketo MM, Colnot S, Robine S, Lamarque D, Laurent-Puig P, Perret C, Romagnolo B: A genetic study of the role of the Wnt/beta-catenin signalling in Paneth cell differentiation. Dev Biol; 2008 Dec 15;324(2):288-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A genetic study of the role of the Wnt/beta-catenin signalling in Paneth cell differentiation.
  • Wnt/beta-catenin signalling plays a key role in the homeostasis of the intestinal epithelium.
  • Whereas its role in the maintenance of the stem cell compartment has been clearly demonstrated, its role in the Paneth cell fate remains unclear.
  • We performed genetic studies to elucidate the functions of the Wnt/beta-catenin pathway in Paneth cell differentiation.
  • We analysed mice with inducible gain-of-function mutations in the Wnt/beta-catenin pathway and mice with a hypomorphic beta-catenin allele that have not been previously described.
  • We demonstrated that acute activation of Wnt/beta-catenin signalling induces de novo specification of Paneth cells in both the small intestine and colon and that colon cancers resulting from Apc mutations expressed many genes involved in Paneth cell differentiation.
  • This suggests a key role for the Wnt/beta-catenin pathway in Paneth cell differentiation.
  • We also showed that a slight decrease in beta-catenin gene dosage induced a major defect in Paneth cell differentiation, but only a modest effect on crypt morphogenesis.
  • Overall, our findings show that a high level of beta-catenin activation is required to determine Paneth cell fate and that fine tuning of beta-catenin signalling is critical for correct Paneth cell lineage.
  • [MeSH-major] Cell Differentiation. Paneth Cells / metabolism. Signal Transduction. Wnt Proteins / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Adenoma / genetics. Animals. Cell Lineage. Cell Proliferation. Colorectal Neoplasms / genetics. Gene Deletion. Gene Dosage. Gene Expression Profiling. Gene Expression Regulation. Genes, APC. Humans. Mice. Mutation

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  • (PMID = 18948094.001).
  • [ISSN] 1095-564X
  • [Journal-full-title] Developmental biology
  • [ISO-abbreviation] Dev. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Wnt Proteins; 0 / beta Catenin
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63. Genelhu MC, Gobbi H, Arantes DC, Cardoso SV, Cassali GD: Immunolocalization of beta-catenin in pleomorphic adenomas and carcinomas ex-pleomorphic adenomas of salivary glands. Appl Immunohistochem Mol Morphol; 2007 Sep;15(3):273-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunolocalization of beta-catenin in pleomorphic adenomas and carcinomas ex-pleomorphic adenomas of salivary glands.
  • Beta-catenin plays a central role in cadherin/catenin cell-cell adhesion complex and is involved in cell signaling pathway.
  • Change in beta-catenin distribution has been associated with several human cancers including salivary gland tumors.
  • We studied the immunolocalization of beta-catenin in a series of pleomorphic adenomas (PA) and carcinomas ex-pleomorphic adenomas (Ca ex-PA).
  • Ten samples of PA and ten of Ca ex-PA were evaluated by immunohistochemistry using streptavidin-biotin-peroxidase technique and a monoclonal antibody against beta-catenin (E-5).
  • Cell membrane/cytoplasmic staining of beta-catenin was observed in normal gland parenchyma, PA, and in well-differentiated Ca ex-PA.
  • Cytoplasmic/nuclear beta-catenin staining was observed in poorly differentiated carcinomas and, interestingly, in one case of PA.
  • Our data showed decreased cell membrane beta-catenin expression in higher-grade tumors suggesting that beta-catenin may play an important role in histologic differentiation and transition to malignant phenotype of Ca ex-PA.

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  • (PMID = 17721271.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / beta Catenin
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64. Feng Y, Bommer GT, Zhai Y, Akyol A, Hinoi T, Winer I, Lin HV, Cadigan KM, Cho KR, Fearon ER: Drosophila split ends homologue SHARP functions as a positive regulator of Wnt/beta-catenin/T-cell factor signaling in neoplastic transformation. Cancer Res; 2007 Jan 15;67(2):482-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Drosophila split ends homologue SHARP functions as a positive regulator of Wnt/beta-catenin/T-cell factor signaling in neoplastic transformation.
  • Among other effects, certain Wnts stabilize the beta-catenin protein, leading to the ability of beta-catenin to activate T-cell factor (TCF)-mediated transcription.
  • Mutations resulting in constitutive beta-catenin stabilization underlie development of several human cancers.
  • We have assessed the role of SHARP, a human homologue of spen, in Wnt/beta-catenin/TCF function in mammalian cells.
  • We found that SHARP gene and protein expression is elevated in human colon and ovarian endometrioid adenocarcinomas and mouse colon adenomas and carcinomas carrying gene defects leading to beta-catenin dysregulation.
  • When ectopically expressed, the silencing mediator for retinoid and thyroid receptors/histone deacetylase 1-associated repressor protein (SHARP) protein potently enhanced beta-catenin/TCF transcription of a model reporter gene and cellular target genes.
  • Inhibition of endogenous SHARP function via RNA inhibitory (RNAi) approaches antagonized beta-catenin/TCF-mediated activation of target genes.
  • The effect of SHARP on beta-catenin/TCF-regulated genes was mediated via a functional interaction between SHARP and TCF. beta-Catenin-dependent neoplastic transformation of RK3E cells was enhanced by ectopic expression of SHARP, and RNAi-mediated inhibition of endogenous SHARP in colon cancer cells inhibited their transformed growth.
  • In toto, our findings implicate SHARP as an important positive regulator of Wnt signaling in cancers with beta-catenin dysregulation.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Colonic Neoplasms / metabolism. Homeodomain Proteins / physiology. Nuclear Proteins / physiology. Wnt Proteins / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Animals. HCT116 Cells. Humans. Mice. Mice, Transgenic. Signal Transduction. Transcriptional Activation

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  • (PMID = 17234755.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA082223; United States / NCI NIH HHS / CA / CA085463; United States / NCI NIH HHS / CA / CA094172
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / SPEN protein, human; 0 / Wnt Proteins; 0 / beta Catenin
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65. 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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66. Chen G, Jiang Q, You Z, Yao J, Mou L, Lin X, Shen X, You T, Lin Q, Wen J, Lin L: Regulation of GSK-3 beta in the proliferation and apoptosis of human thyrocytes investigated using a GSK-3 beta-targeting RNAi adenovirus expression vector: involvement the Wnt/beta-catenin pathway. Mol Biol Rep; 2010 Jul;37(6):2773-9
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  • [Title] Regulation of GSK-3 beta in the proliferation and apoptosis of human thyrocytes investigated using a GSK-3 beta-targeting RNAi adenovirus expression vector: involvement the Wnt/beta-catenin pathway.
  • Disorders in the proliferation and apoptosis of thyrocytes may induce goitre, adenoma and carcinoma in the thyroid.
  • The Wnt/beta-catenin pathway has been demonstrated to be involved in the regulation of cell proliferation, differentiation and apoptosis in various cell lines.
  • Results showed that the expression of beta-catenin protein in primary human thyrocytes was increased after GSK-3beta-targeting RNAi adenovirus infection, the proliferation of primary human thyrocytes was significantly stimulated using Bromodeoxyuridine (BrdU) assay, while cell apoptosis was slightly affected which was observed through flow cytometry.
  • It is concluded that the Wnt/beta-catenin pathway plays a significant role in the regulation of the proliferation of primary human thyrocytes.
  • [MeSH-minor] Adenoviridae Infections / genetics. Cell Proliferation. Down-Regulation. Genetic Vectors / genetics. Humans. Time Factors. Wnt Proteins / metabolism. beta Catenin / metabolism

