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1. National Toxicology Program: Toxicology and carcinogenesis studies of alpha-methylstyrene (Cas No. 98-83-9) in F344/N rats and B6C3F1 mice (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2007 Nov;(543):1-210
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Toxicology and carcinogenesis studies of alpha-methylstyrene (Cas No. 98-83-9) in F344/N rats and B6C3F1 mice (inhalation studies).
  • alpha-Methylstyrene is used in the production of acrylonitrile-butadiene-styrene resins and copolymers, which improve the impact and heat-resistant properties of polymers, specialty grades of plastics, rubber, and protective coatings. alpha-Methylstyrene also moderates polymerization rates and improves product clarity in coatings and resins.
  • Low molecular weight liquid polymers are used as plasticizers in paints, waxes, adhesives, and plastics. alpha-Methylstyrene was nominated by the U.S.
  • Male and female F344/N rats and B6C3F1 mice were exposed to alpha-methylstyrene (99.5% pure) by inhalation for 3 months or 2 years.
  • Genetic toxicology studies were conducted in Salmonella typhimurium, cultured Chinese hamster ovary cells, and mouse peripheral blood erythrocytes.
  • 3-MONTH STUDY IN RATS: Groups of 10 male and 10 female rats were exposed by whole-body inhalation to alpha-methylstyrene at concentrations of 0, 75, 150, 300, 600, or 1,000 ppm for 6 hours per day, 5 days per week for 14 weeks.
  • Consistent with the hyaline droplet accumulation, an exposure-related increase in alpha2μ-globulin was detected in the kidneys of males exposed to alpha-methylstyrene.
  • Morphologic changes were not detected in the liver.
  • 3-MONTH STUDY IN MICE: Groups of 10 male and 10 female mice were exposed by whole-body inhalation to alpha-methylstyrene at concentrations of 0, 75, 150, 300, 600, or 1,000 ppm for 6 hours per day, 5 days per week for 14 weeks.
  • Minimal to mild centrilobular hypertrophy was present in the livers of male and female mice exposed to 600 or 1,000 ppm alpha-methylstyrene.
  • 2-YEAR STUDY IN RATS: Groups of 50 male and 50 female rats were exposed by whole body inhalation to alpha-methylstyrene at concentrations of 0, 100, 300, or 1,000 ppm for 6 hours per day, 5 days per week, except holidays, for 105 weeks.
  • Two 1,000 ppm males and one 300 ppm male had renal tubule carcinomas, and one 300 ppm male had a renal tubule adenoma.
  • Because of the neoplasms observed in 300 and 1,000 ppm males at the end of the 2-year study and the finding of alpha2μ-globulin accumulation in the kidneys at 3 months, which is often associated with kidney neoplasms, additional step sections of kidney were prepared; additional males with focal hyperplasia or adenoma were identified.
  • The incidences of renal tubule adenoma and carcinoma (combined) in the 1,000 ppm males were significantly greater than those in the chamber controls when the single and step sections were combined.
  • The incidence of mononuclear cell leukemia in 1,000 ppm males was significantly increased compared to the chamber controls.
  • In the nose, the incidences of basal cell hyperplasia were significantly increased in all exposed groups of males and females, and the incidences of degeneration of the olfactory epithelium were increased in 1,000 ppm males and females and 300 ppm females.
  • 2-YEAR STUDY IN MICE: Groups of 50 male and 50 female mice were exposed by whole body inhalation to alpha-methylstyrene at concentrations of 0, 100, 300, or 600 ppm for 6 hours per day, 5 days per week, except holidays, for 105 weeks.
  • The incidences of hepatocellular adenoma or carcinoma (combined) were significantly increased in the 100 and 600 ppm males and in all exposed groups of females.
  • The incidences of hepatocellular adenoma were significantly increased in all exposed groups of females, and the incidences in all exposed groups of males and females exceeded the historical range for chamber controls.
  • GENETIC TOXICOLOGY: alpha-Methylstyrene was not mutagenic in four strains of Salmonella typhimurium, with or without rat or hamster liver metabolic activation enzymes (S9).
  • alpha-Methylstyrene did not induce chromosomal aberrations in cultured Chinese hamster ovary cells, with or without S9 activation, but did significantly increase the frequency of sister chromatid exchanges in cultures exposed in the presence of S9.
  • CONCLUSIONS: Under the conditions of this 2-year inhalation study, there was some evidence of carcinogenic activity of alpha-methylstyrene in male F344/N rats based on increased incidences of renal tubule adenomas and carcinomas (combined).
  • The increased incidence of mononuclear cell leukemia in 1,000 ppm male F344/N rats may have been related to alpha-methylstyrene exposure.
  • There was no evidence of carcinogenic activity of alpha-methylstyrene in female F344/N rats exposed to 100, 300, or 1,000 ppm.
  • There was equivocal evidence of carcinogenic activity of alpha-methylstyrene in male B6C3F1 mice based on marginally increased incidences of hepatocellular adenoma or carcinoma (combined).
  • There was clear evidence of carcinogenic activity of alpha-methylstyrene in female B6C3F1 mice based on increased incidences of hepatocellular adenomas and carcinomas.
  • Exposure of rats to alpha-methylstyrene resulted in kidney toxicity, which in males exhibited some features of alpha2μ-globulin nephropathy.
  • Exposure to alpha-methylstyrene resulted in nonneoplastic lesions of the nose in male and female rats and mice and of the liver and kidney in female mice.
  • [MeSH-minor] Animals. Body Weight / drug effects. CHO Cells. Cricetinae. Cricetulus. DNA Damage. Female. Inhalation Exposure. Kidney / drug effects. Kidney / pathology. Kidney Neoplasms / chemically induced. Kidney Neoplasms / pathology. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / pathology. Liver Neoplasms / chemically induced. Liver Neoplasms / pathology. Male. Mice. Mice, Inbred Strains. Micronuclei, Chromosome-Defective / chemically induced. Nose Diseases / chemically induced. Rats. Rats, Inbred F344

  • Hazardous Substances Data Bank. ALPHA-METHYL STYRENE .
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  • (PMID = 18685715.001).
  • [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 / Air Pollutants, Occupational; 0 / Carcinogens; 0 / Mutagens; 0 / Styrenes; 98-83-9 / alpha-methylstyrol
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2. Lewis RB, Lattin GE Jr, Paal E: Pancreatic endocrine tumors: radiologic-clinicopathologic correlation. Radiographics; 2010 Oct;30(6):1445-64
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  • [Title] Pancreatic endocrine tumors: radiologic-clinicopathologic correlation.
  • Pancreatic endocrine tumors (PETs) are primarily well-differentiated tumors composed of cells that resemble normal islet cells but that arise from pancreatic ductal cells.
  • They are classified as functioning or nonfunctioning according to their associated clinical symptoms; insulinoma, gastrinoma, and glucagonoma are the most common functioning PETs.
  • Most are sporadic, but some are associated with familial syndromes such as multiple endocrine neoplasia type 1, von Hippel-Lindau syndrome, and neurofibromatosis type 1.
  • At imaging, PETs typically appear as well-defined hypervascular masses, a finding indicative of their rich capillary network.
  • Cystic change, calcification, and necrosis are common in large tumors, which are associated with a poorer prognosis and a higher prevalence of local and vascular invasion and metastases than are smaller tumors.
  • Poorly differentiated PETs are rare and have an infiltrative appearance; patients with such tumors have a poor prognosis.
  • Knowledge of the characteristic clinical, pathologic, and radiologic features of PETs is important in the evaluation and management of patients with a suspected clinical syndrome or a pancreatic mass.
  • [MeSH-major] Diagnostic Imaging. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / epidemiology. Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / epidemiology. Carcinoma, Islet Cell / pathology. Diagnosis, Differential. Humans. Multiple Endocrine Neoplasia Type 1 / pathology. Neurofibromatosis 1 / pathology. Prevalence. von Hippel-Lindau Disease / pathology

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  • [Copyright] © RSNA, 2010.
  • (PMID = 21071369.001).
  • [ISSN] 1527-1323
  • [Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc
  • [ISO-abbreviation] Radiographics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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3. Gupta N, Jadhav K, Ahmed MB, Amberkar VS: Basal cell adenoma in a relatively rare site. J Oral Maxillofac Pathol; 2009 Jul;13(2):101-4
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  • [Title] Basal cell adenoma in a relatively rare site.
  • Basal cell adenoma (BCA) of the salivary glands is an uncommon type of monomorphic adenoma.
  • Histologically, it is seen as nests of isomorphic cells and interlaced trabeculae with a prominent basal membrane.
  • There is also slack, hyaline stroma with absence of a myxoid or chondroid component.
  • We describe a case of BCA of palatal minor salivary glands, a rare site for its occurrence.

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  • [ISSN] 0973-029X
  • [Journal-full-title] Journal of oral and maxillofacial pathology : JOMFP
  • [ISO-abbreviation] J Oral Maxillofac Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3162860
  • [Keywords] NOTNLM ; Basal cell adenoma / alpha smooth muscle actin / monomorphic adenoma / pancytokeratin / squamous morules
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4. Couvelard A, O'Toole D, Turley H, Leek R, Sauvanet A, Degott C, Ruszniewski P, Belghiti J, Harris AL, Gatter K, Pezzella F: Microvascular density and hypoxia-inducible factor pathway in pancreatic endocrine tumours: negative correlation of microvascular density and VEGF expression with tumour progression. Br J Cancer; 2005 Jan 17;92(1):94-101
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  • [Title] Microvascular density and hypoxia-inducible factor pathway in pancreatic endocrine tumours: negative correlation of microvascular density and VEGF expression with tumour progression.
  • Tumour-associated angiogenesis is partly regulated by the hypoxia-inducible factor (HIF) pathway.
  • The aim of this study is to evaluate angiogenesis and expression of HIF-related molecules in a series of patients with pancreatic endocrine tumours (PETs).
  • The expression of vascular endothelial growth factor (VEGF), HIF-1alpha, HIF-2alpha and carbonic anhydrase 9 (CA9) was examined by immunohistochemistry in 45 patients with PETs and compared to microvascular density (MVD), endothelial proliferation, tumour stage and survival.
  • The regulation of HIF signalling appears to be specific in pancreatic endocrine tumours.
  • [MeSH-major] Adenoma, Islet Cell / blood supply. Adenoma, Islet Cell / metabolism. Neovascularization, Pathologic. Pancreatic Neoplasms / blood supply. Pancreatic Neoplasms / metabolism. Vascular Endothelial Growth Factors / metabolism
  • [MeSH-minor] Adult. Basic Helix-Loop-Helix Transcription Factors. Carbonic Anhydrases / metabolism. Disease Progression. Female. Humans. Hypoxia-Inducible Factor 1, alpha Subunit. Male. Microcirculation. Transcription Factors / metabolism

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  • (PMID = 15558070.001).
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Transcription Factors; 0 / Vascular Endothelial Growth Factors; 0 / endothelial PAS domain-containing protein 1; EC 4.2.1.1 / Carbonic Anhydrases
  • [Other-IDs] NLM/ PMC2361752
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5. Dourakis SP, Alexopoulou A, Georgousi KK, Delladetsima JK, Tolis G, Archimandritis AJ: Glucagonoma syndrome: survival 21 years with concurrent liver metastases. Am J Med Sci; 2007 Sep;334(3):225-7
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  • [Title] Glucagonoma syndrome: survival 21 years with concurrent liver metastases.
  • A patient who survived for 21 years since initial discovery of glucagonoma with concurrent liver metastases is described.
  • Psychiatric symptoms, weight loss, necrolytic migratory erythema, diarrhea, and diabetes mellitus developed gradually after diagnosis of the tumor.
  • The longevity of this patient may be related to the slow tumor growth expressed histologically by ischemic necrosis of the malignant cells and in imaging by extensive tumor calcifications, a very rare finding in this type of the tumor.
  • [MeSH-major] Glucagonoma / pathology. Liver Neoplasms / secondary. Pancreatic Neoplasms / pathology


6. Couvelard A, Deschamps L, Rebours V, Sauvanet A, Gatter K, Pezzella F, Ruszniewski P, Bedossa P: Overexpression of the oxygen sensors PHD-1, PHD-2, PHD-3, and FIH Is associated with tumor aggressiveness in pancreatic endocrine tumors. Clin Cancer Res; 2008 Oct 15;14(20):6634-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of the oxygen sensors PHD-1, PHD-2, PHD-3, and FIH Is associated with tumor aggressiveness in pancreatic endocrine tumors.
  • PURPOSE: Tumor hypoxia is associated with poor prognosis and resistance to treatment.
  • Our aim was to assess the expression of proteins that act as cellular oxygen sensors, directly regulating the hypoxia inducible factor (HIF) pathway, i.e., prolyl hydroxylase domain proteins (PHD)-1, PHD-2, PHD-3, and FIH in pancreatic endocrine tumors (PET).
  • The results were correlated with histoprognostic factors including Ki-67 index, presence of a fibrotic focus, and microvascular density (MVD).
  • FIH stromal expression was found in 23% of PETs and correlated with higher FIH nuclear expression (P = 0.0004) and poorer disease-free survival (P = 0.0018).
  • CONCLUSION: HIF regulatory proteins are highly expressed in PET and their expression is correlated with tumor metastases, tumor recurrence, and prognosis.
  • [MeSH-major] Cell Hypoxia. Dioxygenases / metabolism. Pancreatic Neoplasms / metabolism. Procollagen-Proline Dioxygenase / metabolism. Repressor Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Adenoma, Islet Cell / metabolism. Adenoma, Islet Cell / pathology. Adult. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / secondary. Cell Differentiation. Cell Proliferation. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Hypoxia-Inducible Factor-Proline Dioxygenases. Immunoenzyme Techniques. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lymphatic Metastasis. Male. Microcirculation. Mixed Function Oxygenases. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / metabolism. Neovascularization, Pathologic. Tissue Array Analysis

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  • (PMID = 18927305.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Repressor Proteins; EC 1.- / Mixed Function Oxygenases; EC 1.13.11.- / Dioxygenases; EC 1.14.11.- / HIF1AN protein, human; EC 1.14.11.2 / EGLN1 protein, human; EC 1.14.11.2 / Procollagen-Proline Dioxygenase; EC 1.14.11.29 / EGLN3 protein, human; EC 1.14.11.29 / Hypoxia-Inducible Factor-Proline Dioxygenases
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7. Nicol MR, Papacleovoulou G, Evans DB, Penning TM, Strachan MW, Advani A, Johnson SJ, Quinton R, Mason JI: Estrogen biosynthesis in human H295 adrenocortical carcinoma cells. Mol Cell Endocrinol; 2009 Mar 5;300(1-2):115-20
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  • [Title] Estrogen biosynthesis in human H295 adrenocortical carcinoma cells.
  • The direct secretion of estradiol by adrenocortical tumors requires, in addition to the expression of aromatase (CYP19), the expression of one or more of the reductive 17beta-hydroxysteroid dehydrogenases.
  • The expression of CYP19 transcripts and protein were markedly induced in the H295 adrenocortical carcinoma cell line after treatment with either forskolin or vasoactive intestinal peptide (VIP).
  • The reductive type 5 17beta-hydroxysteroid dehydrogenase (AKR1C3) was also constitutively expressed in the H295 cells but neither its mRNA transcript nor protein levels were altered after forskolin or VIP treatment.
  • Western immunoblotting of an estrogen-secreting adrenal carcinoma revealed notable levels of both aromatase and AKR1C3 expression while an aldosterone-producing adrenal adenoma lacked aromatase expression and showed a reduced level of AKR1C3 expression.
  • Immunohistochemistry of the carcinoma-bearing adrenal revealed localization of AKR1C3 not only in the tumor but also principally in the zona reticularis of the normal adrenal tissue.

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  • (PMID = 19026713.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA090744-07; United States / NCI NIH HHS / CA / R01 CA090744; United States / NCI NIH HHS / CA / R01 CA090744-07; United States / NCI NIH HHS / CA / R01-CA90744
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Estrogens; 1F7A44V6OU / Colforsin; 37221-79-7 / Vasoactive Intestinal Peptide; EC 1.1.- / 17-Hydroxysteroid Dehydrogenases; EC 1.1.- / 3-Hydroxysteroid Dehydrogenases; EC 1.1.1.- / AKR1C3 protein, human; EC 1.1.1.- / Hydroxyprostaglandin Dehydrogenases; EC 1.1.1.145 / 3 beta-hydroxysteroid dehydrogenase type II; EC 1.1.1.145 / Progesterone Reductase; EC 1.14.14.1 / Aromatase; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase
  • [Other-IDs] NLM/ NIHMS99072; NLM/ PMC2673546
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8. Wezensky SJ, Hanks TS, Wilkison MJ, Ammons MC, Siemsen DW, Gauss KA: Modulation of PLAGL2 transactivation by positive cofactor 2 (PC2), a component of the ARC/Mediator complex. Gene; 2010 Feb 15;452(1):22-34
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  • The pleomorphic adenoma gene (PLAG) family of transcription factors regulates a wide range of physiological processes, including cell proliferation, tissue-specific gene regulation, and embryonic development, although little is known regarding the mechanisms that regulate PLAG protein activity.
  • We show that PC2 cooperates with PLAGL2 and PU.1 to enhance the activity of a known PLAGL2 target promoter (NCF2).
  • The PLAGL2-binding element in the NCF2 promoter consisted of the core sequence of the bipartite PLAG1 consensus site, but lacked the G-cluster motif, and was recognized by PLAGL2 zinc fingers 5 and 6.
  • Co-immunoprecipitation and promoter-reporter studies reveal that the effect of PC2 on PLAGL2 target promoter activity was conferred via the C-terminus of PLAGL2, the region that is required for PC2 binding and contains the PLAGL2 activation domain.
  • Importantly, chromatin immunoprecipitation analysis and PC2 knockdown studies confirmed that endogenous PC2 protein associated with the NCF2 promoter in MM1 cells in the region occupied by PLAGL2, and was required for PLAGL2 target promoter activity in TNF-alpha-treated MM1 cells, respectively.