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  • (PMID = 19757160.001).
  • [ISSN] 1573-4978
  • [Journal-full-title] Molecular biology reports
  • [ISO-abbreviation] Mol. Biol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Wnt Proteins; 0 / beta Catenin; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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67. Kamei Y, Kito K, Takeuchi T, Imai Y, Murase R, Ueda N, Kobayashi N, Abe Y: Human scribble accumulates in colorectal neoplasia in association with an altered distribution of beta-catenin. Hum Pathol; 2007 Aug;38(8):1273-81
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  • [Title] Human scribble accumulates in colorectal neoplasia in association with an altered distribution of beta-catenin.
  • Furthermore, the overexpression and distribution of hScrib was observed to extensively overlap with the cytoplasmic accumulation of beta-catenin.
  • Like beta-catenin, the intense immunoreactivity of hScrib was often observed in small adenomas, thus, suggesting that hScrib could be involved in an early step of colon carcinogenesis.
  • In an immunofluorescence analysis on cultured cell lines, the loss of membranous staining of hScrib was observed according to the cytoplasmic translocation of beta-catenin.
  • We herein demonstrate that the accumulation of hScrib protein might therefore be involved in colon carcinogenesis while also providing a possible link between hScrib and beta-catenin.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Biomarkers, Tumor / metabolism. Colorectal Neoplasms / pathology. Membrane Proteins / metabolism. Tumor Suppressor Proteins / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Blotting, Western. Cell Line, Tumor. Female. Fluorescent Antibody Technique, Indirect. Humans. Immunoenzyme Techniques. Male. Middle Aged

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  • (PMID = 17509663.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Membrane Proteins; 0 / SCRIB protein, human; 0 / Tumor Suppressor Proteins; 0 / beta Catenin
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68. Dewa Y, Nishimura J, Jin M, Kawai M, Saegusa Y, Harada T, Shibutani M, Mitsumori K: Molecular expression analysis of beta-naphthoflavone-induced hepatocellular tumors in rats. Toxicol Pathol; 2009 Jun;37(4):446-55
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  • [Title] Molecular expression analysis of beta-naphthoflavone-induced hepatocellular tumors in rats.
  • The present study was performed to characterize molecular expression levels of preneoplastic and neoplastic lesions induced by beta-naphthoflavone (BNF), an aryl hydrocarbon receptor (AhR) agonist in rat hepatocarcinogenesis.
  • Immunohistochemically, BNF increased the number of proliferating cell nuclear antigen (PCNA)-positive cells in altered foci (2.3-fold) and HCAs (6.7-fold) compared with the surrounding tissue and decreased the staining of cell cycle regulators (P21, C/EBPalpha).
  • These results suggest that enhanced cell proliferation and protection against oxidative stress play an important role in BNF-induced hepatocarcinogenesis in rats.
  • [MeSH-major] Adenoma, Liver Cell / chemically induced. Enzyme Inhibitors / toxicity. Liver Neoplasms / chemically induced. beta-Naphthoflavone / toxicity
  • [MeSH-minor] Animals. Body Weight. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Cell Proliferation. Data Interpretation, Statistical. Disease Models, Animal. Gene Expression Profiling. Histone Deacetylase 1. Histone Deacetylases / metabolism. Immunohistochemistry. Liver / metabolism. Liver / pathology. Oxidative Stress / genetics. Proliferating Cell Nuclear Antigen / metabolism. Rats. Receptors, Aryl Hydrocarbon / agonists. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19389873.001).
  • [ISSN] 1533-1601
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; 0 / Proliferating Cell Nuclear Antigen; 0 / Receptors, Aryl Hydrocarbon; 6051-87-2 / beta-Naphthoflavone; EC 3.5.1.98 / Hdac1 protein, rat; EC 3.5.1.98 / Histone Deacetylase 1; EC 3.5.1.98 / Histone Deacetylases
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69. Cetani F, Pardi E, Banti C, Collecchi P, Viacava P, Borsari S, Fanelli G, Naccarato AG, Saponaro F, Berti P, Miccoli P, Pinchera A, Marcocci C: Beta-catenin activation is not involved in sporadic parathyroid carcinomas and adenomas. Endocr Relat Cancer; 2010 Mar;17(1):1-6

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  • [Title] Beta-catenin activation is not involved in sporadic parathyroid carcinomas and adenomas.
  • Aberrant accumulation of beta-catenin has been found in various types of human tumors.
  • The aim of this study was to evaluate whether Wnt/beta-catenin signaling is activated in parathyroid carcinomas and adenomas.
  • Immunostaining of beta-catenin was performed in all carcinomas and in 66 adenomas (including three atypical).
  • Normal parathyroid showed a homogeneous distinct outer cell membrane staining in the majority of cells and no nuclear staining.
  • With the exception of one carcinoma, which had a negative membrane staining, all other samples showed a membrane staining which was similar to that of the normal parathyroid. beta-Catenin expression was heterogeneous with a range of positive cells between 5 and 80%, independently of tumor type.
  • Our results suggest that the Wnt/beta-catenin signaling pathway is not involved in the development of parathyroid carcinomas and adenomas.
  • [MeSH-major] Adenoma / physiopathology. Carcinoma / physiopathology. Neoplasm Proteins / physiology. Parathyroid Neoplasms / physiopathology. Signal Transduction / physiology. Wnt Proteins / physiology. beta Catenin / physiology
  • [MeSH-minor] Cell Transformation, Neoplastic / genetics. Cytoplasm / chemistry. DNA Mutational Analysis. Exons / genetics. Humans. Membrane Proteins / analysis

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  • (PMID = 19755524.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Wnt Proteins; 0 / beta Catenin
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70. Cavard C, Terris B, Grimber G, Christa L, Audard V, Radenen-Bussiere B, Simon MT, Renard CA, Buendia MA, Perret C: Overexpression of regenerating islet-derived 1 alpha and 3 alpha genes in human primary liver tumors with beta-catenin mutations. Oncogene; 2006 Jan 26;25(4):599-608
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  • [Title] Overexpression of regenerating islet-derived 1 alpha and 3 alpha genes in human primary liver tumors with beta-catenin mutations.
  • The Wnt/beta-catenin signaling pathway is activated in many human hepatocellular carcinomas (HCC).
  • We tried to identify the genes involved in carcinogenesis and progression of HCC with beta-catenin mutations.
  • We used PCR-based subtractive hybridization to compare gene expression between malignant and benign components of a human HCC occurring in pre-existing adenoma activated for beta-catenin.
  • Using siRNA directed against beta-catenin, we demonstrated that REG3A is a target of beta-catenin signaling in Huh7 hepatoma cells.
  • The upregulation of REG3A and REG1A expression is significantly correlated to the beta-catenin status in 42 HCC and 28 hepatoblastomas characterized for their beta-catenin status.
  • [MeSH-major] Antigens, Neoplasm / genetics. Biomarkers, Tumor / genetics. Carcinoma, Hepatocellular / genetics. Gene Expression Regulation, Neoplastic. Lectins, C-Type / genetics. Lithostathine / genetics. Liver Neoplasms / genetics. Mutation. beta Catenin / genetics
  • [MeSH-minor] Adenoma / genetics. Adult. Cell Line, Tumor. Colonic Neoplasms / genetics. Hepatoblastoma / genetics. Humans. Male. Signal Transduction