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  • [Copyright] Published by Elsevier B.V.
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  • (PMID = 20025940.001).
  • [ISSN] 1879-0038
  • [Journal-full-title] Gene
  • [ISO-abbreviation] Gene
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / RR-016455; United States / NCRR NIH HHS / RR / P20 RR16455-08; United States / NCRR NIH HHS / RR / RR-020185; United States / NCRR NIH HHS / RR / P20 RR024237-026650; United States / NCRR NIH HHS / RR / RR-024237; United States / NCRR NIH HHS / RR / RR024237-026650; United States / NCRR NIH HHS / RR / P20 RR024237; United States / NCRR NIH HHS / RR / P20 RR016455; United States / NCRR NIH HHS / RR / P20 RR020185
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MED15 protein, human; 0 / Mediator Complex; 0 / Multiprotein Complexes; 0 / PLAGL2 protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA-Binding Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / proto-oncogene protein Spi-1; 67763-97-7 / Insulin-Like Growth Factor II; EC 1.6.3.1 / NADPH Oxidase; EC 1.6.3.1 / NCF2 protein, human
  • [Other-IDs] NLM/ NIHMS166082; NLM/ PMC2815083
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9. Iino K, Oki Y, Yamashita M, Matsushita F, Hayashi C, Yogo K, Nishizawa S, Yamada S, Maekawa M, Sasano H, Nakamura H: Possible relevance between prohormone convertase 2 expression and tumor growth in human adrenocorticotropin-producing pituitary adenoma. J Clin Endocrinol Metab; 2010 Aug;95(8):4003-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Possible relevance between prohormone convertase 2 expression and tumor growth in human adrenocorticotropin-producing pituitary adenoma.
  • CONTEXT: Methods for preoperative diagnosis of prohormone convertase 2 (PC2)-positive ACTH-producing pituitary adenomas (APPAs) have not been established.
  • OBJECTIVE: This study was designed to understand the meaning of plasma alphaMSH levels and the role of cell proliferation-signaling molecules in PC2-positive APPAs.
  • RESULTS: Nine adenomas (47.4%) were immunopositive for PC2 and were large and invasive in nature.
  • Eight adenomas (42.1%) were immunopositive for both PC2 and p-Akt, and seven others (36.8%) were immunonegative for both, suggesting significant coexpression of PC2 and p-Akt in tumors.
  • CONCLUSIONS: Our study suggests that PC2 expression and Akt phosphorylation are related at the molecular level, resulting in a change in cell cycle and an increase in pituitary adenoma size.
  • An elevation of plasma alphaMSH could conjecture the activation of the phosphatidylinositol 3/Akt cascade in PC2-positive APPAs and may become a valuable clinical marker of tumor growth in Cushing's disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Proprotein Convertase 2 / metabolism. alpha-MSH / blood

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  • (PMID = 20501680.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 581-05-5 / alpha-MSH; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.21.94 / Proprotein Convertase 2
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10. Li W, Gomez E, Zhang Z: Immunohistochemical expression of stromal cell-derived factor-1 (SDF-1) and CXCR4 ligand receptor system in hepatocellular carcinoma. J Exp Clin Cancer Res; 2007 Dec;26(4):527-33
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  • [Title] Immunohistochemical expression of stromal cell-derived factor-1 (SDF-1) and CXCR4 ligand receptor system in hepatocellular carcinoma.
  • The alpha-chemokine stromal cell-derived factor-1 (SDF-1) and its receptor CXCR4 have been recognized for their roles in regulating neoangiogenesis.
  • Formalin-fixed paraffin-embedded tissue sections of 28 HCC, 7 hepatocellular adenoma (HA), 26 cirrotic nodules (CN) and 16 normal liver tissues (NLT) were immunostained for SDF-1 and CXCR4.
  • SDF-1 and CXCR4 are detected in sinusoidal endothelial cells in HCC tissue, and their expressions are significantly higher than in non-HCC tissues.
  • Overexpressions of SDF-1 and CXCR4 in sinusoidal endothelial cells in HCC suggest that the SDF-1/CXCR4 pathway plays a possible role in HCC progression through neoangiogenesis.
  • [MeSH-minor] Endothelial Cells / metabolism. Humans. Immunohistochemistry. Neovascularization, Pathologic. Signal Transduction

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  • (PMID = 18365549.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Chemokine CXCL12; 0 / Receptors, CXCR4
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11. Chaw L, Krop TM, Hood AF: What is your diagnosis? Necrolytic migratory erythema associated with a glucagonoma. Cutis; 2008 Jan;81(1):25, 30-2
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  • [Title] What is your diagnosis? Necrolytic migratory erythema associated with a glucagonoma.
  • [MeSH-major] Erythema / etiology. Glucagonoma / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes / pathology. Skin / pathology. Skin Diseases / etiology
  • [MeSH-minor] Female. Glucagon / blood. Humans. Middle Aged

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  • (PMID = 18306843.001).
  • [ISSN] 0011-4162
  • [Journal-full-title] Cutis
  • [ISO-abbreviation] Cutis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-92-5 / Glucagon
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12. Rao VP, Poutahidis T, Ge Z, Nambiar PR, Boussahmain C, Wang YY, Horwitz BH, Fox JG, Erdman SE: Innate immune inflammatory response against enteric bacteria Helicobacter hepaticus induces mammary adenocarcinoma in mice. Cancer Res; 2006 Aug 1;66(15):7395-400
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  • Here we report that infecting Rag2-deficient C57BL/6 Apc(Min/+) mice with an intestinal bacterial pathogen, Helicobacter hepaticus, significantly promotes mammary carcinoma in females and enhances intestinal adenoma multiplicity by a tumor necrosis factor alpha (TNFalpha)-dependent mechanism.
  • The mammary and intestinal tumor development as well as the increase in proinflammatory mediators is suppressed by adoptive transfer of interleukin 10-competent CD4+CD45RB(lo)CD25+ regulatory (T(R)) cells.
  • Furthermore, prior exposure of donor mice to H. hepaticus significantly enhances antitumor potency of their T(R) cells.
  • Interestingly, these microbially experienced T(R) cells suppress tumorigenesis more effectively in recipient mice irrespective of their tumor etiology.
  • These data suggest that infections with enteric pathogens enhance T(R)-cell potency and protect against epithelial cancers later in life, potentially explaining paradoxical increases in cancer risk in developed countries having more stringent hygiene practices.

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  • (PMID = 16885333.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / T32 RR 07036; United States / NIDDK NIH HHS / DK / R01 DK 52413; United States / NIAID NIH HHS / AI / R01 AI 52267-01; United States / NIEHS NIH HHS / ES / P30 ES002109; United States / NCI NIH HHS / CA / R01 CA 67529; United States / NIEHS NIH HHS / ES / P30 ES 02109; United States / NCI NIH HHS / CA / P01 CA 26731; United States / NCI NIH HHS / CA / R01 CA 108854
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Immunoglobulins; 0 / Rag2 protein, mouse; 0 / Receptors, Interleukin-2; 0 / Recombinant Fusion Proteins; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10
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13. Jeannot E, Poussin K, Chiche L, Bacq Y, Sturm N, Scoazec JY, Buffet C, Van Nhieu JT, Bellanné-Chantelot C, de Toma C, Laurent-Puig P, Bioulac-Sage P, Zucman-Rossi J: Association of CYP1B1 germ line mutations with hepatocyte nuclear factor 1alpha-mutated hepatocellular adenoma. Cancer Res; 2007 Mar 15;67(6):2611-6
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  • [Title] Association of CYP1B1 germ line mutations with hepatocyte nuclear factor 1alpha-mutated hepatocellular adenoma.
  • Biallelic somatic mutations of TCF1 coding for hepatocyte nuclear factor 1alpha (HNF1alpha) are found in 50% of the hepatocellular adenoma (HCA) cases usually associated with oral contraception.
  • For 10 genes (CYP1A1, CYP1A2, CYP3A4, CYP3A5, COMT, UGT2B7, NQO1, GSTM1, GSTP1, and GSTT1), we did not find mutations nor differences in the allele distribution among 32 women presenting HNF1alpha-mutated adenomas compared with 58 controls.
  • In contrast, we identified a CYP1B1 germ line heterozygous mutation in 4 of 32 women presenting HNF1alpha-mutated adenomas compared with none in 58 controls.
  • [MeSH-major] Adenoma, Liver Cell / genetics. Cytochrome P-450 Enzyme System / genetics. Germ-Line Mutation. Hepatocyte Nuclear Factor 1-alpha / genetics. Liver Neoplasms / genetics
  • [MeSH-minor] Adolescent. Adult. Alleles. Aryl Hydrocarbon Hydroxylases. Child. Cytochrome P-450 CYP1B1. Female. Genetic Predisposition to Disease. Genotype. Humans. Middle Aged. Mutagenesis, Site-Directed. Pedigree

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  • (PMID = 17363580.001).
  • [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 / Hepatocyte Nuclear Factor 1-alpha; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / CYP1B1 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP1B1
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14. Yoshida D, Kim K, Noha M, Teramoto A: Anti-apoptotic action by hypoxia inducible factor 1-alpha in human pituitary adenoma cell line, HP-75 in hypoxic condition. J Neurooncol; 2006 Jul;78(3):217-25
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  • [Title] Anti-apoptotic action by hypoxia inducible factor 1-alpha in human pituitary adenoma cell line, HP-75 in hypoxic condition.
  • Hypoxia-inducible factor-1 (HIF-1) alpha is the major transcription factor involved in the adaptive response to hypoxia.
  • The purpose of this study was to investigate whether HIF 1-alpha protects HP75 cells, pituitary adenoma cell line from hypoxia induced apoptosis.
  • HP75 was transfected with siRNA targeting HIF 1-alpha mRNA sequences or scrambled RNA duplexes, followed by subjected to hypoxia (1% oxygen) for 24 h, compared with normoxia (21%).
  • Membrane cDNA microarray was examined to detect gene profiling among the cell in normoxia, hypoxia, or hypoxia following the RNAi.
  • A significantly greater proportion of HP75 cells transfected with specific siRNA duplexes and subsequently exposed to hypoxia demonstrated apoptosis to a large extent when compared with non-transfected cells.
  • Transfection with specific siRNA duplexes knocked down HIF 1-alpha mRNA and protein expression in hypoxia-exposed cells by approximately 80%, whereas transfection with scrambled siRNA duplexes had no noticeable effect on HIF 1-alpha expression.
  • Microarray analysis indicated that HIF1-alpha down-regulated caspase-10.
  • These findings strongly suggest that HIF 1-alpha exerts an antiapoptotic role in HP75 in hypoxia.
  • [MeSH-major] Adenoma / metabolism. Apoptosis / physiology. Hypoxia / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Pituitary Neoplasms / metabolism
  • [MeSH-minor] Adaptation, Physiological. Cell Line, Tumor. Cell Survival / genetics. Cell Survival / physiology. DNA Fingerprinting. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. RNA, Messenger / analysis. RNA, Small Interfering. Transfection

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  • (PMID = 16779673.001).
  • [ISSN] 0167-594X
  • [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 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / RNA, Small Interfering
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15. Liu L, Qian J, Singh H, Meiers I, Zhou X, Bostwick DG: Immunohistochemical analysis of chromophobe renal cell carcinoma, renal oncocytoma, and clear cell carcinoma: an optimal and practical panel for differential diagnosis. Arch Pathol Lab Med; 2007 Aug;131(8):1290-7
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  • [Title] Immunohistochemical analysis of chromophobe renal cell carcinoma, renal oncocytoma, and clear cell carcinoma: an optimal and practical panel for differential diagnosis.
  • CONTEXT: The separation of chromophobe renal cell carcinoma, oncocytoma, and clear cell renal cell carcinoma using light microscopy remains problematic in some cases.
  • OBJECTIVE: To determine a practical immunohistochemical panel for the differential diagnosis of chromophobe carcinoma.
  • DESIGN: Vimentin, glutathione S-transferase alpha (GST-alpha), CD10, CD117, cytokeratin (CK) 7, and epithelial cell adhesion molecule (EpCAM) were investigated in 22 cases of chromophobe carcinoma, 17 cases of oncocytoma, and 45 cases of clear cell carcinoma.
  • RESULTS: Vimentin and GST-alpha expression were exclusively observed in clear cell carcinoma.
  • CD10 staining was more frequently detected in clear cell carcinoma (91%) than in chromophobe carcinoma (45%) and oncocytoma (29%).
  • CD117 was strongly expressed in chromophobe carcinoma (82%) and oncocytoma (100%), whereas none of the cases of clear cell carcinomas were immunoreactive.
  • EpCAM protein was expressed in all 22 cases of chromophobe carcinoma in more than 90% of cells, whereas all EpCAM-positive oncocytomas (5/17; 29%) displayed positivity in single cells or small cell clusters.
  • CONCLUSIONS: Using the combination of 3 markers (vimentin, GST-alpha, and EpCAM), we achieved 100% sensitivity and 100% specificity for the differential diagnosis of chromophobe carcinoma, oncocytoma, and clear cell carcinoma.
  • The pattern of "vimentin(-)/GST-alpha(-)" effectively excluded clear cell carcinoma, and homogeneous EpCAM expression confirmed the diagnosis of chromophobe carcinoma rather than oncocytoma.
  • CD117 and CK7 were also useful markers and could be used as second-line markers for the differential diagnosis, with high specificity (100%) and high sensitivity (90% and 86%, respectively).
  • [MeSH-major] Adenocarcinoma, Clear Cell / diagnosis. Adenoma, Oxyphilic / diagnosis. Biomarkers, Tumor / analysis. Carcinoma, Renal Cell / diagnosis. Immunoenzyme Techniques / methods. Kidney Neoplasms / diagnosis. Neoplasm Proteins / analysis
  • [MeSH-minor] Diagnosis, Differential. Fluorescent Antibody Technique, Indirect. Humans. Predictive Value of Tests


16. Sun W, Iijima T, Kano J, Kobayashi H, Li D, Morishita Y, Okubo C, Anami Y, Noguchi M: Frequent aberrant methylation of the promoter region of sterile alpha motif domain 14 in pulmonary adenocarcinoma. Cancer Sci; 2008 Nov;99(11):2177-84
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  • [Title] Frequent aberrant methylation of the promoter region of sterile alpha motif domain 14 in pulmonary adenocarcinoma.
  • Aberrant methylation of promoter CpG islands is known to be a major inactivation mechanism of tumor-suppressor and tumor-related genes.
  • In order to identify novel hypermethylated genes in early stage lung adenocarcinoma, we carried out methylated CpG island amplification, modified suppression subtractive hybridization, and methylation-specific polymerase chain reaction to identify aberrant methylation of CpG islands in the A/J mouse lung adenoma model, which histologically mimics the early stage of human pulmonary adenocarcinoma.
  • Of these two genes, we selected sterile alpha motif domain 14 (SAMD14) and further analyzed its methylation status and expression level by methylation-specific polymerase chain reaction and quantitative real-time polymerase chain reaction.
  • Most of the lung adenocarcinoma cell lines showed suppressed expression of SAMD14 together with hypermethylation at the promoter region, although an immortalized bronchial epithelium cell line (PL16B) did not show hypermethylation and did express SAMD14.
  • Hypermethylation at the CpG site of the SAMD14 promoter region was detected frequently in early invasive adenocarcinoma (8/24, 33.3%) but not in in situ adenocarcinoma (0/7, 0%) or normal lung tissue (0/31, 0%).
  • [MeSH-major] Adenocarcinoma / genetics. DNA Methylation. Lung Neoplasms / genetics. Promoter Regions, Genetic / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. CpG Islands. DNA, Neoplasm / metabolism. Female. Humans. Kinesin / genetics. Kinesin / metabolism. Male. Mice. Mice, Inbred Strains. Middle Aged. Tumor Cells, Cultured