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  • (PMID = 16314847.001).
  • [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 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / Lithostathine; 0 / REG1A protein, human; 0 / beta Catenin; 0 / pancreatitis-associated protein
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71. Di Leo A, Barone M, Maiorano E, Tanzi S, Piscitelli D, Marangi S, Lofano K, Ierardi E, Principi M, Francavilla A: ER-beta expression in large bowel adenomas: implications in colon carcinogenesis. Dig Liver Dis; 2008 Apr;40(4):260-6
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  • [Title] ER-beta expression in large bowel adenomas: implications in colon carcinogenesis.
  • BACKGROUND: A pivotal role of oestrogen receptor-beta has been suggested in colon carcinogenesis in humans.
  • However, few data are available on oestrogen receptor-beta in colorectal pre-cancerous lesions.
  • AIM: In the present study, we evaluated oestrogen receptor-beta expression and its possible correlation with proliferative activity and apoptosis in colorectal adenomas and normal colon tissue.
  • Oestrogen receptor-beta expression, colonocyte proliferation (expressed as PCNA positivity) and apoptosis were evaluated.
  • RESULTS: In adenomatous tissue, a significant reduction of oestrogen receptor-beta was observed compared to normal mucosa (10.1+/-5.5% vs. 44.2+/-13.7; p<0.03), while the expression of oestrogen receptor-alpha remained unvaried.
  • Cell proliferative activity significantly increased in adenomatous tissue compared to normal mucosa (59.3+/-7.1 vs. 18.5+/-8.8; p<0.0001), doubling the PCNA/apoptosis ratio.
  • An inverse correlation was found between oestrogen receptor-beta and PCNA expression in adenomas (r=-0.81), a datum confirmed by confocal microscopy evaluation.
  • CONCLUSIONS: Our data demonstrate, for the first time, a significant reduction of oestrogen receptor-beta expression already in the pre-cancerous phase of colon carcinogenesis.
  • This suggests a role of selective oestrogen receptor-beta agonists in the prevention of colorectal cancer.
  • [MeSH-major] Adenoma / metabolism. Estrogen Receptor beta / metabolism. Intestinal Neoplasms / metabolism

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  • (PMID = 18093886.001).
  • [ISSN] 1590-8658
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Estrogen Receptor beta
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72. 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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73. Eloy C, Lopes JM, Faria G, Moreira H, Brandão A, Silva T, Carneiro F: Clear cell change in colonic polyps. Int J Surg Pathol; 2009 Dec;17(6):438-43
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  • [Title] Clear cell change in colonic polyps.
  • In this study, the pathogenesis of clear cell change in colorectal epithelial lesions was studied.
  • A total of 4 cases of clear cell change (1 hyperplasic polyp and 3 adenomas) were characterized using histochemistry, immunohistochemistry, and electron microscopy.
  • In all, 1 adenoma with clear cell dysplastic glands progressed to adenocarcinoma without clear cell change.
  • Clear cell cytoplasmatic vacuoles were negative for glycogen and mucins (MUC 2, MUC 5AC).
  • Ki-67 LI in clear cell adenoma components was lower than in common adenoma components of the same dysplasia grades (while p53 and beta-catenin were similarly expressed).
  • Ultrastructural features of clear cell change showed features of lipid-like material.
  • Clear cell change is found in hyperplastic and neoplastic lesions of the colon and is not due to the accumulation of glycogen or mucins.
  • A degenerative nature of clear cell change is suggested by the demonstration of lipid-like material in the vacuoles of clear cells.
  • [MeSH-major] Adenocarcinoma, Clear Cell / pathology. Adenoma / pathology. Colon / pathology. Colonic Neoplasms / pathology. Intestinal Polyps / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Cell Count. Cell Nucleus / ultrastructure. Cytoplasm / ultrastructure. Humans. Hyperplasia. Immunoenzyme Techniques. In Vitro Techniques. Ki-67 Antigen / metabolism. Male. Middle Aged

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  • (PMID = 18611940.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen
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74. 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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75. Naishiro Y, Yamada T, Idogawa M, Honda K, Takada M, Kondo T, Imai K, Hirohashi S: Morphological and transcriptional responses of untransformed intestinal epithelial cells to an oncogenic beta-catenin protein. Oncogene; 2005 Apr 28;24(19):3141-53
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  • [Title] Morphological and transcriptional responses of untransformed intestinal epithelial cells to an oncogenic beta-catenin protein.
  • Aberrant transactivation of a certain set of target genes by the beta-catenin and T-cell factor/lymphoid enhancer factor (TCF/LEF) transcription factor complexes has been implicated in the process of intestinal epithelial cells entering early colorectal carcinogenesis.
  • A rat intestinal epithelial cell line IEC6 became elongated, extended protrusions at cell periphery, and increased stress fibers and focal contacts upon the induction of beta-catenin protein stabilized by deletion of the N-terminal glycogen synthase kinase-3beta (GSKbeta) phosphorylation sites (beta-catenin DeltaN89).
  • Those genes included known negative regulators of the Wnt signaling pathway, Sfrp4 and Axin2; extracellular matrix and related molecule, Hxb and Crtl1; cell adhesion and cytoskeletal proteins, Podxl, Igaf4, and Itab6; and molecules involved in the insulin and insulin-like growth factor (IGF) signaling pathways, Enpp1, Igfbp2, and Sgk.
  • We report the finding that insulin-like growth factor-binding protein-2 (IGFBP2) is a direct target gene of the beta-catenin and TCF/LEF complexes.
  • Disruption of the multigene network system regulating cell adhesion and cytoskeleton may be crucial in the initiation of colorectal carcinogenesis.
  • [MeSH-major] Cell Transformation, Neoplastic. Cytoskeletal Proteins / metabolism. Epithelial Cells / metabolism. Gene Expression Regulation, Neoplastic. Intestines / metabolism. Trans-Activators / metabolism. Transcription, Genetic
  • [MeSH-minor] Adenoma / metabolism. Animals. Cell Adhesion. Cell Line. Cell Line, Transformed. Cell Line, Tumor. Cells, Cultured. Chromatin Immunoprecipitation. Colon / metabolism. Colorectal Neoplasms / metabolism. DNA-Binding Proteins / metabolism. Extracellular Matrix / metabolism. Genes, Reporter. Glycogen Synthase Kinase 3 / metabolism. HeLa Cells. Humans. Immunohistochemistry. Intercellular Signaling Peptides and Proteins / metabolism. Intestine, Small / metabolism. Luciferases / metabolism. Lymphoid Enhancer-Binding Factor 1. Male. Mice. Mice, Inbred C57BL. Microscopy, Fluorescence. Oligonucleotide Array Sequence Analysis. Protein Structure, Tertiary. Rats. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Time Factors. Transcription Factors / metabolism. Wnt Proteins. beta Catenin

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  • (PMID = 15735679.001).
  • [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 / CTNNB1 protein, human; 0 / CTNNB1 protein, mouse; 0 / Ctnnb1 protein, rat; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin; EC 1.13.12.- / Luciferases; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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76. Steinbrecher KA, Horowitz NA, Blevins EA, Barney KA, Shaw MA, Harmel-Laws E, Finkelman FD, Flick MJ, Pinkerton MD, Talmage KE, Kombrinck KW, Witte DP, Palumbo JS: Colitis-associated cancer is dependent on the interplay between the hemostatic and inflammatory systems and supported by integrin alpha(M)beta(2) engagement of fibrinogen. Cancer Res; 2010 Apr 1;70(7):2634-43
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  • [Title] Colitis-associated cancer is dependent on the interplay between the hemostatic and inflammatory systems and supported by integrin alpha(M)beta(2) engagement of fibrinogen.
  • More detailed analyses in mice expressing a mutant form of fibrinogen that retains clotting function, but lacks the leukocyte integrin receptor alpha(M)beta(2) binding motif (Fibgamma(390-396A)), revealed that alpha(M)beta(2)-mediated engagement of fibrin(ogen) is mechanistically coupled to local inflammatory processes (e.g., interleukin-6 elaboration) and epithelial alterations that contribute to adenoma formation.
  • Given the importance of antecedent inflammation in the progression of numerous cancers, these studies suggest that therapies targeting fibrin(ogen)-alpha(M)beta(2) interactions may be useful in preventing and/or treating this important subset of malignancies.