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  • (PMID = 18823374.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / KIF21A protein, human; 0 / Kif21a protein, mouse; 0 / Tumor Suppressor Proteins; EC 3.6.1.- / Kinesin
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17. Oberg K: Pancreatic endocrine tumors. Semin Oncol; 2010 Dec;37(6):594-618
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  • [Title] Pancreatic endocrine tumors.
  • Pancreatic endocrine tumors have been steadily growing in incidence and prevalence during the last two decades, showing an incidence of 4-5/1,000,000 population.
  • They represent a heterogeneous group with very varying tumor biology and prognosis.
  • About half of the patients present clinical symptoms and syndromes related to substances released from the tumors (Zollinger-Ellison syndrome, insulinoma, glucagonoma, etc) and the other half are so-called nonfunctioning tumors mainly presenting with symptoms such as obstruction, jaundice, bleeding, and abdominal mass.
  • Ten percent to 15% of the pancreatic endocrine tumors are part of an inherited syndrome such as multiple endocrine neoplasia type 1 (MEN-1), von Hippel-Lindau (VHL), neurofibromatosis, or tuberousclerosis.
  • The diagnosis is based on histopathology demonstrating neuroendocrine features such as positive staining for chromogranin A and specific hormones such as gastrin, proinsulin, and glucagon.
  • Moreover, the biochemical diagnosis includes measurement of chromogranins A and B or specific hormones such as gastrin, insulin, glucagon, and vasoactive intestinal polypeptide (VIP) in the circulation.
  • Surgery is still one of the cornerstones in the management of pancreatic endocrine tumors, but curative surgery is rarely obtained in most cases because of metastatic disease.
  • Cytotoxic drugs, biological agents, such as somatostatin analogs, alpha interferons, mammalian target of rapamycin (mTOR) inhibitors and tyrosine kinase inhibitors are routinely used.
  • Tumor-targeted radioactive treatment is available in many centres in Europe and is effective in patients with tumors that express high content of somatostatin receptors type 2 and 5.
  • In the future, treatment will be based on tumor biology and molecular genetics with the aim of so-called personalized medicine.
  • [MeSH-major] Pancreatic Neoplasms
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Biological Therapy / methods. Biomarkers, Tumor. Humans. Neoplastic Syndromes, Hereditary / diagnosis. Neoplastic Syndromes, Hereditary / therapy. Pancreatectomy. Paraneoplastic Endocrine Syndromes / diagnosis. Paraneoplastic Endocrine Syndromes / therapy


18. Gasparre G, Hervouet E, de Laplanche E, Demont J, Pennisi LF, Colombel M, Mège-Lechevallier F, Scoazec JY, Bonora E, Smeets R, Smeitink J, Lazar V, Lespinasse J, Giraud S, Godinot C, Romeo G, Simonnet H: Clonal expansion of mutated mitochondrial DNA is associated with tumor formation and complex I deficiency in the benign renal oncocytoma. Hum Mol Genet; 2008 Apr 1;17(7):986-95
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  • [Title] Clonal expansion of mutated mitochondrial DNA is associated with tumor formation and complex I deficiency in the benign renal oncocytoma.
  • Here we show a benign tumor type in which mtDNA mutations that lead to complex I (CI) enzyme deficiency are found in all tumors and are the only genetic alteration detected.
  • Actually renal oncocytomas are homogeneous tumors characterized by dense accumulation of mitochondria and we had found that they are deficient in electron transport chain complex I (CI, NADH-ubiquinone oxidoreductase).
  • In this work total sequencing of mtDNA showed that 9/9 tumors harbored point mutations in mtDNA, seven in CI genes, one in complex III, and one in the control region.
  • All tumors were somatically deficient for CI.
  • The clonal amplification of mutated mtDNA in 8/9 tumors demonstrates that these alterations are selected and therefore favor or trigger growth.
  • We hypothesize that functional deficiency of the oxidative phosphorylation CI could create a loop of amplification of mitochondria during cell division, impair substrates oxidation and increase intermediary metabolites availability.
  • [MeSH-major] Adenoma, Oxyphilic / genetics. DNA, Mitochondrial / genetics. Electron Transport Complex I / genetics. Kidney Neoplasms / genetics
  • [MeSH-minor] Cell Culture Techniques. Cell Nucleus / genetics. Cell Proliferation. Citrate (si)-Synthase / metabolism. DNA Mutational Analysis. DNA-Directed DNA Polymerase / genetics. Electron Transport Chain Complex Proteins / genetics. Electron Transport Chain Complex Proteins / metabolism. Gene Amplification. Glucose / metabolism. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. NADH Dehydrogenase / metabolism. Nucleic Acid Hybridization. Oxidative Phosphorylation. RNA, Messenger / genetics. RNA, Messenger / metabolism. Sequence Analysis, DNA

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  • (PMID = 18156159.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Mitochondrial; 0 / Electron Transport Chain Complex Proteins; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; EC 1.6.5.3 / Electron Transport Complex I; EC 1.6.99.3 / NADH Dehydrogenase; EC 2.3.3.1 / Citrate (si)-Synthase; EC 2.7.7.- / POLG protein, human; EC 2.7.7.7 / DNA-Directed DNA Polymerase; IY9XDZ35W2 / Glucose
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19. Pawlikowski M, Winczyk K: Immunohistochemical detection of prothymosin alpha in pituitary adenomas--a new marker of tumor recurrence? Folia Histochem Cytobiol; 2009;47(4):559-62
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  • [Title] Immunohistochemical detection of prothymosin alpha in pituitary adenomas--a new marker of tumor recurrence?
  • Forty pituitary adenomas were immunostained with an antibody raised against the C-terminal fragment (101-109) of human prothymosin alpha (PT alpha).
  • The strong positive immunostaining was found in the subpopulation of cell nuclei and intratumoral vessel walls, while the cytoplasm of adenoma cells was slightly immunopositive.
  • The significantly higher percentage of PT alpha-positive cell nuclei was found in recurrent pituitary adenomas as compared with primary tumors.
  • However, there was no correlation between the percentage of PT alpha-positive cell nuclei and Ki-67 indices.
  • Gonadotropinomas were characterized by higher nuclear PT alpha expression in comparison to other pituitary adenomas, which is probably linked with the high recurrence rate of these tumors.
  • It is suggested that PT alpha immunostaining may be helpful in predicting the pituitary tumor recurrence.
  • Moreover, PT alpha may be also useful as an immunohistochemical marker of the intratumoral microvasculature.

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  • (PMID = 20430720.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Protein Precursors; 0 / prothymosin alpha; 61512-21-8 / Thymosin
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20. 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.
  • 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.
  • 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.
  • [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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21. Levy A: Molecular and trophic mechanisms of tumorigenesis. Endocrinol Metab Clin North Am; 2008 Mar;37(1):23-50, vii
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  • Classical proto-oncogene activation and tumor suppressor mutation are rarely responsible, and no histologic or molecular markers reliably predict behavior.
  • GNAS1 activation and the mutations associated with multiple endocrine neoplasia type 1 and Carney complex, aryl hydrocarbon receptor interacting protein gene mutations, and a narrowing region of chromosome 11q13 in familial isolated acromegaly together account for such a small proportion of pituitary adenomas that the pituitary adenoma pathogenic epiphany is surely yet to come.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Pituitary Neoplasms / pathology
  • [MeSH-minor] Animals. GTP-Binding Protein alpha Subunits, Gs / genetics. GTP-Binding Protein alpha Subunits, Gs / physiology. Humans. Phenotype

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  • (PMID = 18226729.001).
  • [ISSN] 0889-8529
  • [Journal-full-title] Endocrinology and metabolism clinics of North America
  • [ISO-abbreviation] Endocrinol. Metab. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.1.- / GNAS protein, human; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  • [Number-of-references] 125
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22. Wang Y, Hua Q: [Clinical significance of HIF-1 alpha,VEGF and VEGF-C expression in papillary thyroid carcinoma]. Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi; 2007 Mar;21(5):204-6, 208
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  • [Title] [Clinical significance of HIF-1 alpha,VEGF and VEGF-C expression in papillary thyroid carcinoma].
  • OBJECTIVE: To evaluate clinical significance of HIF-1 alpha,VEGF and VEGF-C expression in papillary thyroid carcinoma.
  • METHOD: HIF-1a,VEGF and VEGF-C expression were detected by immunohistochemical method in 73 patients of papillary thyroid carcinoma(group I ), 32 patients of thyroid adenoma(group II) and 35 patients of nodular goiter(group II ) respectively.
  • RESULT: The expression of HIF-1 alpha in group I (75.
  • VEGF and VEGF-C expression had a positive correlation with HIF-1 alpha ( P <0. 05).
  • CONCLUSION: In papillary thyroid carcinoma, HIF-1 alpha, VEGF and VEGF-C expression are significantly increased.
  • Furthermore,VEGF and VEGF-C expression may be regulated by HIF-1 alpha, involving in the process of cancer cell spreading to lymph nodes.
  • [MeSH-major] Carcinoma, Papillary / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Thyroid Neoplasms / metabolism. Vascular Endothelial Growth Factor A / metabolism. Vascular Endothelial Growth Factor C / metabolism

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  • (PMID = 17536453.001).
  • [ISSN] 1001-1781
  • [Journal-full-title] Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology, head, and neck surgery
  • [ISO-abbreviation] Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] Controlled Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / VEGFA protein, human; 0 / VEGFC protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C
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23. Wagner S, Kiupel M, Peterson RA 2nd, Heikinheimo M, Wilson DB: Cytochrome b5 expression in gonadectomy-induced adrenocortical neoplasms of the domestic ferret (Mustela putorius furo). Vet Pathol; 2008 Jul;45(4):439-42
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  • We screened ferret adrenocortical tumor specimens for expression of cytochrome b(5) (cyt b(5)), an allosteric regulator that selectively enhances the 17,20-lyase activity of P450c17.
  • Cyt b(5) immunoreactivity was evident in 24 of 25 (96%) adrenocortical adenomas/carcinomas from ferrets with signs of ectopic sex steroid production.
  • Normal adrenocortical cells lacked cyt b(5), which may account for the low production of adrenal androgens in healthy ferrets.
  • Other markers characteristic of gonadal somatic cells, such as luteinizing hormone receptor, aromatase, and GATA4, were coexpressed with cyt b(5) in some of the tumors.
  • We concluded that cyt b(5) is upregulated during gonadectomy-induced adrenocortical neoplasia and is a marker of androgen synthetic potential in these tumors.

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  • [Cites] Vet Pathol. 2003 Mar;40(2):136-42 [12637752.001]
  • [Cites] J Endocrinol. 1983 Dec;99(3):361-8 [6417256.001]
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  • (PMID = 18587089.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK075618-02; United States / NIDDK NIH HHS / DK / P30 DK052574-09; United States / NIDDK NIH HHS / DK / R01 DK075618-02; United States / NIDDK NIH HHS / DK / DK52574; United States / NIDDK NIH HHS / DK / DK075618; United States / NIDDK NIH HHS / DK / P30 DK052574; United States / NIDDK NIH HHS / DK / R01 DK075618
  • [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 / GATA4 Transcription Factor; 0 / Receptors, LH; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins; 9035-39-6 / Cytochromes b5
  • [Other-IDs] NLM/ NIHMS45245; NLM/ PMC2497446
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24. Antoniades D, Epivatianos A, Markopoulos A, Kolokotronis A, Zaraboukas T: Coexistence of mucous retention cyst and basal cell adenoma arising from the lining epithelium of the cyst. Report of two cases. Med Princ Pract; 2009;18(3):248-52
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  • [Title] Coexistence of mucous retention cyst and basal cell adenoma arising from the lining epithelium of the cyst. Report of two cases.
  • OBJECTIVE: To report 2 cases of coexisting mucous retention cyst and basal cell adenoma arising from the lining epithelium of the cyst.
  • CLINICAL PRESENTATION AND INTERVENTION: Two cases of painless swellings, well-demarcated, soft to palpation, and located in the submucosa of the upper lip were clinically examined with the provisional diagnosis of mucocele or salivary gland tumor.
  • Histological examination showed the presence of a large unilocular cystic cavity in many parts surrounded by single or bilayered lining epithelium composed of flattened to cuboidal cells, and in other parts surrounded by projections of cells arranged in a trabecular pattern far into the cystic cavity.
  • The trabeculae were composed of basal and low columnar cells that sometimes formed small duct-like structures.
  • Immunohistochemistry showed that the lining epithelium of the cystic cavity and the cells of the projections expressed cytokeratin 7 and high-molecular-weight cytokeratins.
  • The cells of the projections were weakly positive for S-100 protein and negative for vimentin and alpha-smooth muscle actin.
  • Based on the results, a diagnosis of coexisting mucous retention cysts and basal cell adenomas arising from the lining epithelium of cysts was made.
  • CONCLUSION: The coexistence of mucous retention cysts and basal cell adenomas arising from the lining epithelium of the cyst is reported.
  • [MeSH-major] Adenoma / complications. Adenoma / pathology. Mucocele / complications. Mucocele / pathology. Salivary Gland Diseases / complications. Salivary Gland Diseases / pathology

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19349732.001).
  • [ISSN] 1423-0151
  • [Journal-full-title] Medical principles and practice : international journal of the Kuwait University, Health Science Centre
  • [ISO-abbreviation] Med Princ Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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25. Kumanov P, Nandipati KC, Tomova A, Robeva R, Agarwal A: Significance of inhibin in reproductive pathophysiology and current clinical applications. Reprod Biomed Online; 2005 Jun;10(6):786-812
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  • It is a glycoprotein hormone secreted by the Sertoli cells of the testis and granulosa and theca cells of the ovary.
  • Current understanding of inhibin physiology and pathology in the human suggests that inhibin B may be of importance as a marker of Sertoli cell function in men with infertility and as a prognostic indicator in women undergoing ovulation induction therapy.
  • Inhibin concentrations are elevated in patients with granulosa cell tumours and in post-menopausal women with mucinous ovarian cancers.
  • Immunoreactivity against the inhibin alpha-subunit was identified in all cases of adrenal cortical adenoma and carcinoma, and levels are suppressed in the malignant prostate disease.
  • [MeSH-minor] Activins / chemistry. Activins / metabolism. Adult. Age Factors. Chromosomes, Human, Y. Exocrine Glands / metabolism. Female. Fertilization in Vitro / methods. Follistatin / chemistry. Follistatin / metabolism. Humans. Infant, Newborn. Male. Menstrual Cycle / physiology. Ovarian Neoplasms / blood. Polycystic Ovary Syndrome / physiopathology. Pregnancy. Sequence Deletion. alpha-Macroglobulins / chemistry. alpha-Macroglobulins / metabolism

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  • (PMID = 15970011.001).
  • [ISSN] 1472-6483
  • [Journal-full-title] Reproductive biomedicine online
  • [ISO-abbreviation] Reprod. Biomed. Online
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Follistatin; 0 / alpha-Macroglobulins; 104625-48-1 / Activins; 57285-09-3 / Inhibins
  • [Number-of-references] 114
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26. Waalkes MP, Liu J, Ward JM, Powell DA, Diwan BA: Urogenital carcinogenesis in female CD1 mice induced by in utero arsenic exposure is exacerbated by postnatal diethylstilbestrol treatment. Cancer Res; 2006 Feb 1;66(3):1337-45
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  • Arsenic alone induced some urogenital system tumors, including mostly benign tumors of the ovary and uterus, and adrenal adenoma.
  • Diethylstilbestrol alone induced some tumors (primarily cervical) but when given after in utero arsenic, it greatly enhanced urogenital tumor incidence, multiplicity, and progression.
  • For instance, compared with the incidence of urogenital malignancies in the control (0%), arsenic alone (9%), and diethylstilbestrol alone (21%) groups, arsenic plus diethylstilbestrol acted synergistically, inducing a 48% incidence of malignant urogenital tumors.
  • Of the urogenital tumors induced by arsenic plus diethylstilbestrol, 80% were malignant, and 55% were multiple site.
  • Arsenic plus diethylstilbestrol increased ovarian, uterine, and vaginal tumors, and urinary bladder proliferative lesions, including three transitional cell carcinomas.
  • Tamoxifen alone did not increase urogenital tumors or affect arsenic-induced neoplasia but did increase arsenic-induced uroepithelial proliferative lesions.
  • Uterine and bladder carcinoma induced by arsenic plus diethylstilbestrol greatly overexpressed estrogen receptor-alpha (ER-alpha) and pS2, an estrogen-regulated gene.
  • In neonatal uteri, prenatal arsenic increased ER-alpha expression and enhanced estrogen-related gene expression induced by postnatal diethylstilbestrol.
  • [MeSH-minor] Animals. Body Weight / drug effects. Drinking / drug effects. Drug Synergism. Estrogen Receptor alpha / biosynthesis. Estrogen Receptor alpha / genetics. Female. Gene Expression / drug effects. Maternal-Fetal Exchange. Mice. Pregnancy. Tamoxifen / toxicity. Uterus / drug effects. Uterus / metabolism. Uterus / physiology

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  • (PMID = 16452187.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CO / N01 CO 12400; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 094ZI81Y45 / Tamoxifen; 731DCA35BT / Diethylstilbestrol; N712M78A8G / Arsenic
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27. Zamora V, Cabanne A, Salanova R, Bestani C, Domenichini E, Marmissolle F, Giacomi N, O'Connor J, Méndez G, Roca E, Buenos Aires and La Plata Argentina Argentum Working Group: Immunohistochemical expression of somatostatin receptors in digestive endocrine tumours. Dig Liver Dis; 2010 Mar;42(3):220-5
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  • The somatostatin receptors types 1-5 expression in a series including 100 gastro-entero-pancreatic endocrine tumours were analysed.
  • METHODS: From a prospectively built database of patients with gastro-entero-pancreatic endocrine tumours referred from three institutions, 100 cases with clinical and pathological data were selected.
  • Somatostatin receptors expression by immunohistochemistry with somatostatin receptor types 1-5 antibodies in tissue paraffin sections were studied and correlated with the histological diagnosis according to the WHO classification, location and functional status.
  • RESULTS: Of the 100 cases, 67 were gastrointestinal tumours, 25 pancreatic and 8 liver metastasis of unknown origin.
  • Thirty-one of them were functioning tumours: 2 insulinomas, 5 gastrinomas, 1 glucagonoma and 23 carcinoids.
  • Somatostatin receptors expression was less frequent in pancreatic than in gastrointestinal tumours.
  • CONCLUSIONS: Immunohistochemistry revealed that somatostatin receptors were highly expressed in both primary and metastatic gastro-entero-pancreatic endocrine tumours with heterogeneous staining distribution.
  • It proved to be a reliable technique even in small tumour samples.