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  • (PMID = 20233870.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N02CB66600; United States / NHLBI NIH HHS / HL / R01 HL085545; United States / NHLBI NIH HHS / HL / R01 HL085545-03; United States / NHLBI NIH HHS / HL / R01 HL085545-04
  • [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 / Carcinogens; 0 / Cytokines; 0 / Fibronectins; 0 / Macrophage-1 Antigen; 9042-14-2 / Dextran Sulfate; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ NIHMS174574; NLM/ PMC4288842
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77. Chen G, Mou LP, Yao J, You TT, Shen XY, Zhu XQ, Qiao YF, Lin M, Fang XW, Zou X, Lin LX: [Construction of GSK-3beta-targeting RNAi adenovirus vector and the influence of Wnt/beta-catenin pathway in proliferation of human thyrocytes]. Zhonghua Yi Xue Za Zhi; 2008 Nov 4;88(40):2821-5

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  • [Title] [Construction of GSK-3beta-targeting RNAi adenovirus vector and the influence of Wnt/beta-catenin pathway in proliferation of human thyrocytes].
  • OBJECTIVE: To construct RNAi recombinant adenoviral expressive vectors specific to glycogen synthase kinase-3beta (GSK-3beta) and to observe its gene knockdown effect on the expression of GSK-3beta, and to explore the effect of Wnt/beta-catenin pathway on the proliferation of human thyrocytes using the RNAi adenovirus vector.
  • Normal human thyrocytes fart from thyroid adenoma were obtained during resection of adenoma, cultured, and infected by the GSK-3beta specific RNAi adenovirus.
  • BrdU method was used to detect the cell proliferation.
  • 72 hours later Western blotting was used to examine the level of beta-catenin.
  • The expression of beta-catenin of the thyrocytes infected with Ad-DEST was significantly higher than those of the Ad-DEST group and un-infected group (both P<0.05).
  • The Wnt/beta-catenin pathway plays an important role in the regulation of proliferation of human thyrocytes.
  • [MeSH-major] Cell Proliferation. Glycogen Synthase Kinase 3 / genetics. RNA Interference. Thyroid Gland / cytology. Wnt Proteins / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Adenoviridae. Cell Line. Genetic Vectors. Humans

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  • (PMID = 19080489.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Wnt Proteins; 0 / beta Catenin; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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78. National Toxicology Program: NTP technical report on the toxicology and carcinogenesis studies of beta-myrcene (CAS No. 123-35-3) in F344/N rats and B6C3F1 mice (Gavage studies). Natl Toxicol Program Tech Rep Ser; 2010 Dec;(557):1-163
Hazardous Substances Data Bank. MYRCENE .

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  • [Title] NTP technical report on the toxicology and carcinogenesis studies of beta-myrcene (CAS No. 123-35-3) in F344/N rats and B6C3F1 mice (Gavage studies).
  • Beta-myrcene, an acyclic unsubstituted monoterpene, and the essential oils which contain it are used as intermediates in the production of terpene alcohols (geraniol, nerol, and linalool), which, in turn, serve as intermediates in the production of aroma and flavor chemicals.
  • Thus beta-myrcene is used widely in cosmetics, soaps, and detergents and as a flavoring additive in food and beverages.
  • Beta-myrcene is also the major constituent of hop and bay oils, which are used in the manufacture of alcoholic beverages.
  • Beta-myrcene was nominated for study by the National Institute of Environmental Health Sciences based on its high production volume, high level of human exposure, and structural relationship to d-limonene, which induced neoplasms in the kidneys of male rats in association with hyaline droplet nephropathy (NTP, 1990).
  • Male and female F344/N rats and B6C3F1 mice were administered beta-myrcene (greater than 90% pure) by gavage for 3 months or 2 years.
  • 3-MONTH STUDY IN RATS: Groups of 10 male and 10 female rats were administered 0, 0.25, 0.5, 1, 2, or 4 g beta-myrcene/kg body weight in corn oil by gavage, 5 days per week for 14 weeks.
  • 3-MONTH STUDY IN MICE: Groups of 10 male and 10 female mice were administered 0, 0.25, 0.5, 1, 2, or 4 g beta-myrcene/kg body weight in corn oil by gavage, 5 days per week for 14 weeks.
  • 2-YEAR STUDY IN RATS: Groups of 50 male and 50 female rats were administered 0, 0.25, 0.5, or 1 g beta-myrcene/kg body weight in corn oil by gavage, 5 days per week for 105 weeks.
  • In the standard evaluation of the kidney, the incidence of renal tubule adenoma was significantly increased in 0.5 g/kg male rats, and the combined incidences of renal tubule adenoma or carcinoma were significantly increased in 0.25 and 0.5 g/kg males.
  • In both the extended evaluation and the combined standard and extended evaluations, the incidences of renal tubule adenoma and the combined incidences of renal tubule adenoma or carcinoma were significantly increased in the 0.25 and 0.5 g/kg groups of males.
  • 2-YEAR STUDY IN MICE: Groups of 50 male and 50 female mice were administered 0, 0.25, 0.5, or 1 g beta-myrcene/kg body weight in corn oil by gavage, 5 days per week for 104 or 105 weeks.
  • Liver neoplasms included hepatocellular adenoma and hepatocellular carcinoma in males and females and hepatoblastoma in males.
  • The incidences of hepatocellular hypertrophy were significantly increased in 0.5 g/kg males and females, as was the incidence of mixed cell focus in 0.5 g/kg females.
  • GENETIC TOXICOLOGY: beta-myrcene did not show evidence of genotoxicity in assays conducted by the NTP.
  • In addition, no significant increase in frequency of micronucleated normochromatic erythrocytes, biomarkers of chromosomal damage, was observed in male or female mice administered beta-myrcene for 3 months by gavage.
  • CONCLUSIONS: Under the conditions of these 2-year gavage studies, there was clear evidence of carcinogenic activity of beta-myrcene in male F344/N rats based on increased incidences of renal tubule neoplasms.
  • There was equivocal evidence of carcinogenic activity of beta-myrcene in female F344/N rats based on increased incidences of renal tubule adenoma.
  • There was clear evidence of carcinogenic activity of beta-myrcene in male B6C3F1 mice based on increased incidences of hepatocellular adenoma, hepatocellular carcinoma, and hepatoblastoma.
  • There was equivocal evidence of carcinogenic activity of beta-myrcene in female B6C3F1 mice based on marginally increased incidences of hepatocellular adenoma and carcinoma.
  • Administration of beta-myrcene induced nonneoplastic lesions in the kidney of male and female rats, nose of male rats, and liver of male and female mice.
  • [MeSH-major] Adenoma / chemically induced. Carcinoma, Hepatocellular / chemically induced. Hepatoblastoma / chemically induced. Kidney Neoplasms / chemically induced. Liver Neoplasms / chemically induced. Monoterpenes / toxicity. Neoplasms, Experimental / chemically induced

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  • (PMID = 21415873.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Monoterpenes; 123-35-3 / beta-myrcene
  • [Investigator] Chan PC; Cesta MF; Sills RC; Bishop JB; Bristol DW; Bucher JR; Chhabra RS; Foster PM; Herbert RA; Hooth MJ; King-Herbert AP; Kissling GE; Malarkey DE; Roycroft JH; Sanders JM; Smith CS; Travlos GS; Walker NJ; Witt KL
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79. Sansom OJ, Reed KR, van de Wetering M, Muncan V, Winton DJ, Clevers H, Clarke AR: Cyclin D1 is not an immediate target of beta-catenin following Apc loss in the intestine. J Biol Chem; 2005 Aug 5;280(31):28463-7
The Lens. Cited by Patents in .

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  • [Title] Cyclin D1 is not an immediate target of beta-catenin following Apc loss in the intestine.
  • Cyclin D1 is postulated to be a target of the canonical Wnt pathway and critical for intestinal adenoma development.
  • Finally in a smaller study, we analyzed whether cyclin D1 deficiency affected adenoma formation 20 days following induced loss of Apc.
  • [MeSH-minor] Adenoma. Animals. Cell Line, Tumor. Colorectal Neoplasms. Gene Deletion. Gene Expression Regulation, Neoplastic. Integrases / metabolism. Intestinal Neoplasms. Mice. Mice, Inbred C57BL. Phenotype. beta Catenin

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  • (PMID = 15946945.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [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 / Cytoskeletal Proteins; 0 / Trans-Activators; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
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80. 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
Xenbase. Xenbase .

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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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81. Wang J, Wang X, Gong W, Mi B, Liu S, Jiang B: Increased expression of beta-catenin, phosphorylated glycogen synthase kinase 3beta, cyclin D1, and c-myc in laterally spreading colorectal tumors. J Histochem Cytochem; 2009 Apr;57(4):363-71
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  • [Title] Increased expression of beta-catenin, phosphorylated glycogen synthase kinase 3beta, cyclin D1, and c-myc in laterally spreading colorectal tumors.
  • This study was performed to characterize the clinicopathological features and examine activation of the Wnt/beta-catenin pathway in LSTs and protruded-type colorectal adenomas (PAs).
  • The expression of E-cadherin, beta-catenin, glycogen synthase kinase-3beta (GSK-3beta), phosphorylated GSK-3beta, (phospho-GSK-3beta), cyclin D1, and c-myc was investigated by immunohistochemical staining on serial sections.
  • Expression of beta-catenin, phospho-GSK-3beta, cyclin D1, and c-myc was significantly increased in LSTs compared with PAs (p<0.05).
  • The level of beta-catenin expression correlated strongly with phospho-GSK-3beta, cyclin D1, and c-myc expression in LSTs but not in PAs.
  • Our findings suggest that activation of the Wnt/beta-catenin pathway is more prevalent in LSTs than in PAs, suggesting that phosphorylation-dependent inactivation of GSK-3beta may be involved in LST carcinogenesis.
  • [MeSH-major] Colorectal Neoplasms / metabolism. Cyclin D1 / biosynthesis. Glycogen Synthase Kinase 3 / biosynthesis. Proto-Oncogene Proteins c-myc / biosynthesis. beta Catenin / biosynthesis
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Biomarkers, Tumor / biosynthesis. Humans. Immunohistochemistry. Phosphorylation

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  • (PMID = 19064714.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ PMC2664982
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82. Gómez-Pérez FJ, Cuevas-Ramos D, Valdés PA, Aguilar-Salinas CA, Mehta R, Rull JA: Beta-cell adenomas without hyperinsulinemia with use of highly specific insulin radioimmunoassays: case report and review of literature. Endocr Pract; 2010 Jul-Aug;16(4):660-3
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  • [Title] Beta-cell adenomas without hyperinsulinemia with use of highly specific insulin radioimmunoassays: case report and review of literature.
  • OBJECTIVE: To report a case of a proinsulin-secreting islet cell adenoma in which the diagnosis was obscured by an ultraspecific insulin assay.
  • A proinsulin-secreting islet cell tumor was diagnosed.
  • CONCLUSION: The diagnosis of a hypoglycemia-producing pancreatic adenoma can be missed when an ultraspecific insulin assay is used.

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  • (PMID = 20439243.001).
  • [ISSN] 1934-2403
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 9035-68-1 / Proinsulin
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83. Wang Y, Giel-Moloney M, Rindi G, Leiter AB: Enteroendocrine precursors differentiate independently of Wnt and form serotonin expressing adenomas in response to active beta-catenin. Proc Natl Acad Sci U S A; 2007 Jul 3;104(27):11328-33
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  • [Title] Enteroendocrine precursors differentiate independently of Wnt and form serotonin expressing adenomas in response to active beta-catenin.
  • Here, we show that specification of enteroendocrine but not Paneth cells occurs independently of Wnt signals by conditional deletion of beta-catenin in immature cells expressing the transcription factor, neurogenin 3.
  • Activation of the Wnt pathway by conditionally deleting exon 3 of the beta-catenin gene at an early stage of enteroendocrine cell differentiation induced small-intestinal adenomas expressing serotonin, a feature not previously described in other tumors induced by Wnt in mice.
  • In contrast, excision of exon 3 of beta-catenin at a later stage of enteroendocrine differentiation did not produce tumors.

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  • (PMID = 17592150.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / T32-DK007542; United States / NIDDK NIH HHS / DK / P30 DK034928; United States / NIDDK NIH HHS / DK / DK67166; United States / NIDDK NIH HHS / DK / DK52870; United States / NIDDK NIH HHS / DK / P30-DK34928; United States / NIDDK NIH HHS / DK / DK43673; United States / NIDDK NIH HHS / DK / T32 DK007542; United States / NIDDK NIH HHS / DK / R01 DK067166; United States / NIDDK NIH HHS / DK / R01 DK043673
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CTNNB1 protein, human; 0 / NEUROG3 protein, human; 0 / Nerve Tissue Proteins; 0 / Wnt Proteins; 0 / beta Catenin; 333DO1RDJY / Serotonin
  • [Other-IDs] NLM/ PMC2040898
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84. Rajakangas J, Misikangas M, Päivärinta E, Mutanen M: Chemoprevention by white currant is mediated by the reduction of nuclear beta-catenin and NF-kappaB levels in Min mice adenomas. Eur J Nutr; 2008 Apr;47(3):115-22
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  • [Title] Chemoprevention by white currant is mediated by the reduction of nuclear beta-catenin and NF-kappaB levels in Min mice adenomas.
  • AIMS OF THE STUDY: To study if white currant is chemopreventive in an experimental model for intestinal tumorigenesis and further study the effects on beta-catenin and NF-kappaB signaling pathways.
  • Cell signaling parameters were analysed from intestinal adenomas and surrounding mucosa by Western blotting and immunohistochemistry.
  • White currant reduced nuclear beta-catenin and NF-kappaB protein levels in the adenomas (P<0.05 and P<0.02, respectively).
  • [MeSH-major] Adenoma / prevention & control. Antineoplastic Agents, Phytogenic / pharmacology. Fruit / chemistry. Intestinal Mucosa / pathology. Intestinal Neoplasms / prevention & control. NF-kappa B / metabolism. beta Catenin / metabolism

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  • (PMID = 18389329.001).
  • [ISSN] 1436-6207
  • [Journal-full-title] European journal of nutrition
  • [ISO-abbreviation] Eur J Nutr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / NF-kappa B; 0 / beta Catenin
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85. 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