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  • [Copyright] 2009 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
  • [CommentIn] Dig Liver Dis. 2010 Mar;42(3):173-4 [20117969.001]
  • (PMID = 19819769.001).
  • [ISSN] 1878-3562
  • [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; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, Somatostatin
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28. Laumonier H, Rullier A, Saric J, Balabaud C, Bioulac-Sage P: Unexpected discovery of 2 cases of hepatocyte nuclear factor 1alpha-mutated infracentimetic adenomatosis. World J Gastroenterol; 2008 Aug 14;14(30):4830-3
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  • We present 2 cases of hepatocyte nuclear factor 1alpha (HNF1alpha)-mutated adenomatosis, discovered for reasons unrelated to this disease, and identified using immunohistochemical methods.
  • These new tools may further our understanding of the link between adenomas/adenomatosis subtypes and their complications, and their association with other abnormalities.

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  • (PMID = 18720549.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA095817
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha
  • [Other-IDs] NLM/ PMC2739350
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29. Mizuno T, Hiraoka H, Yoshioka C, Takeda Y, Matsukane Y, Shimoyama N, Morimoto M, Hayashi T, Okuda M: Superficial necrolytic dermatitis associated with extrapancreatic glucagonoma in a dog. Vet Dermatol; 2009 Feb;20(1):72-9
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  • [Title] Superficial necrolytic dermatitis associated with extrapancreatic glucagonoma in a dog.
  • Based on histopathological findings, blood examinations and necropsy findings, the condition was diagnosed as superficial necrolytic dermatitis associated with a glucagon-secreting extrapancreatic neuroendocrine tumour.
  • Gross necropsy revealed tumour invasion into the spleen, liver, adrenal glands and mesenteric lymph nodes.
  • Immunohistochemical analysis of the neoplastic cells revealed that the tumour was a glucagonoma, consistent with earlier findings of persistent glucagonaemia and hypoaminoacidaemia.
  • [MeSH-major] Dermatitis / veterinary. Dog Diseases / pathology. Glucagonoma / veterinary

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  • (PMID = 19152590.001).
  • [ISSN] 1365-3164
  • [Journal-full-title] Veterinary dermatology
  • [ISO-abbreviation] Vet. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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30. 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.
  • The patient was treated with thyroid radioablation and hormone replacement and followed for 7 years, during which time the tumor grew to 4.6 cm.
  • At transsphenoidal surgery, a tumor consisting of a pituitary adenoma and adamantinomatous craniopharyngiomalike components was resected.
  • Both components were closely intermingled, but there was no evidence of an intermediate morphologic phenotype.
  • 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.
  • This lesion may represent an unusual composite tumor attributable to divergent differentiation of a common precursor.
  • 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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31. Krause W: Skin diseases in consequence of endocrine alterations. Aging Male; 2006 Jun;9(2):81-95
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  • There, knowledge of skin alterations is important not only for dermatologists, but also for endocrinologists and other physicians, because a clinical diagnosis of the underlying disease is often possible.
  • These include acanthosis nigricans, diseases due to alterations of androgen metabolism, carcinoid syndrome, diseases due to alterations of corticosteroid metabolism, diseases in association with diabetes mellitus, diseases due to alterations of estrogen metabolism, genetic syndromes including dermatological and endocrine symptoms, the glucagonoma syndrome, diseases due to dysfunctions of growth hormone secretion, diseases in association with Merkel cells of the skin, diseases due to dysfunctions of the thyroid gland, diseases to alteration of vitamin D metabolism, and vitiligo and disorders of pigmentation.
  • [MeSH-minor] Androgens / deficiency. Androgens / secretion. Estrogens / deficiency. Estrogens / secretion. Glucagonoma / etiology. Malignant Carcinoid Syndrome / etiology. Thyroid Hormones / deficiency. Thyroid Hormones / secretion. Vitamin D / secretion. Vitiligo / etiology

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  • (PMID = 16916743.001).
  • [ISSN] 1368-5538
  • [Journal-full-title] The aging male : the official journal of the International Society for the Study of the Aging Male
  • [ISO-abbreviation] Aging Male
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Estrogens; 0 / Thyroid Hormones; 1406-16-2 / Vitamin D
  • [Number-of-references] 71
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32. Davies K, Conlon KC: Neuroendocrine tumors of the pancreas. Curr Gastroenterol Rep; 2009 Apr;11(2):119-27
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  • [Title] Neuroendocrine tumors of the pancreas.
  • Pancreatic endocrine tumors are rare neoplasms accounting for less than 5% of pancreatic malignancies.
  • They are broadly classified into either functioning tumors (insulinomas, gastrinomas, glucagonomas, VIPomas, and somatostatinomas) or nonfunctioning tumors.
  • The diagnosis of these tumors is difficult and requires a careful history and examination combined with laboratory tests and radiologic imaging.
  • Signs and symptoms are usually related to hormone hypersecretion in the case of functioning tumors and to tumor size or metastases with nonfunctioning tumors.
  • Surgical resection remains the treatment of choice even in the face of metastatic disease.
  • Further development of novel diagnostic and treatment modalities offers potential to greatly improve quality of life and prolong disease-free survival for patients with pancreatic endocrine tumors.
  • [MeSH-major] Adenoma, Islet Cell. Carcinoma, Islet Cell. Pancreatic Neoplasms
  • [MeSH-minor] Algorithms. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Catheter Ablation. Chemoembolization, Therapeutic / methods. Evidence-Based Medicine. Gastrins / secretion. Glucagon / secretion. Humans. Insulin / secretion. Quality of Life. Somatostatin / secretion. Survival Analysis. Treatment Outcome

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  • (PMID = 19281699.001).
  • [ISSN] 1534-312X
  • [Journal-full-title] Current gastroenterology reports
  • [ISO-abbreviation] Curr Gastroenterol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gastrins; 0 / Insulin; 51110-01-1 / Somatostatin; 9007-92-5 / Glucagon
  • [Number-of-references] 44
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33. Hong J, Abudula R, Chen J, Jeppesen PB, Dyrskog SE, Xiao J, Colombo M, Hermansen K: The short-term effect of fatty acids on glucagon secretion is influenced by their chain length, spatial configuration, and degree of unsaturation: studies in vitro. Metabolism; 2005 Oct;54(10):1329-36
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  • [Title] The short-term effect of fatty acids on glucagon secretion is influenced by their chain length, spatial configuration, and degree of unsaturation: studies in vitro.
  • The influence of fatty acids on beta cell function has been well established whereas little is known about the role of fatty acids on alpha cell function.
  • The aim of our study was to investigate the short-term effects of chain length, spatial configuration, and degree of unsaturation of fatty acids on glucagon secretion from isolated mouse islets and alpha tumor cell 1 clone 6 cells (alpha TC1-6 cells).
  • Glucagon release was measured with different saturated and unsaturated fatty acids as well as cis and trans isomers of fatty acids at low and high glucose.
  • Palmitate (0.1-0.5 mmol/L) immediately stimulated glucagon release in a dose-dependent manner from both isolated islets and alpha TC 1-6 cells.
  • The longer chain length of saturated fatty acids, the higher glucagon responses were obtained.
  • The average fold increase in glucagon to saturated fatty acids (0.3 mmol/L) compared to control was octanoate 1.5, laurate 2.0, myristate 2.9, palmitate 5.4, and stearate 6.2, respectively.
  • Saturated fatty acids were more effective than unsaturated fatty acids in stimulating glucagon secretion.
  • Fatty acids immediately stimulate glucagon secretion from isolated mouse islets pancreatic alpha cells.
  • [MeSH-major] Fatty Acids / pharmacology. Glucagon / secretion

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  • (PMID = 16154432.001).
  • [ISSN] 0026-0495
  • [Journal-full-title] Metabolism: clinical and experimental
  • [ISO-abbreviation] Metab. Clin. Exp.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids; 0 / Insulin; 9007-92-5 / Glucagon
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34. Katori H, Nozawa A, Tsukuda M: Expression of epidermal growth factor receptor, transforming growth factor-alpha and Ki-67 in relationship to malignant transformation of pleomorphic adenoma. Acta Otolaryngol; 2007 Nov;127(11):1207-13
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  • [Title] Expression of epidermal growth factor receptor, transforming growth factor-alpha and Ki-67 in relationship to malignant transformation of pleomorphic adenoma.
  • The data support the hypothesis that increased epidermal growth factor receptor (EGFR) and transforming growth factor (TGF)-alpha expression is associated with early events in malignant transformation of pleomorphic adenoma (PA).
  • OBJECTIVE: In the present study, we attempted to identify EGFR and TGF-alpha expression and Ki-67 index in carcinoma ex-pleomorphic adenoma (Ca ex-PA) and PA.
  • We also compared the presence of EGFR and TGF-alpha and Ki-67 index with clinical data.
  • MATERIALS AND METHODS: The tissues were stained with monoclonal antibodies to EGFR, TGF-alpha and Ki-67.
  • RESULTS: As regards the association of patients' prognosis with EGFR staining and Ki-67 index, a significant increase was observed in patients who died or had residual disease compared with patients who were alive without disease.
  • In the immunohistochemical analysis of EGFR and TGF-alpha and Ki67 index, a significant increase was observed in Ca ex-PA, especially with adenocarcinoma, compared with PA and sialadenitis.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. Biomarkers, Tumor / biosynthesis. Cell Transformation, Neoplastic. Ki-67 Antigen / genetics. Receptor, Epidermal Growth Factor / biosynthesis. Salivary Gland Neoplasms / metabolism. Transforming Growth Factor alpha / biosynthesis

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  • (PMID = 17851915.001).
  • [ISSN] 0001-6489
  • [Journal-full-title] Acta oto-laryngologica
  • [ISO-abbreviation] Acta Otolaryngol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Transforming Growth Factor alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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35. Brown RL, Muzzafar T, Wollman R, Weiss RE: A pituitary carcinoma secreting TSH and prolactin: a non-secreting adenoma gone awry. Eur J Endocrinol; 2006 May;154(5):639-43
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  • [Title] A pituitary carcinoma secreting TSH and prolactin: a non-secreting adenoma gone awry.
  • To our knowledge, only one case of a TSH-secreting carcinoma has previously been reported.
  • We describe here a second patient with a pituitary carcinoma producing TSH and prolactin (PRL).
  • Except for mildly increased PRL and elevated alpha-subunit, hormone evaluation was normal.
  • Pathologic examination revealed a chromophobe adenoma with increased mitotic forms.
  • Nine months later, the patient underwent further debulking of metastatic disease.
  • Although development of a carcinoma from a pituitary adenoma is very rare (<0.5%), macroadenomas that become hormonally active should be suspect for transformation into pituitary cancer.

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  • (PMID = 16645009.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK07011; United States / NCRR NIH HHS / RR / RR00055; United States / NCRR NIH HHS / RR / RR18372
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin
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36. Ozenne V, Paradis V, Vullierme MP, Vilgrain V, Leblanc T, Belghiti J, Imbert A, Valla DC, Degos F: Liver tumours in patients with Fanconi anaemia: a report of three cases. Eur J Gastroenterol Hepatol; 2008 Oct;20(10):1036-9
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  • Fanconi anaemia is an autosomal recessive disease, causing secondary aplastic anaemia and congenital abnormalities, associated with an increased risk of tumours.
  • Liver cell adenoma and hepatocellular carcinoma have rarely been described.
  • Alpha-fetoprotein levels were normal in all cases.
  • Patient 2 had hepatic nodules diagnosed at routine examination with radiological features of adenomas.
  • The patient underwent resection, which showed liver cell adenoma with foci of carcinoma.
  • Patient 3 had three nodules, with radiological and histological diagnosis of adenoma.
  • In patients with Fanconi anaemia, androgen therapy and iron overload may contribute to the development of liver cell adenoma and hepatocellular carcinoma.
  • Hepatocellular carcinoma may occur as a transformation of liver cell adenoma.
  • [MeSH-major] Adenoma, Liver Cell / etiology. Carcinoma, Hepatocellular / etiology. Fanconi Anemia / complications. Liver Neoplasms / etiology

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  • (PMID = 18787475.001).
  • [ISSN] 1473-5687
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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37. Igaz P: MEN1 clinical background. Adv Exp Med Biol; 2009;668:1-15
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  • Multiple endocrine neoplasia Type 1 (MEN1) is a rare hereditary tumor syndrome predisposing to tumor development in several endocrine organs.
  • Its major manifestations include hyperparathyroidism, tumors of endocrine pancreas and pituitary.
  • Beside these three, several other endocrine (adrenocortical, foregut carcinoid) and nonendocrine (lipoma, angiofibroma, collagenoma, ependymoma, meningioma) tumors have been described to be associated with this syndrome.
  • Both familial and sporadic forms of the disease are known.
  • The diagnosis of MEN1 can be established if two of the three major manifestations are found in the same patient, whereas the diagnosis of familial MEN1 requires one MEN1 patient and a first degree relative with at least one MEN1 manifestation.
  • Both benign (parathyroid, anterior pituitary) and malignant (gastrinoma, glucagonoma) lesions may develop in MEN1 patients.
  • Regular surveillance of MEN1 gene mutation carriers is necessary to reveal disease manifestations.
  • Several diagnostic modalities can be used to screen for and to examine MEN1-related tumors.
  • The therapy of MEN1-associated tumors requires specific approach in some cases, as multiple tumors and recurrence is frequently observed.
  • [MeSH-minor] Adult. Child. Child, Preschool. Diagnosis, Differential. Genetic Predisposition to Disease. Genetic Testing. Humans. Middle Aged. Multiple Endocrine Neoplasia Type 2a / genetics. Multiple Endocrine Neoplasia Type 2a / pathology. Multiple Endocrine Neoplasia Type 2a / physiopathology. Mutation. Young Adult

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  • (PMID = 20175448.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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38. Paner GP, Luthringer DJ, Amin MB: Best practice in diagnostic immunohistochemistry: prostate carcinoma and its mimics in needle core biopsies. Arch Pathol Lab Med; 2008 Sep;132(9):1388-96
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  • CONTEXT: The unrelenting challenge encountered when differentiating limited-volume prostate carcinoma and sometimes subtle variants from its many morphologic mimics has increased the use of ancillary immunohistochemistry in routine prostate needle biopsies.
  • The availability of prostate cancer-associated and basal cell-associated markers has been an invaluable addition to diagnostic surgical pathology.
  • OBJECTIVE: To review commonly used immunohistochemical stains, including innovative combinations, for confirmation or differential diagnosis of prostate carcinoma, and to propose appropriately constructed panels using morphologic patterns in prostate needle biopsies.
  • CONCLUSIONS: Basal cell-associated markers p63, high-molecular-weight cytokeratin 34 beta E12, cytokeratin 5/6 or a cocktail containing p63 and high-molecular-weight cytokeratin 34 beta E12 or cytokeratin 5/6 and prostate carcinoma-specific marker alpha-methylacyl coenzyme A (coA) racemase alone or in combination are useful adjuncts in confirming prostatic carcinoma that either lacks diagnostic, qualitative or quantitative features or that has an unusual morphologic pattern (eg, atrophic, pseudohyperplastic) or is in the setting of prior treatment.
  • The combination of alpha-methylacyl coA racemase positivity with negative staining for basal cell-associated markers supports a malignant diagnosis in the appropriate morphologic context.
  • Dual chromogen basal cell- associated markers (p63 [nuclear] and high-molecular-weight cytokeratin 34 beta E12/cytokeratin 5/6 [cytoplasmic]) and alpha-methylacyl coA racemase in an antibody cocktail provide greater sensitivity for the basal cell layer, easing evaluation and minimizing loss of representation of the focal area interest because the staining is performed on one slide.
  • In the posttreatment setting, pancytokeratin facilitates detection of subtle-treated cancer cells.
  • Prostate-specific antigen and prostatic acid phosphatase markers are helpful in excluding secondary malignancies involving the prostate, such as urothelial carcinoma, and occasionally in excluding nonprostatic benign mimickers, such as nephrogenic adenoma, mesonephric gland hyperplasia, and Cowper glands.
  • [MeSH-major] Biomarkers, Tumor / analysis. Biopsy, Needle. Immunohistochemistry / methods. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Humans. Male