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  • (PMID = 17977470.001).
  • [ISSN] 0007-1145
  • [Journal-full-title] The British journal of nutrition
  • [ISO-abbreviation] Br. J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cadherins; 0 / Dietary Fats; 0 / Neoplasm Proteins; 0 / beta Catenin; 136601-57-5 / Cyclin D1; 9005-80-5 / Inulin
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86. 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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87. Oda E, Nakamura Y, Yamamoto M, Kojiro M: Immunohistochemical distribution of tubulin beta II in human normal and neoplastic tissues. Kurume Med J; 2005;52(4):117-25
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  • [Title] Immunohistochemical distribution of tubulin beta II in human normal and neoplastic tissues.
  • In mammals, there are seven beta-tubulins and six alpha-tubulins.
  • Each beta-tubulin isotype has a unique tissue distribution.
  • The purpose of this study was to describe the distribution of tubulin beta II in normal and neoplastic human tissues with immunohistochemical techniques.
  • Immunohistochemical staining for tubulin beta II was performed using a monoclonal antibody, KNY379 developed in our laboratory.
  • Tubulin beta II was detected in various normal tissues, particularly in fetal and neonatal tissues, such as the nervous system, pulmonary alveoli, bronchioles and bronchi, colon, pancreatic ducts and acini, renal convoluted tubuli, skin epidermis, body cavity mesothelial cells, smooth muscle and thymus.
  • In neoplastic tissues, tubulin beta II immunoreactivity was detected in various nervous system neoplasms and other neoplasms such as pancreatic solid cystic carcinoma, pleomorphic adenoma, Warthin's tumor, nephroblastoma, basal cell carcinoma and malignant mesothelioma.
  • We conclude that our monoclonal antibody, KNY379, may be useful as a marker of nervous system neoplasm, pancreatic solid cystic carcinoma, pleomorphic adenoma, Warthin's tumor, nephroblastoma, basal cell carcinoma and malignant mesothelioma.

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  • (PMID = 16639982.001).
  • [ISSN] 0023-5679
  • [Journal-full-title] The Kurume medical journal
  • [ISO-abbreviation] Kurume Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Protein Isoforms; 0 / Tubulin
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88. Moon WS, Park HS, Lee H, Pai R, Tarnawski AS, Kim KR, Jang KY: Co-expression of cox-2, C-met and beta-catenin in cells forming invasive front of gallbladder cancer. Cancer Res Treat; 2005 Jun;37(3):171-6
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  • [Title] Co-expression of cox-2, C-met and beta-catenin in cells forming invasive front of gallbladder cancer.
  • Our previous studies have demonstrated that prostaglandin E(2) (PGE(2)), generated by cyclooxygenase 2 (Cox-2), transactivates epidermal growth factor receptor (EGFR), c-Met and beta-catenin; thus, enhancing colon cancer cell growth and invasiveness in vitro.
  • To determine whether these findings are applicable to clinical conditions, we examined the expression and cellular localization/co-localization of Cox-2, c-Met, beta-catenin, EGFR and c-erbB2 in gallbladder cancer.
  • MATERIALS AND METHODS: Thirty-five specimens of invasive gallbladder cancer, 8 in situ carcinoma and 7 adenoma specimens were immunostained with specific antibodies against Cox-2, c-Met, beta-catenin, EGFR and c-erbB2.
  • RESULTS: Cox-2, c-Met, beta-catenin, c-erbB2 and EGFR were over-expressed in 80, 74, 71, 62 and 11% of invasive gallbladder cancers, respectively. beta-catenin was expressed in 80% of non-malignant specimens, exclusively in the cell membrane, while the cancer specimens showed cytoplasmic and/or nuclear staining.
  • Significantly higher Cox-2, c-Met and beta-catenin expressions were present in cancer cells of the invasive front than in the tumor central areas (p<0.001), and these expressions were significantly (p=0.01) associated with the invasion depth.
  • Co-expressions of Cox-2, c-Met, beta-catenin and c-erbB2 were present in 42% of the specimens in cancer cells forming the invasive front.
  • CONCLUSION: The overexpressions, and often co-localizations, of Cox-2, c-Met and beta-catenin in cancer cells forming the invasive front indicate their local interactions and important roles in invasion.


89. Hirata K, Ajiki T, Okazaki T, Horiuchi H, Fujita T, Kuroda Y: Frequent occurrence of abnormal E-cadherin/beta-catenin protein expression in advanced gallbladder cancers and its association with decreased apoptosis. Oncology; 2006;71(1-2):102-10
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  • [Title] Frequent occurrence of abnormal E-cadherin/beta-catenin protein expression in advanced gallbladder cancers and its association with decreased apoptosis.
  • OBJECTIVE: Our aim is to assess the clinicopathological significance of E-cadherin and beta-catenin expression, as well as their association with apoptosis in gallbladder cancers.
  • METHODS: The expression of E-cadherin and beta-catenin proteins was examined in 4 biliary tract cancer cell lines and 49 gallbladder cancer specimens by immunofluorescent or immunohistochemical methods and Western blotting.
  • The apoptotic status was evaluated in the cell lines by poly(ADP-ribose) polymerase Western blotting and in the tumors by the TdT-mediated dUTP nick end labeling assay.
  • RESULTS: Expression of poly(ADP-ribose) polymerase (apoptosis) was only seen in cell lines that expressed both E-cadherin and beta-catenin.
  • Reduced expression of E-cadherin and beta-catenin was frequently seen in advanced gallbladder cancer cases (61 and 83%, respectively) relative to pT1 cases (25 and 63%, respectively).
  • Cases with reduced expression of both had lower apoptotic indices and showed a worse prognosis compared with cases with reduced expression of either E-cadherin or beta-catenin (p = 0.04 and 0.049, respectively).
  • CONCLUSIONS: The expression of E-cadherin or beta-catenin frequently diminishes as the tumor progresses, and abnormalities of E-cadherin and beta-catenin expression were associated with decreased apoptosis in gallbladder cancers.
  • [MeSH-major] Apoptosis. Biomarkers, Tumor / metabolism. Cadherins / metabolism. Gallbladder Neoplasms / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Aged. Biliary Tract Neoplasms / metabolism. Biliary Tract Neoplasms / pathology. Epithelium / metabolism. Epithelium / pathology. Female. Fluorescent Antibody Technique. Humans. Immunoenzyme Techniques. Lymphatic Metastasis / pathology. Male. Neoplasm Staging. Poly(ADP-ribose) Polymerases / metabolism. Prognosis. Survival Rate

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  • (PMID = 17341890.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDH1 protein, human; 0 / CTNNB1 protein, human; 0 / Cadherins; 0 / beta Catenin; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
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90. Yachida S, Mudali S, Martin SA, Montgomery EA, Iacobuzio-Donahue CA: Beta-catenin nuclear labeling is a common feature of sessile serrated adenomas and correlates with early neoplastic progression after BRAF activation. Am J Surg Pathol; 2009 Dec;33(12):1823-32
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  • [Title] Beta-catenin nuclear labeling is a common feature of sessile serrated adenomas and correlates with early neoplastic progression after BRAF activation.
  • Recent observations indicate that some sessile serrated adenomas (SSAs) have aberrant beta-catenin nuclear labeling, implicating the Wnt pathway in the molecular progression of SSAs to colorectal carcinoma.
  • We sought to expand upon this finding by characterizing beta-catenin expression in the full spectrum of serrated colorectal polyps, and correlating these findings with the genetic status of BRAF, KRAS and CTNNB1.
  • Immunolabeling for beta-catenin confirmed the presence of abnormal nuclear accumulation in SSAs, with 35/54 (67%) SSAs showing nuclear labeling compared with 0/12 hyperplastic polyps.
  • When SSAs were further analyzed with respect to the presence or absence of conventional epithelial dysplasia, nuclear beta-catenin labeling was seen in 8/27 (29%) SSAs without dysplasia (SSA) but in 27/27 (100%) of SSAs with dysplasia (P=0.000001).
  • Sequencing of genomic DNA extracted from a subset of hyperplastic polyps, SSAs, SSAs with dysplasia, TSAs and tubular adenomas failed to identify any CTNNB1 mutations to account for abnormal beta-catenin nuclear labeling.