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  • (PMID = 18788849.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 47
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39. La Rosa S, Uccella S, Dainese L, Marchet S, Placidi C, Vigetti D, Capella C: Characterization of c-kit (CD117) expression in human normal pituitary cells and pituitary adenomas. Endocr Pathol; 2008;19(2):104-11
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  • [Title] Characterization of c-kit (CD117) expression in human normal pituitary cells and pituitary adenomas.
  • c-kit (CD117) is a tyrosine kinase receptor involved in the proliferation, differentiation, and secretory functions of various cells.
  • In experimental animal models, c-kit has been detected in the pars intermedia of the normal pituitary gland and in alpha-melanocyte-stimulating-hormone-positive adenomas and it has been suggested that it plays a role in regulating adrenocorticotropic hormone (ACTH) secretion.
  • To the best of our knowledge, the expression of c-kit in normal human pituitary cells and in pituitary adenomas has never been reported, so the possible biological role of this receptor in the control of pituitary hormone secretion remains unclear.
  • The aim of this study was to evaluate the immunohistochemical expression of c-kit in normal human pituitary glands and in a series of 62 well-characterized pituitary adenomas.
  • In normal adenohypophyses, several cells, mainly located in the central mucoid wedge, showed a c-kit immunoreactivity (IR).
  • Double label immunostaining procedures showed that the c-kit-IR cells corresponded to ACTH cells.
  • Out of 62 adenomas, 15 (24%) were c-kit-IR, including 7/16 (44%) ACTH cell, 3/7 (42%) null cell, 4/11 (36%) alpha-subunit cell, and 1/11 (10%) follicle-stimulating hormone-luteinizing hormone cell adenomas.
  • By contrast, all ten prolactin cell and seven growth hormone cell adenomas were c-kit negative.
  • [MeSH-major] Adenoma / metabolism. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism. Proto-Oncogene Proteins c-kit / biosynthesis
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adolescent. Adult. Aged. Blotting, Western. Child. Female. Follicle Stimulating Hormone / blood. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Growth Hormone-Secreting Pituitary Adenoma / pathology. Humans. Immunohistochemistry. Luteinizing Hormone / blood. Male. Middle Aged. Paraffin Embedding. Prolactinoma / metabolism. Prolactinoma / pathology. Tissue Fixation

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  • (PMID = 18568298.001).
  • [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] 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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40. Gin VC, Zacharias M: Glucagonoma: anaesthetic management. Anaesth Intensive Care; 2009 Mar;37(2):329-30
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  • [Title] Glucagonoma: anaesthetic management.
  • [MeSH-major] Anesthesia, General / methods. Glucagonoma / surgery. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Blood Glucose / analysis. Female. Glucagon / blood. Humans. Middle Aged

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  • (PMID = 19400510.001).
  • [ISSN] 0310-057X
  • [Journal-full-title] Anaesthesia and intensive care
  • [ISO-abbreviation] Anaesth Intensive Care
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Blood Glucose; 9007-92-5 / Glucagon
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41. Simonenko VB, Dulin PA, Beliaev LB, Makanin MA, Dem'ianenko AV, Zykova AA, Zhuravleva SI, Kolesnikova VN: [A case of pancreatic glucagonoma]. Klin Med (Mosk); 2007;85(8):67-70
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  • [Title] [A case of pancreatic glucagonoma].
  • Neuroendocrine tumor consisting of pancreatic alpha-cells -- glucagonoma -- is a very rare finding (one case per two million people a year).
  • This functionally active, usually malignant tumor has typical clinical manifestations.
  • Glucagonoma syndrome is a disease that has an original clinical picture that includes necrolytic migrating erythema with secondary bullous dermatitis, glucose tolerance disorder or diabetes mellitus, weight loss, anemia, hypoaminoacidemia, venous thrombosis, and alimentary and mental disturbances.
  • By the time diagnosis is made, 60 to 70% of glucagonomas already give metastases, and even small glucagonomas should be considered tumors with unknown malignant potential or malignant tumors.
  • Glucagonomas grow slowly, and patients live long (the survival median is approximately 15 years).
  • [MeSH-major] Glucagonoma / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 17926496.001).
  • [ISSN] 0023-2149
  • [Journal-full-title] Klinicheskaia meditsina
  • [ISO-abbreviation] Klin Med (Mosk)
  • [Language] rus
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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42. Tran N, McLean T, Zhang X, Zhao CJ, Thomson JM, O'Brien C, Rose B: MicroRNA expression profiles in head and neck cancer cell lines. Biochem Biophys Res Commun; 2007 Jun 22;358(1):12-7
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  • [Title] MicroRNA expression profiles in head and neck cancer cell lines.
  • In this study, the relative expression of 261 mature miRNA genes was determined in nine head and neck cancer cell lines using an oligonucleotide array platform.
  • Thirty-three miRNAs in the array were found to be highly expressed and 22 showed low levels of expression in all cell lines.
  • Potential targets of validated miRNAs included tumor suppressor genes, kinesin family member 1B isoform alpha (KIF1B), and hypermethylated in cancer 2 (HIC2), and pleomorphic adenoma gene 1 (PLAG1).
  • This study provides the largest genomewide survey of mature miRNA transcripts in head and neck cancer cell lines.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Head and Neck Neoplasms / metabolism. MicroRNAs / metabolism
  • [MeSH-minor] Cell Line, Tumor. DNA-Binding Proteins / metabolism. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Kinesin / metabolism. Nerve Tissue Proteins / metabolism. Oligonucleotide Array Sequence Analysis

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  • (PMID = 17475218.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / KIF1B protein, human; 0 / MicroRNAs; 0 / Nerve Tissue Proteins; 0 / PLAG1 protein, human; EC 3.6.1.- / Kinesin
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43. Warner RR: Enteroendocrine tumors other than carcinoid: a review of clinically significant advances. Gastroenterology; 2005 May;128(6):1668-84
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  • [Title] Enteroendocrine tumors other than carcinoid: a review of clinically significant advances.
  • Only relatively recently has there been an increased clinical recognition and characterization of the heterogeneous group of rare gastroenteropancreatic neuroendocrine neoplasms.
  • This review summarizes the derivation of these tumors and the advances in their diagnosis and treatment over the past decade and a half.
  • They are varied in their biological behavior and clinical courses and, depending on their cell type, can produce different hormones causing distinct clinical endocrine syndromes (insulinoma [hypoglycemia], gastrinoma [Zollinger-Ellison syndrome (ZES)], vasoactive intestinal peptideoma [VIPoma], watery diarrhea, hypokalemia-achlorhydria [WDHA], glucagonoma [glucagonoma syndrome], and so forth).
  • In addition to surgery for cure or palliation (by excision and a variety of other cytoreductive techniques), they each are treated with anti-hormonal agents or drugs targeted to each tumor's specific product or its effects.
  • Because of their usual slow rate of growth it is recommended that, even when they are advanced and incurable, unlike in patients with common and more malignant cancers, patients with neuroendocrine tumors often can be palliated and appear to survive longer when managed with an active approach using sequential multimodality treatment.
  • [MeSH-major] Carcinoma, Neuroendocrine. Gastrointestinal Neoplasms
  • [MeSH-minor] Carcinoid Tumor. Humans

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  • (PMID = 15887158.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 222
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44. Takehara K, Sakai H, Shono T, Irie J, Kanetake H: Proliferative activity and genetic changes in adrenal cortical tumors examined by flow cytometry, fluorescence in situ hybridization and immunohistochemistry. Int J Urol; 2005 Feb;12(2):121-7
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  • [Title] Proliferative activity and genetic changes in adrenal cortical tumors examined by flow cytometry, fluorescence in situ hybridization and immunohistochemistry.
  • BACKGROUND: To determine differences in biological features among different adrenal tumors, we investigated the DNA ploidy, numerical chromosomal aberration and proliferative activity in human adrenal cortical neoplasms.
  • METHODS: Our study included six adrenal cortical adenomas with Cushing syndrome, 12 adenomas with hyperaldosteronism, three non-functioning adenomas and three adrenal cortical carcinomas.
  • For FISH analysis, we used an alpha-centromeric enumeration probe for chromosome 17.
  • RESULTS: The mean Ki-67 labeling index (LI) of adrenal cortical carcinomas was markedly higher than that of adrenal cortical adenomas (209.4 vs 8.7).
  • In functional adrenal cortical adenomas, the LI was significantly lower in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004), although FCM results indicated that tetraploid patterns were more frequently observed in the former type.
  • Tumor size was significantly smaller in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004).
  • Chromosome 17 showed disomy in all adrenal cortical adenomas, whereas chromosome 17 abnormalities were found in two of three adrenal cortical carcinomas.
  • CONCLUSIONS: Our study characterized various biological features of benign and malignant adrenal cortical tumors.
  • The use of a combination of markers might provide additional information to assist our understanding of the clinical behavior of an individual adrenal cortical tumor.
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adult. Aged. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Carcinoma / genetics. Carcinoma / metabolism. Carcinoma / pathology. Cell Proliferation. Chromosomes, Human, Pair 17. Cushing Syndrome / genetics. Cushing Syndrome / metabolism. Cushing Syndrome / pathology. DNA, Neoplasm / genetics. Female. Humans. Hyperaldosteronism / genetics. Hyperaldosteronism / metabolism. Hyperaldosteronism / pathology. Ki-67 Antigen / metabolism. Male. Middle Aged. Ploidies. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15733104.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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45. Halsey MA, Calder KB, Mathew R, Schlauder S, Morgan MB: Expression of alpha-methylacyl-CoA racemase (P504S) in sebaceous neoplasms. J Cutan Pathol; 2010 Apr;37(4):446-51
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  • [Title] Expression of alpha-methylacyl-CoA racemase (P504S) in sebaceous neoplasms.
  • BACKGROUND: Alpha-methylacyl-CoA racemase (AMACR), also known as P504S, is a protein that plays an important role in mitochondrial and peroxisomal beta-oxidation of branched-chain fatty acid and bile acid intermediates.
  • AMACR has been established as a valuable diagnostic marker for prostate cancer and has recently been shown to be useful in the diagnosis of colorectal carcinoma.
  • METHODS: Five samples of normal sebaceous glands as well as five cases each of sebaceous hyperplasia (SH), sebaceous adenoma (SA), basal cell carcinoma (BCC) with sebaceous differentiation and extraocular sebaceous carcinoma (SC) were evaluated for immunohistochemical (IHC) expression of AMACR.
  • CONCLUSIONS: The expression of AMACR is increased in benign sebaceous glands and SH; with decreasing AMACR expression in tumors with less sebaceous differentiation (i.e.
  • [MeSH-major] Adenoma / enzymology. Carcinoma / enzymology. Racemases and Epimerases / metabolism. Sebaceous Gland Neoplasms / enzymology. Sebaceous Glands / enzymology

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  • (PMID = 19638170.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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46. Tomita T: Lymphatic vessel endothelial hyaluronan receptor 1 immunocytochemical staining for pancreatic islets and pancreatic endocrine tumors. Pancreas; 2007 Nov;35(4):e18-22
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  • [Title] Lymphatic vessel endothelial hyaluronan receptor 1 immunocytochemical staining for pancreatic islets and pancreatic endocrine tumors.
  • OBJECTIVES: Immunocytochemical staining for lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) is able to recognize lymphatic vessel endothelium and pancreatic endocrine cells (PETs).
  • Pancreatic endocrine tumors were studied for LYVE-1 immunocytochemical staining compared with normal pancreatic islets to detect possible presence of LYVE-1 in PETs.
  • METHODS: Twenty-five cases of primary and metastatic PETs were immunocytochemically stained for LYVE-1, including insulinomas, glucagonomas, somatostatinoma, pancreatic polypeptidomas, gastrinomas, and nonfunctioning tumors.
  • RESULTS: All normal pancreatic islet cells were positive for LYVE-1, whereas 2 cases of 25 PETs, 1 each of gastrinoma and nonfunctioning tumor, were positive for LYVE-1, retaining immunocytochemical reactivity of islet cells.
  • CONCLUSIONS: Normal pancreatic islets were positive for LYVE-1, whereas only 2 of 25 PETs were positive, suggesting that most PETs lost LYVE-1 or contained below detectable levels of LYVE-1.
  • The presence of LYVE-1 in pancreatic islets and in some PETs may suggest structure-function relationship of LYVE-1/lymphatic vessel in hormone synthesis and secretion.
  • [MeSH-major] Gastrinoma / chemistry. Glucagonoma / chemistry. Immunohistochemistry. Insulinoma / chemistry. Islets of Langerhans / chemistry. Pancreatic Neoplasms / chemistry. Somatostatinoma / chemistry. Vesicular Transport Proteins / analysis

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  • (PMID = 18090227.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / LYVE1 protein, human; 0 / Vesicular Transport Proteins
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47. Prout TM, Taylor AJ: Case of the season: glucagonoma syndrome. Semin Roentgenol; 2005 Jan;40(1):4-7
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  • [Title] Case of the season: glucagonoma syndrome.
  • [MeSH-major] Glucagonoma / radiography. Pancreatic Neoplasms / radiography
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Middle Aged. Syndrome. Tomography, X-Ray Computed


48. Marogy G, De Man M, Verslype C: Necrolytic migratory erythaema and glucagonoma syndrome. Acta Clin Belg; 2009 Jan-Feb;64(1):70-1
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  • [Title] Necrolytic migratory erythaema and glucagonoma syndrome.
  • [MeSH-major] Erythema / etiology. Glucagonoma / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Female. Humans. Middle Aged. Syndrome


49. Jalali M, Krishnamurthy S: Comparison of immunomarkers for the identification of adrenocortical cells in cytology specimens. Diagn Cytopathol; 2005 Aug;33(2):78-82
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  • [Title] Comparison of immunomarkers for the identification of adrenocortical cells in cytology specimens.
  • We studied the immunoreactivity of three antibodies--A103, calretinin, and inhibin alpha in destained Papanicolaou (Pap) smears and cell-blocks of 40 fine-needle aspiration biopsy cases of adrenocortical lesions (35 cases of hyperplasia/adenoma and 5 cases of carcinoma).
  • Five cases of carcinoma (4) and melanoma (1) metastases to the adrenal gland and five cases of renal-cell carcinoma were also included for comparison.
  • In benign adrenocortical lesions, A103 staining was noted in 82% of the destained Pap smears and in 92% of cell-blocks.
  • In malignant adrenocortical lesions, A103 staining was noted in 50% of the destained Pap smears and in 80% of cell-blocks.
  • In comparison, calretinin staining was noted in 6% and 50% of destained smears and in 78% and 60% of the cell-blocks of benign and malignant adrenocortical lesions.
  • Inhibin alpha was not positive in any of the smears and showed the lowest level of positivity in the cell-block sections, namely in 11% of the benign lesions and 25% of the malignant lesions.
  • The sensitivity of A103 was 90% on cell-blocks and 74% on smears, that of calretinin 75% on cell-blocks and 11% on smears, and that of inhibin alpha, 13% on cell-blocks alone.
  • Our data show A103 to be the immunomarker with the highest sensitivity for identifying cells of adrenocortical origin in destained Pap's smears and cell-block sections with, however, a lower specificity when compared with calretinin and inhibin alpha.
  • Calretinin is comparable in sensitivity with A103 on cell-block sections alone and not on smears.
  • The results of this study suggest that if metastatic melanoma in adrenal gland is not a consideration then A103 is the marker of choice for identifying cells of adrenocortical origin in the limited material available for diagnostic purposes in cytology specimens.
  • [MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / pathology. Biomarkers, Tumor / metabolism. Inhibins / metabolism. Neoplasms / pathology. S100 Calcium Binding Protein G / metabolism

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16007649.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Biomarkers, Tumor; 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / S100 Calcium Binding Protein G; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins
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50. Edwards RA, Witherspoon M, Wang K, Afrasiabi K, Pham T, Birnbaumer L, Lipkin SM: Epigenetic repression of DNA mismatch repair by inflammation and hypoxia in inflammatory bowel disease-associated colorectal cancer. Cancer Res; 2009 Aug 15;69(16):6423-9
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  • [Title] Epigenetic repression of DNA mismatch repair by inflammation and hypoxia in inflammatory bowel disease-associated colorectal cancer.
  • However, tumors in germ-line MMR-deficient mouse models lack these histopathologic features.
  • Mice lacking the heterotrimeric G protein alpha subunit Gialpha2 develop chronic colitis and multifocal, right-sided cancers with mucinous histopathology, similar to human MMR-deficient colorectal cancer.
  • Chromatin immunoprecipitation identified increased binding of the transcriptional repressor DEC-1 to the proximal Mlh1 promoter in hypoxic YAMC cells and colitic Gialpha2-/- crypts.
  • Treating Gialpha2-/- mice with the histone deacetylase inhibitor suberoylanilide hydroxamic acid significantly decreased colitis activity and rescued MLH1 expression in crypt epithelial cells, which was associated with increased acetyl histone H3 levels and decreased DEC-1 binding at the proximal Mlh1 promoter, consistent with a histone deacetylase-dependent mechanism.