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  • (PMID = 19745699.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA106610; United States / NCI NIH HHS / CA / K08 CA106610-05; United States / NCI NIH HHS / CA / CA106610
  • [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 / CTNNB1 protein, human; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / beta Catenin; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS139736; NLM/ PMC2788075
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91. Takeda K, Kinoshita I, Shimizu Y, Ohba Y, Itoh T, Matsuno Y, Shichinohe T, Dosaka-Akita H: Clinicopathological significance of expression of p-c-Jun, TCF4 and beta-Catenin in colorectal tumors. BMC Cancer; 2008;8:328
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinicopathological significance of expression of p-c-Jun, TCF4 and beta-Catenin in colorectal tumors.
  • BACKGROUND: A recent study has shown that phosphorylated c-Jun (p-c-Jun) interacts with TCF4 to form a complex that cooperatively enhances their transcriptional activity in the presence of beta-Catenin, and that their interaction is critical for mouse intestinal tumorigenesis.
  • RESULTS: Expression of p-c-Jun, TCF4 and beta-Catenin were significantly higher in adenomas than in the adjacent normal epithelia.
  • Expression of p-c-Jun and beta-Catenin in HGINs and adenocarcinomas were also significantly higher than in the adjacent normal epithelia. p-c-Jun expression, but not TCF4 and beta-Catenin, was higher in adenomas and HGINs than in adenocarcinomas, in which p-c-Jun expression was negatively correlated with pT stage progression.
  • Furthermore, significant correlations of expression were observed between p-c-Jun and TCF4 (r = 0.25, p = 0.04), TCF4 and beta-Catenin (r = 0.30, p = 0.01), p-c-Jun and MMP7 (r = 0.26, p = 0.03), and TCF4 and MMP7 (r = 0.39, p = 0.0008), respectively.
  • CONCLUSION: These results suggest that nuclear expression of p-c-Jun, TCF4 and beta-Catenin have important roles in human colorectal tumor development and that p-c-Jun may play a pivotal role in the earlier stages of tumor development.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenoma / metabolism. Colorectal Neoplasms / metabolism. DNA-Binding Proteins / metabolism. Proto-Oncogene Proteins c-jun / metabolism. Transcription Factors / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Basic Helix-Loop-Helix Leucine Zipper Transcription Factors. Binding Sites / genetics. Cell Transformation, Neoplastic. Female. Gene Expression. Humans. Immunohistochemistry. Male. Matrix Metalloproteinase 7 / chemistry. Matrix Metalloproteinase 7 / genetics. Matrix Metalloproteinase 7 / metabolism. Middle Aged. Neoplasm Staging. Phosphorylation. Protein Binding / genetics. Transcription Factor AP-1 / chemistry. Transcription Factor AP-1 / metabolism. Transcriptional Activation

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  • (PMID = 18992165.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins c-jun; 0 / TCF4 protein, human; 0 / Transcription Factor AP-1; 0 / Transcription Factors; 0 / beta Catenin; EC 3.4.24.23 / MMP7 protein, human; EC 3.4.24.23 / Matrix Metalloproteinase 7
  • [Other-IDs] NLM/ PMC2585585
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92. 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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93. Souazé F, Viardot-Foucault V, Roullet N, Toy-Miou-Leong M, Gompel A, Bruyneel E, Comperat E, Faux MC, Mareel M, Rostène W, Fléjou JF, Gespach C, Forgez P: Neurotensin receptor 1 gene activation by the Tcf/beta-catenin pathway is an early event in human colonic adenomas. Carcinogenesis; 2006 Apr;27(4):708-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neurotensin receptor 1 gene activation by the Tcf/beta-catenin pathway is an early event in human colonic adenomas.
  • Alterations in the Wnt/APC (adenomatous polyposis coli) signalling pathway, resulting in beta-catenin/T cell factor (Tcf)-dependent transcriptional gene activation, are frequently detected in familial and sporadic colon cancers.
  • Consequently, we observed the activation of NT1 receptor gene by agents causing beta-catenin cytosolic accumulation, as well as a strong decline of endogenous receptor when wt-APC was restored.
  • We corroborated the Wnt/APC signalling pathway on the NT1 receptor promoter activation with human colon carcinogenesis, and showed that NT1 receptor gene activation was perfectly correlated with nuclear or cytoplasmic beta-catenin localization while NT1 receptor was absent when beta-catenin was localized at the cell-cell junction in early adenomas of patients with familial adenomatous polyposis, hereditary non-polyposis colorectal cancer and loss of heterozygosity tumours.
  • In this report we establish a novel link in vitro between the Tcf/beta-catenin pathway and NT1 receptor promoter activation.
  • [MeSH-major] Adenoma / genetics. Colonic Neoplasms / genetics. Receptors, Neurotensin / biosynthesis. TCF Transcription Factors / physiology. beta Catenin / physiology
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / physiology. Cell Proliferation. Cell Survival. Cell Transformation, Neoplastic. Humans. Loss of Heterozygosity. Promoter Regions, Genetic. Signal Transduction. Up-Regulation. Wnt Proteins / physiology

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  • (PMID = 16299383.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [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 / Receptors, Neurotensin; 0 / TCF Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin; 0 / neurotensin type 1 receptor
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94. Bataille F, Rogler G, Modes K, Poser I, Schuierer M, Dietmaier W, Ruemmele P, Mühlbauer M, Wallner S, Hellerbrand C, Bosserhoff AK: Strong expression of methylthioadenosine phosphorylase (MTAP) in human colon carcinoma cells is regulated by TCF1/[beta]-catenin. Lab Invest; 2005 Jan;85(1):124-36
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  • [Title] Strong expression of methylthioadenosine phosphorylase (MTAP) in human colon carcinoma cells is regulated by TCF1/[beta]-catenin.
  • To examine MTAP RNA and protein expression, we screened six colon carcinoma cell lines and human primary colon epithelial cells by RT-PCR and immunoblotting.
  • MTAP expression was confirmed in vivo by immunohistochemical staining of normal colon tissue compared to adenoma and colon carcinoma.
  • Interestingly, we found strong MTAP mRNA and protein expression by colon carcinoma cell lines but no expression by colonic epithelial cells.
  • To analyse the regulation of MTAP expression, promoter studies were performed and revealed control of MTAP expression by LEF/TCF/beta-catenin.
  • In addition, the recently postulated association between MTAP activity and interferon (IFN) sensitivity was confirmed in colon epithelial cells showing only little response to IFN-gamma, in contrast to the carcinoma cell lines.
  • [MeSH-minor] Breast Neoplasms / enzymology. Breast Neoplasms / pathology. Cell Line, Tumor. Cell Proliferation. Fluorescent Antibody Technique, Indirect. Hepatocyte Nuclear Factor 1. Hepatocyte Nuclear Factor 1-alpha. Humans. Intestinal Mucosa / enzymology. Melanoma / enzymology. Melanoma / pathology. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Skin Neoplasms / enzymology. Skin Neoplasms / pathology. Up-Regulation. beta Catenin

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  • (PMID = 15492751.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / Trans-Activators; 0 / Transcription Factors; 0 / beta Catenin; 126548-29-6 / Hepatocyte Nuclear Factor 1; EC 2.4.2.1 / Purine-Nucleoside Phosphorylase; EC 2.4.2.28 / 5'-methylthioadenosine phosphorylase
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95. 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