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  • (PMID = 19638594.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA98626; United States / NIEHS NIH HHS / ES / Z01 ES101643; United States / NCI NIH HHS / CA / R01 CA098626; United States / NIDDK NIH HHS / DK / K08 DK59816; United States / NIDDK NIH HHS / DK / R21 DK071591-01A2; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R56 CA098626; United States / NCI NIH HHS / CA / P30 CA062203; United States / NIDDK NIH HHS / DK / K08 DK059816; United States / NIDDK NIH HHS / DK / R21 DK071591; United States / NIDDK NIH HHS / DK / DK071591-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Mlh1 protein, mouse; 0 / Nuclear Proteins; 58IFB293JI / vorinostat; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / Pms2 protein, mouse; EC 3.6.5.1 / GTP-Binding Protein alpha Subunit, Gi2; EC 6.5.1.- / DNA Repair Enzymes
  • [Other-IDs] NLM/ NIHMS127354; NLM/ PMC2748849
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51. El-Rayes BF, Ali S, Philip PA, Sarkar FH: Protein kinase C: a target for therapy in pancreatic cancer. Pancreas; 2008 May;36(4):346-52
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  • [Title] Protein kinase C: a target for therapy in pancreatic cancer.
  • OBJECTIVES: Protein kinase C (PKC) is involved in tumor growth and apoptosis and hence represents a potential target for cancer therapy.
  • This study investigated the expression of PKC in pancreatic tumor tissue in comparison to adjacent normal tissue and determined the modulation of PKC by bryostatin-1 (BRYO) on pancreatic cancer cell lines.
  • METHODS: Pancreatic tissue was obtained from 18 patients who had a resection (14 with ductal adenocarcinoma and 4 with adenoma and high-grade dysplasia).
  • HPAC cells were treated with gemcitabine and BRYO and in sequential and concomitant combination.
  • To evaluate cell viability, apoptosis, and electrophoretic mobility shift assay, 3-(4,5-dimetylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, enzyme-linked immunosorbent assay, and nuclear factor kappaB (NF-kappaB) assays were used.
  • RESULTS: As compared with the adjacent normal tissue, PKC-alpha, PKC-beta1, and PKC-delta were higher in the tumor; PKC-epsilon was higher in the normal tissue.
  • Pretreatment with gemcitabine followed by BRYO resulted in decreased cell viability, increased apoptosis, and inhibited NF-kappaB than either agent alone or BRYO followed by gemcitabine.
  • CONCLUSION: Protein kinase C is overexpressed and activated in pancreatic cancer as compared with normal tissue.
  • Inhibition of PKC could sensitize pancreatic cancer cell lines to the effects of gemcitabine.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Isoenzymes / antagonists & inhibitors. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / enzymology. Protein Kinase C / antagonists & inhibitors
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / enzymology. Adenocarcinoma / pathology. Adenoma / drug therapy. Adenoma / enzymology. Adenoma / pathology. Bryostatins / administration & dosage. Cell Survival / drug effects. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Humans. Protein Kinase Inhibitors / therapeutic use. Reference Values

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  • (PMID = 18437080.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bryostatins; 0 / Isoenzymes; 0 / Protein Kinase Inhibitors; 0W860991D6 / Deoxycytidine; 37O2X55Y9E / bryostatin 1; B76N6SBZ8R / gemcitabine; EC 2.7.11.13 / Protein Kinase C
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52. Jarufe NP, Coldham C, Orug T, Mayer AD, Mirza DF, Buckels JA, Bramhall SR: Neuroendocrine tumours of the pancreas: predictors of survival after surgical treatment. Dig Surg; 2005;22(3):157-62
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  • [Title] Neuroendocrine tumours of the pancreas: predictors of survival after surgical treatment.
  • AIMS: Neuroendocrine tumours of pancreatic and duodenal origin (NETP) are rare and we present a significant experience from a single centre.
  • RESULTS: Twenty-four patients had functioning tumours (16 insulinomas, 3 gastrinomas, 2 somatostatinomas, 1 vipoma, 1 glucagonoma and 1 carcinoid tumour).
  • [MeSH-major] Neuroendocrine Tumors / surgery. Pancreatic Neoplasms / surgery

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16043962.001).
  • [ISSN] 0253-4886
  • [Journal-full-title] Digestive surgery
  • [ISO-abbreviation] Dig Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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53. Ladeiro Y, Couchy G, Balabaud C, Bioulac-Sage P, Pelletier L, Rebouissou S, Zucman-Rossi J: MicroRNA profiling in hepatocellular tumors is associated with clinical features and oncogene/tumor suppressor gene mutations. Hepatology; 2008 Jun;47(6):1955-63
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  • [Title] MicroRNA profiling in hepatocellular tumors is associated with clinical features and oncogene/tumor suppressor gene mutations.
  • Molecular classifications defining new tumor subtypes have been recently refined with genetic and transcriptomic analyses of benign and malignant hepatocellular tumors.
  • Here, we performed microRNA (miRNA) profiling in two series of fully annotated liver tumors to uncover associations between oncogene/tumor suppressor mutations and clinical and pathological features.
  • Expression levels of 250 miRNAs in 46 benign and malignant hepatocellular tumors were compared to those of 4 normal liver samples with quantitative reverse-transcriptase polymerase chain reaction. miRNAs associated with genetic and clinical characteristics were validated in a second series of 43 liver tumor samples and 16 nontumor samples. miRNA profiling unsupervised analysis classified samples in unique clusters characterized by histological features (tumor/nontumor, P < 0.001; benign/malignant tumors, P < 0.01; inflammatory adenoma and focal nodular hyperplasia, P < 0.01), clinical characteristics [hepatitis B virus (HBV) infection, P < 0.001; alcohol consumption, P < 0.05], and oncogene/tumor suppressor gene mutations [beta-catenin, P < 0.01; hepatocyte nuclear factor 1alpha (HNF1alpha), P < 0.01].
  • Our study identified and validated miR-224 overexpression in all tumors and miR-200c, miR-200, miR-21, miR-224, miR-10b, and miR-222 specific deregulation in benign or malignant tumors.
  • Moreover, miR-96 was overexpressed in HBV tumors, and miR-126* was down-regulated in alcohol-related hepatocellular carcinoma.
  • Down-regulations of miR-107 and miR-375 were specifically associated with HNF1alpha and beta-catenin gene mutations, respectively. miR-375 expression was highly correlated to that of beta-catenin-targeted genes as miR-107 expression was correlated to that of HNF1alpha in a small interfering RNA cell line model.
  • CONCLUSION: Hepatocellular tumors may have a distinct miRNA expression fingerprint according to malignancy, risk factors, and oncogene/tumor suppressor gene alterations.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Gene Expression Profiling / methods. Genes, Tumor Suppressor. Liver Neoplasms / genetics. MicroRNAs / genetics. Mutation / genetics
  • [MeSH-minor] Gene Expression Regulation, Neoplastic. Hepatocyte Nuclear Factor 1-alpha / genetics. Hepatocyte Nuclear Factor 1-alpha / metabolism. Humans. Phenotype. Risk Factors. Tumor Cells, Cultured. beta Catenin / genetics. beta Catenin / metabolism

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  • [CommentIn] Hepatology. 2008 Jun;47(6):1807-9 [18506877.001]
  • (PMID = 18433021.001).
  • [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 / Hepatocyte Nuclear Factor 1-alpha; 0 / MicroRNAs; 0 / beta Catenin
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54. 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.
  • The functional development of pituitary cells depends on the expression of a combination of transcription factors and co-factors.
  • The glycoprotein hormone alpha subunit (alpha SU) is the first hormone to be expressed during pituitary development.
  • In addition to being expressed in follicle-stimulating hormone, luteinizing hormone (LH), and TSH cells, alpha SU is reported to co-localize with GH in pituitary cells.
  • 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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55. Frulio N, Laumonier H, Balabaud C, Trillaud H, Bioulac-Sage P: Hepatic congestion plays a role in liver stiffness. Hepatology; 2009 Nov;50(5):1674-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adenoma, Liver Cell / blood supply. Adenoma, Liver Cell / metabolism. Adenoma, Liver Cell / physiopathology. Hepatocyte Nuclear Factor 1-alpha / metabolism. Humans. Liver Neoplasms / blood supply. Liver Neoplasms / metabolism. Liver Neoplasms / physiopathology

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  • [CommentOn] Hepatology. 2008 Dec;48(6):2089 [19003902.001]
  • (PMID = 19670411.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha
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56. Ju J, Hao X, Lee MJ, Lambert JD, Lu G, Xiao H, Newmark HL, Yang CS: A gamma-tocopherol-rich mixture of tocopherols inhibits colon inflammation and carcinogenesis in azoxymethane and dextran sulfate sodium-treated mice. Cancer Prev Res (Phila); 2009 Feb;2(2):143-52
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  • We investigated the effects of a gamma-tocopherol-rich mixture of tocopherols (gamma-TmT, containing 57% gamma-T, 24% delta-T, and 13% alpha-T) on colon carcinogenesis in azoxymethane (AOM)/dextran sulfate sodium (DSS)-treated mice.
  • In the AOM/DSS-treated mice, dietary gamma-TmT treatment resulted in a significantly lower colon inflammation index (52% of the control) on day 7 and number of colon adenomas (9% of the control) on week 7. gamma-TmT treatment also resulted in higher apoptotic index in adenomas, lower prostaglandin E2, leukotriene B4, and nitrotyrosine levels in the colon, and lower prostaglandin E2, leukotriene B4, and 8-isoprostane levels in the plasma on week 7.
  • In experiment 2 with AOM/DSS- treated mice sacrificed on week 21, dietary 0.17% or 0.3% gamma-TmT treatment, starting 1 week before the AOM injection, significantly inhibited adenocarcinoma and adenoma formation in the colon (to 17-33% of the control).

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  • (PMID = 19155443.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA072720; United States / NIEHS NIH HHS / ES / ES05022; United States / NIEHS NIH HHS / ES / P30 ES005022; United States / NCI NIH HHS / CA / P30 CA072720-12; United States / NIEHS NIH HHS / ES / ES005022-109003; United States / NIEHS NIH HHS / ES / P30 ES005022-109003; United States / NCI NIH HHS / CA / CA72720; United States / NCI NIH HHS / CA / CA072720-12
  • [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 / Antioxidants; 0 / Carcinogens; 1HGW4DR56D / Leukotriene B4; 27415-26-5 / 8-epi-prostaglandin F2alpha; 3604-79-3 / 3-nitrotyrosine; 42HK56048U / Tyrosine; 8EF1Z1238F / gamma-Tocopherol; 9042-14-2 / Dextran Sulfate; B7IN85G1HY / Dinoprost; K7Q1JQR04M / Dinoprostone; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ NIHMS172441; NLM/ PMC2821738
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57. Jeannot E, Mellottee L, Bioulac-Sage P, Balabaud C, Scoazec JY, Tran Van Nhieu J, Bacq Y, Michalak S, Buob D, Groupe d'étude Génétique des Tumeurs Hépatiques (INSERM Network), Laurent-Puig P, Rusyn I, Zucman-Rossi J: Spectrum of HNF1A somatic mutations in hepatocellular adenoma differs from that in patients with MODY3 and suggests genotoxic damage. Diabetes; 2010 Jul;59(7):1836-44
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  • [Title] Spectrum of HNF1A somatic mutations in hepatocellular adenoma differs from that in patients with MODY3 and suggests genotoxic damage.
  • A subtype of hepatocellular adenoma (HCA) is also caused by biallelic somatic HNF1A mutations (H-HCA), and rare HCA may be related to MODY3.

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  • (PMID = 20393147.001).
  • [ISSN] 1939-327X
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES010126; United States / NIEHS NIH HHS / ES / R01-ES-15241; United States / NIEHS NIH HHS / ES / R01 ES015241; United States / NIAAA NIH HHS / AA / R01-AA-16258; United States / NIAAA NIH HHS / AA / R01 AA016258
  • [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 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha
  • [Other-IDs] NLM/ PMC2889786
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58. van den Broek FJ, de Graaf EJ, Dijkgraaf MG, Reitsma JB, Haringsma J, Timmer R, Weusten BL, Gerhards MF, Consten EC, Schwartz MP, Boom MJ, Derksen EJ, Bijnen AB, Davids PH, Hoff C, van Dullemen HM, Heine GD, van der Linde K, Jansen JM, Mallant-Hent RC, Breumelhof R, Geldof H, Hardwick JC, Doornebosch PG, Depla AC, Ernst MF, van Munster IP, de Hingh IH, Schoon EJ, Bemelman WA, Fockens P, Dekker E: Transanal endoscopic microsurgery versus endoscopic mucosal resection for large rectal adenomas (TREND-study). BMC Surg; 2009;9:4
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  • [Title] Transanal endoscopic microsurgery versus endoscopic mucosal resection for large rectal adenomas (TREND-study).
  • BACKGROUND: Recent non-randomized studies suggest that extended endoscopic mucosal resection (EMR) is equally effective in removing large rectal adenomas as transanal endoscopic microsurgery (TEM).
  • Furthermore, EMR appears to be associated with fewer complications.The aim of this study is to compare the cost-effectiveness and cost-utility of TEM and EMR for the resection of large rectal adenomas.
  • Patients with a rectal adenoma > or = 3 cm, located between 1-15 cm ab ano, will be randomized to a TEM- or EMR-treatment strategy.
  • For TEM, patients will be treated under general anesthesia, adenomas will be dissected en-bloc by a full-thickness excision, and patients will be admitted to the hospital.
  • Residual adenoma that is visible during the first surveillance endoscopy at 3 months will be removed endoscopically in both treatment strategies and is considered as part of the primary treatment.
  • 4) disease specific and general quality of life;.
  • A cost-effectiveness and cost-utility analysis of EMR against TEM for large rectal adenomas will be performed from a societal perspective with respectively the costs per recurrence free patient and the cost per quality adjusted life year as outcome measures.
  • Based on comparable recurrence rates for TEM and EMR of 3.3% and considering an upper-limit of 10% for EMR to be non-inferior (beta-error 0.2 and one-sided alpha-error 0.05), 89 patients are needed per group.
  • DISCUSSION: The TREND study is the first randomized trial evaluating whether TEM or EMR is more cost-effective for the treatment of large rectal adenomas.
  • [MeSH-major] Adenoma / surgery. Endoscopy / economics. Rectal Neoplasms / surgery

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  • (PMID = 19284647.001).
  • [ISSN] 1471-2482
  • [Journal-full-title] BMC surgery
  • [ISO-abbreviation] BMC Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2664790
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59. Kazanjian KK, Reber HA, Hines OJ: Resection of pancreatic neuroendocrine tumors: results of 70 cases. Arch Surg; 2006 Aug;141(8):765-9; discussion 769-70
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  • [Title] Resection of pancreatic neuroendocrine tumors: results of 70 cases.
  • HYPOTHESIS: Neuroendocrine tumors of the pancreas can be managed surgically with excellent outcomes.
  • PATIENTS: Seventy consecutive patients who underwent resection for pancreatic neuroendocrine tumors between January 1, 1990, and December 31, 2005.
  • RESULTS: Of the 70 patients, 50 (71.4%) had nonfunctional tumors.
  • Thirty-seven patients (52.9%) had neuroendocrine carcinomas and 13 (18.6%) had benign islet cell neoplasms.
  • Twenty patients had functional tumors.
  • Of these 20 patients, 16 had insulinomas, 2 had glucagonomas, and 2 had gastrinomas.
  • Patients undergoing enucleation as compared with those not undergoing enucleation were younger (mean age, 39 vs 51 years, respectively; P = .009) and had smaller tumors (mean tumor size, 2 vs 5 cm, respectively; P<.001).
  • With a median follow-up of 50 months, the 5-year actuarial survival for the patients with malignant neuroendocrine carcinomas (n = 37) was 77%, and all of the patients with functional tumors are alive.
  • CONCLUSIONS: This single-institutional case series demonstrates that pancreatic neuroendocrine tumors can be safely resected without mortality and with minimal morbidity.
  • The presence of lymphovascular invasion can be used to classify neuroendocrine tumors as malignant, and this appears to predict survival.
  • Patients with malignant tumors can expect long-term survival even in the setting of metastatic disease.
  • [MeSH-major] Neuroendocrine Tumors / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / surgery. Pancreaticoduodenectomy / methods

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  • (PMID = 16924083.001).
  • [ISSN] 0004-0010
  • [Journal-full-title] Archives of surgery (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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60. Chen YT, Tu JJ, Kao J, Zhou XK, Mazumdar M: Messenger RNA expression ratios among four genes predict subtypes of renal cell carcinoma and distinguish oncocytoma from carcinoma. Clin Cancer Res; 2005 Sep 15;11(18):6558-66
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  • [Title] Messenger RNA expression ratios among four genes predict subtypes of renal cell carcinoma and distinguish oncocytoma from carcinoma.
  • PURPOSE: Morphologic distinction among clear cell, papillary, and chromophobe types of renal cell carcinoma (RCC) can be difficult, as is the differential diagnosis between oncocytoma and RCC.
  • Whether these renal tumors can be distinguished by their mRNA expression profile of a few selected genes was examined.
  • EXPERIMENTAL DESIGN: The expression of four genes in renal tumor was evaluated by quantitative reverse transcription-PCR: carbonic anhydrase IX (CA9), methylacyl-CoA racemase (AMACR), parvalbumin (PVALB), and chloride channel kb (CLCNKB).
  • Thirty-one fresh-frozen and 63 formalin-fixed, paraffin-embedded tumor specimens were analyzed.
  • RESULTS: CA9 expression was highest in clear cell carcinoma and lowest in chromophobe RCC and in oncocytoma.
  • PVALB was highest in chromophobe RCC, variable in oncocytoma, and low in clear cell and papillary types.
  • The mRNA expression ratios among these genes (i.e., CA9/AMACR and AMACR/CLCNKB ratios) further accentuate the gene expression differences among these tumors, and a molecular diagnostic algorithm was established.
  • This algorithm accurately classified the 31 fresh-frozen tumors into 14 clear cell, 5 papillary, 6 chromophobe, and 6 oncocytomas.
  • In the formalin-fixed group, the molecular criteria accurately classified the cases into 15 clear cell, 16 papillary, and 32 in the chromophobe/oncocytoma group but could only separate some, but not all, oncocytomas from chromophobe RCC.
  • [MeSH-minor] Adenocarcinoma, Clear Cell / genetics. Adenocarcinoma, Clear Cell / pathology. Adenoma, Oxyphilic / genetics. Adenoma, Oxyphilic / pathology. Algorithms. Anion Transport Proteins / genetics. Antigens, Neoplasm / genetics. Carbonic Anhydrases / genetics. Carcinoma, Renal Cell / genetics. Carcinoma, Renal Cell / pathology. Chloride Channels / genetics. Diagnosis, Differential. Humans. Membrane Proteins / genetics. Racemases and Epimerases / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. beta-Defensins / genetics

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  • (PMID = 16166433.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anion Transport Proteins; 0 / Antigens, Neoplasm; 0 / CLCNKB protein, human; 0 / Chloride Channels; 0 / DEFB1 protein, human; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / beta-Defensins; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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61. Technau K, Renkl A, Norgauer J, Ziemer M: Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma. Eur J Dermatol; 2005 Mar-Apr;15(2):110-2
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  • [Title] Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma.
  • Necrolytic migratory erythema is a cutaneous paraneoplastic manifestation, which is usually associated with a glucagon-secreting pancreatic tumor.
  • However, it also may occur in other circumstances in which serum glucagon is elevated, as in hepatic cirrhosis.
  • Rarely, necrolytic migratory erythema is reported in association with a jejunal and rectal adenocarcinoma or villous atrophy of the small intestine without any evidence for increased serum glucagon levels.
  • In this context we report the case of an 85-year-old male with myelodysplastic syndrome who developed typical necrolytic migratory erythema without glucagonoma syndrome or evidence for other pancreatic or liver disease.
  • We suggest that, in addition to the diseases listed, myelodysplastic syndrome might be able to cause necrolytic migratory erythema.
  • [MeSH-major] Erythema / complications. Glucagonoma / complications. Myelodysplastic Syndromes / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes / complications


62. Luo F, Brooks DG, Ye H, Hamoudi R, Poulogiannis G, Patek CE, Winton DJ, Arends MJ: Mutated K-ras(Asp12) promotes tumourigenesis in Apc(Min) mice more in the large than the small intestines, with synergistic effects between K-ras and Wnt pathways. Int J Exp Pathol; 2009 Oct;90(5):558-74
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  • Summary K-ras mutations are found in 40-50% of human colorectal adenomas and carcinomas, but their functional contribution remains incompletely understood.
  • Here, we show that a conditional mutant K-ras mouse model (K-ras(Asp12)/Cre), with transient intestinal Cre activation by beta-Naphthoflavone (beta-NF) treatment, displayed transgene recombination and K-ras(Asp12) expression in the murine intestines, but developed few intestinal adenomas over 2 years.
  • The numbers of adenomas in the small intestine and large intestine were significantly (P < 0.01) increased by 1.5-fold and 5.7-fold, respectively, in K-ras(Asp12)/Cre/Apc(Min/+) mice compared with Apc(Min/+) mice, with the more marked increase in adenoma prevalence in the large intestine.
  • K-ras(Asp12) increased activation of Mapk and Akt signalling pathway targets phospho-extracellular signal-regulated kinase (pErk) and pAkt, and increased relative expression levels of Wnt pathway targets vascular endothelial growth factor (VEGF), gastrin, cyclo-oxygenase 2 (Cox2) and T-cell lymphoma invasion and metastasis 1 (Tiam1) in K-ras(Asp12)/Cre/Apc(Min/+) adenomas compared with that of Apc(Min/+) adenomas, although other Wnt signalling pathway target genes such as Peroxisome proliferator-activated receptor delta (PPARd), matrix metalloproteinase 7 (MMP7), protein phosphatase 1 alpha (PP1A) and c-myc remained unchanged.
  • In conclusion, intestinal expression of K-ras(Asp12) promotes mutant Apc-initiated intestinal adenoma formation in vivo more in the large intestine than the small intestine, with evidence of synergistic co-operation between mutant K-ras and Apc involving increased expression of some Wnt-pathway target genes.

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  • (PMID = 19765110.001).
  • [ISSN] 1365-2613
  • [Journal-full-title] International journal of experimental pathology
  • [ISO-abbreviation] Int J Exp Pathol
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / Wnt Proteins; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Oncogene Protein p21(ras); EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ PMC2768154
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63. Krysiak R, Okopień B, Herman ZS: [Rare pancreatic endocrine tumors]. Przegl Lek; 2008;65(4):209-16
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  • [Title] [Rare pancreatic endocrine tumors].
  • [Transliterated title] Rzadkie guzy endokrynne trzustki.
  • Functional pancreatic endocrine tumors other than gastrinoma and insulinoma are quite rare.
  • Some of these tumors may be part of multiple endocrine neoplasia type one (MEN-1) syndrome or phakomatoses.
  • Depending on their cell type, functional pancreatic endocrine tumors may cause distinct clinical endocrine syndromes, such as the 'glucagonoma syndrome', Verner-Morrison syndrome and the 'somatostatinoma syndrome'.
  • Currently, the only curative treatment for islet cell tumors is complete surgical resection.
  • The medical treatment of endocrine pancreatic tumours consists of somatostatin analogues, chemotherapy, and interferon-alpha.
  • The purpose of this manuscript is to provide an overview of the contemporary etiopathogenesis, diagnosis and treatment of rare pancreatic endocrine tumors.
  • [MeSH-major] Glucagonoma / diagnosis. Glucagonoma / therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy. Somatostatinoma / diagnosis. Somatostatinoma / therapy. Vipoma / diagnosis. Vipoma / therapy
  • [MeSH-minor] Humans. Rare Diseases / diagnosis. Rare Diseases / therapy

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  • (PMID = 18724549.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Number-of-references] 47
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64. Xue HD, Liu W, Sun H, Merges R, Wang X, Zhang XN, Wang Y, Zhao WM, Chen JH, Jin ZY: Spectrum of functioning islet cell tumor on multislice computed tomography: experience on 70 patients. Chin Med Sci J; 2008 Mar;23(1):1-9
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  • [Title] Spectrum of functioning islet cell tumor on multislice computed tomography: experience on 70 patients.
  • OBJECTIVE: To review experience in preoperative detection of islet cell tumors using multislice computed tomography (MSCT) and summarize various imaging features of functioning islet cell tumors on enhanced MSCT.
  • METHODS: Seventy patients with clinical or pathological diagnosis of functioning pancreatic islet cell tumor between October 2003 and February 2007 were included in this retrospective study.
  • Surgery and pathology reports were used to confirm the diagnosis, localization, and size of tumors.
  • RESULTS: Totally, 73 functioning islet cell tumors including 65 benign insulinomas, 2 benign glucagonomas, 3 malignant insulinomas, and 3 malignant glucagonomas were pathologically diagnosed.
  • Tumors in only two cases were not found by MSCT.
  • In 67 benign lesions, 32 showed typical enhancement style, 21 showed prolonged enhancement in portal venous phase, 4 showed delayed enhancement, 4 had iso-dense enhancement with normal pancreatic parenchyma, 2 had no enhancement at all in arterial phase and portal venous phase, and 4 had inhomogeneous enhancement with necrosis or cyst-formation.
  • Patchy or spotty calcifications were found in 3 of the 67 tumors.
  • In 6 malignant islet cell tumors, vessel invasion (2/6) and bowel invasion (1/6) were seen.
  • CONCLUSIONS: Pancreatic islet cell tumor may display a wide spectrum of presentations in MSCT.
  • Tumors with unusual appearances often present as diagnostic challenges.
  • Non-contrast and post-contrast multiphase scans are recommended for the localization of functioning islet cell tumors.

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  • (PMID = 18437902.001).
  • [ISSN] 1001-9294
  • [Journal-full-title] Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih
  • [ISO-abbreviation] Chin. Med. Sci. J.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] China
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65. Gentschev I, Fensterle J, Schmidt A, Potapenko T, Troppmair J, Goebel W, Rapp UR: Use of a recombinant Salmonella enterica serovar Typhimurium strain expressing C-Raf for protection against C-Raf induced lung adenoma in mice. BMC Cancer; 2005 Feb 9;5:15
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  • [Title] Use of a recombinant Salmonella enterica serovar Typhimurium strain expressing C-Raf for protection against C-Raf induced lung adenoma in mice.
  • Therefore these proteins are potential targets for immunotherapy and a possible basis for vaccine development against tumors.
  • In this study we analyzed the functionality of a new live C-Raf vaccine based on an attenuated Salmonella enterica serovar Typhimurium aroA strain in two Raf dependent lung tumor mouse models.
  • METHODS: The antigen C-Raf has been fused to the C-terminal secretion signal of Escherichia coli alpha-hemolysin and expressed in secreted form by an attenuated aroA Salmonella enterica serovar Typhimurium strain via the alpha-hemolysin secretion pathway.
  • The effect of the immunization with this recombinant C-Raf strain on wild-type C57BL/6 or lung tumor bearing transgenic BxB mice was analyzed using western blot and FACS analysis as well as specific tumor growth assays.
  • Immunization of wild-type C57BL/6 or tumor bearing mice provoked specific C-Raf antibody and T-cell responses.
  • Most importantly, the vaccine strain significantly reduced tumor growth in two transgenic mouse models of Raf oncogene-induced lung adenomas.
  • [MeSH-major] Adenoma / prevention & control. Cancer Vaccines / immunology. Escherichia coli Proteins / immunology. Hemolysin Proteins / immunology. Lung Neoplasms / prevention & control. Proto-Oncogene Proteins c-raf / immunology. Salmonella typhimurium / immunology


66. Zatelli MC, Piccin D, Vignali C, Tagliati F, Ambrosio MR, Bondanelli M, Cimino V, Bianchi A, Schmid HA, Scanarini M, Pontecorvi A, De Marinis L, Maira G, degli Uberti EC: Pasireotide, a multiple somatostatin receptor subtypes ligand, reduces cell viability in non-functioning pituitary adenomas by inhibiting vascular endothelial growth factor secretion. Endocr Relat Cancer; 2007 Mar;14(1):91-102
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  • [Title] Pasireotide, a multiple somatostatin receptor subtypes ligand, reduces cell viability in non-functioning pituitary adenomas by inhibiting vascular endothelial growth factor secretion.
  • Somatostatin (SRIF) analogs have been employed in medical therapy of non-functioning pituitary adenomas (NFA), with contrasting results.
  • Previous evidence showed that SRIF can exert its antiproliferative effects by reducing vascular endothelial growth factor (VEGF) secretion and action, and that VEGF expression may be related to pituitary tumor growth.
  • The aim of our study was to clarify the possible effects of a multireceptor SRIF ligand on VEGF secretion and cell proliferation in human NFA primary cultures.
  • We assessed the expression of SRIF receptors (SSTR1-5), the in vitro effects on VEGF secretion, and on cell viability of SRIF and of the stable SRIF analog pasireotide (SOM230), which activates SSTR1, 2, 3, and 5.
  • Twenty-five NFA were examined by RT-PCR for expression of alpha-subunit, SSTR, VEGF, and VEGF receptors 1 (VEGF-R1) and 2 (VEGF-R2).
  • All NFA samples expressed alpha-sub, VEGF and VEGFR-1 and 2, while SSTR expression pattern was highly variable.
  • VEGF secretion and cell viability were reduced by SRIF and pasireotide in the 'responder' group, but not in the 'non-responder' group, including NFA expressing SSTR5.
  • In addition, SRIF and pasireotide completely abrogated the promoting effects of VEGF on NFA cell viability.
  • Our data demonstrate that pasireotide can inhibit NFA cell viability by inhibiting VEGF secretion, and suggest that the multireceptor-SSTR agonist pasireotide might be useful in medical therapy of selected NFA.
  • [MeSH-major] Adenoma / secretion. Oligopeptides / pharmacology. Pituitary Neoplasms / secretion. Somatostatin / pharmacology. Vascular Endothelial Growth Factor A / secretion
  • [MeSH-minor] Adult. Aged. Cell Survival / drug effects. Female. Hormones / pharmacology. Humans. Ligands. Male. RNA, Messenger / metabolism. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism

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  • (PMID = 17395978.001).
  • [ISSN] 1351-0088
  • [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 / Hormones; 0 / Ligands; 0 / Oligopeptides; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / Vascular Endothelial Growth Factor A; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide
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67. Hanson PL, Aylwin SJ, Monson JP, Burrin JM: FSH secretion predominates in vivo and in vitro in patients with non-functioning pituitary adenomas. Eur J Endocrinol; 2005 Mar;152(3):363-70
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  • [Title] FSH secretion predominates in vivo and in vitro in patients with non-functioning pituitary adenomas.
  • OBJECTIVE: Non-functioning pituitary adenomas (NFPAs) are characterised by the lack of symptoms of hormone hypersecretory syndromes but in vitro studies have demonstrated that tumour cells may stain for gonadotrophins and/or their alpha- or beta-subunits.
  • In this study, we aimed to examine the pattern of secretion of LH and FSH from a series of pituitary adenomas cultured in vitro and where data were available to relate the results to pre-operative serum gonadotrophin levels.
  • Peritumorous 'normal' pituitary cell cultures from 20 additional pituitary tumour patients were used for comparison with the NFPA group.
  • Peritumorous 'normal' pituitary cells released LH and FSH in a reversed ratio (median LH:FSH ratio = 3.6:1, P < 0.01 compared with NFPAs).
  • By demonstrating that NFPAs cultured in vitro reflect the in vivo situation of preferential secretion of FSH, it may be possible in future to perform functional studies using this system to elucidate the cellular and molecular mechanisms involved in the development of an imbalance in gonadotroph cells preferentially overproducing FSH in NFPAs.