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  • (PMID = 18490924.001).
  • [ISSN] 1476-5594
  • [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 / DNA Primers; 0 / Transforming Growth Factor beta; 0 / Vascular Endothelial Growth Factor A; EC 2.7.11.1 / Braf protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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96. Tang Y, Katuri V, Srinivasan R, Fogt F, Redman R, Anand G, Said A, Fishbein T, Zasloff M, Reddy EP, Mishra B, Mishra L: Transforming growth factor-beta suppresses nonmetastatic colon cancer through Smad4 and adaptor protein ELF at an early stage of tumorigenesis. Cancer Res; 2005 May 15;65(10):4228-37
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  • [Title] Transforming growth factor-beta suppresses nonmetastatic colon cancer through Smad4 and adaptor protein ELF at an early stage of tumorigenesis.
  • Although transforming growth factor-beta (TGF-beta) is both a suppressor and promoter of tumorigenesis, its contribution to early tumor suppression and staging remains largely unknown.
  • In search of the mechanism of early tumor suppression, we identified the adaptor protein ELF, a beta-spectrin from stem/progenitor cells committed to foregut lineage.
  • ELF activates and modulates Smad4 activation of TGF-beta to confer cell polarity, to maintain cell architecture, and to inhibit epithelial-to-mesenchymal transition.
  • Analysis of development of colon cancer in (adult) elf+/-/Smad4+/-, elf+/-, Smad4+/-, and gut epithelial cells from elf-/- mutant mouse embryos pinpoints the defect to hyperplasia/adenoma transition.
  • This study indicates that by modulating Smad 4, ELF has a key role in TGF-beta signaling in the suppression of early colon cancer.
  • [MeSH-minor] Animals. Apoptosis / physiology. Cell Growth Processes / physiology. Humans. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Mice. Mice, Knockout. Smad4 Protein. Transforming Growth Factor beta

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  • (PMID = 15899814.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK56111; United States / NIDDK NIH HHS / DK / R01 DK58637
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / SMAD4 protein, human; 0 / Smad4 Protein; 0 / Smad4 protein, mouse; 0 / Trans-Activators; 0 / Transforming Growth Factor beta; 12634-43-4 / Spectrin
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97. Xian X, Håkansson J, Ståhlberg A, Lindblom P, Betsholtz C, Gerhardt H, Semb H: Pericytes limit tumor cell metastasis. J Clin Invest; 2006 Mar;116(3):642-51
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  • [Title] Pericytes limit tumor cell metastasis.
  • Previously we observed that neural cell adhesion molecule (NCAM) deficiency in beta tumor cells facilitates metastasis into distant organs and local lymph nodes.
  • Here, we show that NCAM-deficient beta cell tumors grew leaky blood vessels with perturbed pericyte-endothelial cell-cell interactions and deficient perivascular deposition of ECM components.
  • Conversely, tumor cell expression of NCAM in a fibrosarcoma model (T241) improved pericyte recruitment and increased perivascular deposition of ECM molecules.
  • Together, these findings suggest that NCAM may limit tumor cell metastasis by stabilizing the microvessel wall.
  • To directly address whether pericyte dysfunction increases the metastatic potential of solid tumors, we studied beta cell tumorigenesis in primary pericyte-deficient Pdgfb(ret/ret) mice.
  • This resulted in beta tumor cell metastases in distant organs and local lymph nodes, demonstrating a role for pericytes in limiting tumor cell metastasis.
  • These data support a new model for how tumor cells trigger metastasis by perturbing pericyte-endothelial cell-cell interactions.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Neoplasm Metastasis / pathology. Neoplasm Metastasis / prevention & control. Pancreatic Neoplasms / pathology. Pericytes / physiology
  • [MeSH-minor] Animals. Cell Communication / genetics. Endothelium, Vascular / metabolism. Endothelium, Vascular / pathology. Fibrosarcoma / blood supply. Fibrosarcoma / genetics. Fibrosarcoma / metabolism. Fibrosarcoma / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Neovascularization, Pathologic / metabolism. Neural Cell Adhesion Molecules / deficiency. Neural Cell Adhesion Molecules / genetics. Neural Cell Adhesion Molecules / physiology

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  • (PMID = 16470244.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neural Cell Adhesion Molecules
  • [Other-IDs] NLM/ PMC1361347
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98. Hsu HH, Cheng SF, Chen LM, Liu JY, Chu CH, Weng YJ, Li ZY, Lin CS, Lee SD, Kuo WW, Huang CY: Over-expressed estrogen receptor-alpha up-regulates hTNF-alpha gene expression and down-regulates beta-catenin signaling activity to induce the apoptosis and inhibit proliferation of LoVo colon cancer cells. Mol Cell Biochem; 2006 Sep;289(1-2):101-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Over-expressed estrogen receptor-alpha up-regulates hTNF-alpha gene expression and down-regulates beta-catenin signaling activity to induce the apoptosis and inhibit proliferation of LoVo colon cancer cells.
  • Patients that received E(2) replacement therapy were found to have a reduction in the incidence of colon adenoma and carcinoma.
  • The results clearly demonstrated that overexpressed ERalpha with or without E(2) (10(-8) M) treatment could activate caspase -8, -9, and 3 and induce DNA fragmentation in LoVo cell.
  • In addition, E(2) plus ERalpha significantly upregulated p21 and p27 levels and downregulated the beta-catenin and its target genes, cyclin D1 and Rb, which regulate the cell cycle and cell proliferation.
  • The results indicate that E(2) plus overexpressed ERalpha induce LoVo cell apoptosis might mediate through the increase of hTNF-alpha gene expression, which in turn activate caspase-8, -9 and caspase-3 and lead to the DNA fragmentation and apoptosis.
  • E(2) plus ERalpha also showed the downregulation of beta-catenin signalings implicating the suppression of proliferation and metastasis of colorectal cells.
  • [MeSH-major] Apoptosis. Colonic Neoplasms / pathology. Estrogen Receptor alpha / metabolism. Gene Expression Regulation. Signal Transduction. Tumor Necrosis Factor-alpha / genetics. beta Catenin / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / metabolism. Caspases / metabolism. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Proliferation. DNA Fragmentation. Down-Regulation / genetics. Estrogens / pharmacology. Female. Humans. Male. Middle Aged. Promoter Regions, Genetic / drug effects. Transfection. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / metabolism. Up-Regulation / genetics. Wnt Proteins / metabolism

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  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 16628468.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cell Cycle Proteins; 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / TNF protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; 0 / Wnt Proteins; 0 / beta Catenin; EC 3.4.22.- / Caspases
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99. Desai AA, McGuigan JE, Draganov P: Zollinger-Ellison phenotype in the absence of hypergastrinemia and islet-cell tumor. Int J Gastrointest Cancer; 2005;35(2):157-61
MedlinePlus Health Information. consumer health - Diarrhea.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Zollinger-Ellison phenotype in the absence of hypergastrinemia and islet-cell tumor.
  • Patients with the Zollinger-Ellison syndrome are characterized by islet-cell tumors, striking gastric acid hypersecretion, and peptic ulcer disease.
  • It is a rare syndrome caused by non-beta cell islet-cell tumors (gastrinomas) located in or in proximity to the pancreas.
  • We describe a patient presenting with clinical manifestations characteristic of the ZES with strikingly elevated gastric acid secretion,multiple ulcers in the first and second portions of the duodenum and diarrhea, but in absence of islet-cell tumor and/or hypergastrinemia.
  • [MeSH-minor] Adenoma, Islet Cell. Gastrins / blood. Humans. Male. Middle Aged. Pancreatic Neoplasms. Phenotype

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  • (PMID = 15879632.001).
  • [ISSN] 1537-3649
  • [Journal-full-title] International journal of gastrointestinal cancer
  • [ISO-abbreviation] Int J Gastrointest Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gastrins
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100. 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
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
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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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