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  • (PMID = 15757852.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
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68. Shia J, Klimstra DS, Nitzkorski JR, Low PS, Gonen M, Landmann R, Weiser MR, Franklin WA, Prendergast FG, Murphy L, Tang LH, Temple L, Guillem JG, Wong WD, Paty PB: Immunohistochemical expression of folate receptor alpha in colorectal carcinoma: patterns and biological significance. Hum Pathol; 2008 Apr;39(4):498-505
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  • [Title] Immunohistochemical expression of folate receptor alpha in colorectal carcinoma: patterns and biological significance.
  • Folate receptor alpha (FRalpha) has emerged as a potential cancer therapy target with several folate-linked therapeutic agents currently undergoing clinical trials.
  • In addition, FRalpha expression in tumors may offer prognostic significance.
  • We used tissue microarrays containing 152 normal colorectal mucosa samples, 42 adenomas, 177 primary, and 52 metastatic colorectal carcinomas.
  • FRalpha positivity was more frequent in carcinomas (33% in primaries and 44% in metastases) than in normal mucosa or adenoma (7% in both) (P < .001).
  • Positive staining in primary carcinomas also correlated with a worse 5-year disease-specific survival (P = .04) on univariate but not multivariate analysis.
  • Thus, our data show that there is selective expression of FRalpha in some colorectal cancers, providing a foundation for investigating the use of folate conjugates for imaging and therapy of colorectal tumors.
  • [MeSH-major] Carcinoma / diagnosis. Carrier Proteins / analysis. Colorectal Neoplasms / diagnosis. Receptors, Cell Surface / analysis

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  • (PMID = 18342661.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 2 P01 CA65930-05A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Folate Receptors, GPI-Anchored; 0 / Receptors, Cell Surface
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69. Rao VP, Poutahidis T, Ge Z, Nambiar PR, Horwitz BH, Fox JG, Erdman SE: Proinflammatory CD4+ CD45RB(hi) lymphocytes promote mammary and intestinal carcinogenesis in Apc(Min/+) mice. Cancer Res; 2006 Jan 1;66(1):57-61
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  • Here, we apply a widely used T-cell transfer paradigm, involving adoptive transfer of proinflammatory CD4+ CD45RB(hi) (T(E)) cells to induce inflammatory bowel disease (IBD) in mice, to investigate roles of inflammation on carcinogenesis in the Apc(Min/+) mouse model of intestinal polyposis.
  • We find that transfer of T(E) cells significantly increases adenoma multiplicity and features of malignancy in recipient Apc(Min/+) mice.
  • Surprisingly, we find that female Apc(Min/+) recipients of T(E) cells also rapidly develop mammary tumors.
  • Both intestinal polyposis and mammary adenocarcinoma are abolished by cotransfer of anti-inflammatory CD4+ CD45RB(lo) regulatory lymphocytes or by neutralization of key proinflammatory cytokine tumor necrosis factor-alpha.
  • Lastly, down-regulation of cyclooxygenase-2 and c-Myc expression is observed coincident with tumor regression.
  • These findings define a novel mouse model of inflammation-driven mammary carcinoma and suggest that epithelial carcinogenesis can be mitigated by anti-inflammatory cells and cytokines known to regulate IBD in humans and mice.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / immunology. Adenoma / genetics. Adenoma / immunology. Adoptive Transfer. Animals. Disease Models, Animal. Down-Regulation. Epithelial Cells / immunology. Epithelial Cells / pathology. Female. Genes, APC. Genes, myc / genetics. Inflammatory Bowel Diseases / immunology. Intestinal Polyps / genetics. Intestinal Polyps / immunology. Male. Mice. Mice, Inbred C57BL. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 16397216.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA26731; United States / NIEHS NIH HHS / ES / P30ES02109; United States / NIAID NIH HHS / AI / R01 AI50952; United States / NIDDK NIH HHS / DK / R01 DK52413; United States / NCI NIH HHS / CA / R01CA108854; United States / NCI NIH HHS / CA / R01CA67529; United States / NCRR NIH HHS / RR / T32RR07036
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; EC 3.1.3.48 / Antigens, CD45
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70. Furuse C, Sousa SO, Nunes FD, Magalhães MH, Araújo VC: Myoepithelial cell markers in salivary gland neoplasms. Int J Surg Pathol; 2005 Jan;13(1):57-65
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  • [Title] Myoepithelial cell markers in salivary gland neoplasms.
  • We compared the immunoexpression of 5 myoepithelial cell (MEC) markers (alpha-smooth-muscle actin, calponin, h-caldesmon, vimentin, and S-100-protein) using 16 pleomorphic adenomas (PA), 15 adenoid cystic carcinomas (ACC), and 3 epithelial-myoepithelial carcinomas (EMC) of salivary glands.
  • The alpha-smooth-muscle actin was useful for identification of MECs, especially in cribriform and tubular ACC, followed by EMC.
  • Calponin was similar to alpha-smooth-muscle actin, except for polygonal and plasmacytoid cells of PA and for solid ACC, which showed alpha-smooth-muscle actin negative and calponin positive.
  • Vimentin immunostained all MEC types, and was negative in luminal cells.
  • S-100 protein was expressed both in the nuclei and cytoplasm of MECs and luminal cells, especially in PA.
  • The best way to identify MEC is using alpha-smooth-muscle actin or calponin, plus vimentin, since in tumors MECs are hardly ever fully differentiated.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. Biomarkers, Tumor / metabolism. Carcinoma, Adenoid Cystic / metabolism. Myoepithelioma / metabolism. Salivary Gland Neoplasms / metabolism

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  • (PMID = 15735856.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Biomarkers, Tumor; 0 / Calcium-Binding Proteins; 0 / Microfilament Proteins; 0 / S100 Proteins; 0 / Vimentin; 0 / calponin
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71. Mikkelsen CS, Mikkelsen DB, Vestergaard V, Clemmensen O, Nielsen HO, Bygum A: [Glucagonoma syndrome without diabetes mellitus]. Ugeskr Laeger; 2008 Nov 17;170(47):3876
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  • [Title] [Glucagonoma syndrome without diabetes mellitus].
  • Computerised tomography and endoscopic ultrasound showed a solid tumour of the pancreas.
  • A blood sample showed an increased level of glucagon without diabetes.
  • Glucagonoma syndrome is characterized by glucagon overproduction, diabetes, depression, deep venous thrombosis and necrolytic migrating erythema.
  • Glucagonoma is frequently diagnosed late which increases the risk of metastases.
  • It is important not to rule out glucagonoma in patients with a relevant clinical picture but without diabetes.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis


72. Yang J, Zhou GW, Chen X, Wei Y, Peng CH, Ning G, Li HW: [Diagnosis and treatment of multiple endocrine neoplasia type 1 related pancreatic endocrine tumors]. Zhonghua Wai Ke Za Zhi; 2009 Mar 1;47(5):329-32
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  • [Title] [Diagnosis and treatment of multiple endocrine neoplasia type 1 related pancreatic endocrine tumors].
  • OBJECTIVE: To summarize the experience on diagnosis and treatment of multiple endocrine neoplasia type 1 (MEN-1) related pancreatic endocrine tumors (PET).
  • The other patient was diagnosed as glucagonoma clinically.
  • [MeSH-major] Multiple Endocrine Neoplasia Type 1 / diagnosis. Multiple Endocrine Neoplasia Type 1 / surgery. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / surgery


73. 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.
  • To permit robust routine diagnosis to allow for HCA subtype classification, we searched new useful markers.
  • 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.
  • 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)).
  • CONCLUSION: We refined HCA classification and its phenotypic correlations, providing a routine test to classify hepatocellular adenomas using simple and robust immunohistochemistry.
  • [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


74. Rotondo F, Kovacs K, Scheithauer BW, Horvath E, Bell CD, Lloyd RV, Cusimano M: Immunohistochemical expression of SNAP-25 protein in adenomas of the human pituitary. Appl Immunohistochem Mol Morphol; 2008 Oct;16(5):477-81
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  • [Title] Immunohistochemical expression of SNAP-25 protein in adenomas of the human pituitary.
  • SNAP-25, a synaptosome-associated exocytosis protein of 25 kd mw, plays an important role in the secretory activity of several endocrine cells.
  • In the present study, we investigated surgically removed pituitary adenomas including 40 prolactin (PRL), 31 growth hormone, 5 adrenocorticotropic hormone, 5 thyroid-stimulating hormone, 14 follicle-stimulating hormone/luteinizing hormone/alpha-subunit-producing tumors, and 5 null cell adenomas.
  • Among the 40 patients with PRL-producing pituitary adenoma, 16 had been preoperatively treated with the dopamine agonist bromocriptine.
  • Similarly, of the 31 patients with GH-producing pituitary adenomas, 15 had been treated with the long-acting somatostatin analog, octreotide.
  • All tumors were subjected to transsphenoidal surgery, formalin-fixed, routinely processed, and paraffin-embedded.
  • Immunostaining for SNAP-25 (streptavidin-biotin peroxidase complex method) showed that 10 PRL-producing adenomas were strongly immunoreactive.
  • Immunopositivity was mainly cell membrane in distribution but several cells showed mild cytoplasmic staining.
  • Among GH-producing adenomas, SNAP-25 was seen in 5 cases; reactivity being mild-to-moderate, membrane-bound, and cytoplasmic.
  • Other adenoma types were virtually immunonegative.
  • It is conceivable that SNAP-25 plays an important role in PRL release and is involved in the bromocriptine-induced suppression of PRL secretion from PRL-producing adenoma cells.

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  • (PMID = 18633321.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SNAP25 protein, human; 0 / Synaptosomal-Associated Protein 25; 12629-01-5 / Human Growth Hormone; 3A64E3G5ZO / Bromocriptine; 9002-62-4 / Prolactin; RWM8CCW8GP / Octreotide
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75. Cooper O, Ben-Shlomo A, Bonert V, Bannykh S, Mirocha J, Melmed S: Silent corticogonadotroph adenomas: clinical and cellular characteristics and long-term outcomes. Horm Cancer; 2010 Apr;1(2):80-92
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  • [Title] Silent corticogonadotroph adenomas: clinical and cellular characteristics and long-term outcomes.
  • Silent corticotrophins adenomas (SCAs) are clinically silent and non-secreting but immunostain positively for ACTH.
  • We compared preoperative and postoperative clinical results and tumor cytogenesis in 25 SCAs and 84 nonfunctioning adenomas in 109 consecutive patients diagnosed pre-operatively with nonfunctioning pituitary adenomas.
  • Preoperative SCA presentation was similar to that observed for nonfunctioning adenomas.
  • However, SCAs recurred postoperatively at a median of 3 years vs. 8 years for nonfunctioning adenomas (p<0.0001).
  • Fifty-four percent of patients with SCAs had new onset postoperative hypopituitarism vs. 17% of nonfunctioning adenomas (p<0.025).
  • SCAs (n=18) were immunopositive for ACTH, cytoplasmic and nuclear SF-1, NeuroD1, DAX-1, and alpha-gonadotropin subunit, but Tpit negative, and co-expression of tumor ACTH with either SF-1 or LH was detected.
  • In contrast, functional corticotroph adenomas (n=11) were immunopositive for ACTH, nuclear SF-1, NeuroD1, and Tpit, but negative for DAX-1, a gonadotroph cell transcription factor.
  • Gonadotroph adenomas (n=23) were immunonegative for ACTH and Tpit but positive for nuclear SF-1, NeuroD1, and DAX-1.
  • SCA electron microscopy demonstrated ultrastructural features consistent with corticotroph and gonadotroph cells.
  • As SCAs exhibit features consistent with both corticotroph and gonadotroph cytologic origin, we propose a pathologic and clinically distinct classification of SCAs as silent corticogonadotroph adenomas.

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  • (PMID = 20717480.001).
  • [ISSN] 1868-8500
  • [Journal-full-title] Hormones & cancer
  • [ISO-abbreviation] Horm Cancer
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK007770-08; United States / NCI NIH HHS / CA / R01 CA075979-08; United States / NIDDK NIH HHS / DK / T32 DK007770; United States / NIDDK NIH HHS / DK / T32 DK07770; United States / NIDDK NIH HHS / DK / DK007770-08; United States / NCI NIH HHS / CA / CA 075979; United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / CA075979-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gonadotropins
  • [Keywords] NOTNLM ; Corticotroph adenoma / Gonadotroph adenoma / Nonfunctioning adenoma / Pituitary adenoma
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76. 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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  • In mammals, there are seven beta-tubulins and six alpha-tubulins.
  • 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.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Blotting, Western. Child, Preschool. Humans. Immunohistochemistry. Infant. Mesothelioma / chemistry. Middle Aged. Protein Isoforms

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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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77. Salcedo R, Worschech A, Cardone M, Jones Y, Gyulai Z, Dai RM, Wang E, Ma W, Haines D, O'hUigin C, Marincola FM, Trinchieri G: MyD88-mediated signaling prevents development of adenocarcinomas of the colon: role of interleukin 18. J Exp Med; 2010 Aug 2;207(8):1625-36
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  • The inability of Myd88(-/-) mice to heal ulcers generated upon injury creates an altered inflammatory environment that induces early alterations in expression of genes encoding proinflammatory factors, as well as pathways regulating cell proliferation, apoptosis, and DNA repair, resulting in a dramatic increase in adenoma formation and progression to infiltrating adenocarcinomas with frequent clonal mutations in the beta-catenin gene.

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  • (PMID = 20624890.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / CCR NIH HHS / RC / HHSN261200800001C; United States / NCI NIH HHS / CA / HHSN261200800001E; United States / PHS HHS / / HHSN261200800001E; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Il18r1 protein, mouse; 0 / Interleukin-18; 0 / Interleukin-18 Receptor alpha Subunit; 0 / Myd88 protein, mouse; 0 / Myeloid Differentiation Factor 88; 0 / Receptors, Interleukin-1 Type I; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, mouse; 0 / beta Catenin; 9042-14-2 / Dextran Sulfate; EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2; EC 6.5.1.- / DNA Repair Enzymes; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ PMC2916129
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78. 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
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  • [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.
  • However, the mechanisms of ERalpha effects on colorectal cancer cells remained un-clear.
  • LoVo cells were transient transfected to overexpress ERalpha, DNA fragmentation and the activated caspases measurements were performed to evaluate apoptotic effects.
  • 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.
  • At the same time, overexpressed ERalpha plus E(2) significantly increases the expression and promoter activity of hTNF-alpha, and the DNA fragmentation effect induced by E(2) plus ERalpha were reduced by the addition of hTNF antibody (0.1 ng(ml).
  • 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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  • (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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79. Clemo NK, Collard TJ, Southern SL, Edwards KD, Moorghen M, Packham G, Hague A, Paraskeva C, Williams AC: BAG-1 is up-regulated in colorectal tumour progression and promotes colorectal tumour cell survival through increased NF-kappaB activity. Carcinogenesis; 2008 Apr;29(4):849-57
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  • [Title] BAG-1 is up-regulated in colorectal tumour progression and promotes colorectal tumour cell survival through increased NF-kappaB activity.
  • Although expression of the anti-apoptotic protein Bcl-2-associated athanogene-1 (BAG-1) has been reported as up-regulated in a number of malignancies, we show for the first time that BAG-1 is over-expressed in medium/large-sized colorectal adenomas and carcinomas compared with normal epithelium.
  • To investigate whether expression of BAG-1 is important for colorectal tumour cell survival, microarray analysis was carried out on the HCT116 colorectal carcinoma cell line following transfection with BAG-1 small interfering RNA (siRNA).
  • Analysis identified altered expression of a subset of potential nuclear factor-kappaB (NF-kappaB)-regulated genes.
  • Inhibition of NF-kappaB activity using BAG-1 siRNA or the NF-kappaB inhibitor BAY-117082 suppressed HCT116 cell yield and induced apoptosis; combined treatment had no additive effect, suggesting that the decrease in cell yield associated with knock down of BAG-1 expression is mediated via inhibition of NF-kappaB.
  • Of clinical relevance, BAG-1 siRNA sensitized colorectal carcinoma cells to apoptosis induced by potential therapeutic agent TRAIL as well as tumour necrosis factor-alpha, both inducers of NF-kappaB activity.
  • It is proposed that, by inhibiting NF-kappaB, suppression of BAG-1 could represent a novel strategy to impede colorectal cancer cell survival and as an adjuvant increase sensitivity to current therapeutic regimes.
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Carcinoma / genetics. Carcinoma / pathology. Cell Line, Tumor. Cell Survival / genetics. Disease Progression. Humans. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Tumor Cells, Cultured

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  • (PMID = 18204076.001).
  • [ISSN] 1460-2180
  • [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 / BCL2-associated athanogene 1 protein; 0 / DNA-Binding Proteins; 0 / NF-kappa B; 0 / RNA, Small Interfering; 0 / Transcription Factors
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80. Law AY, Lai KP, Ip CK, Wong AS, Wagner GF, Wong CK: Epigenetic and HIF-1 regulation of stanniocalcin-2 expression in human cancer cells. Exp Cell Res; 2008 May 1;314(8):1823-30
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  • [Title] Epigenetic and HIF-1 regulation of stanniocalcin-2 expression in human cancer cells.
  • Here we reported that STC2 expression was sporadically abrogated in human cancer cells by transcriptional silencing associated with CpG island promoter hypermethylation.
  • Direct sequencing of bisulfite-modified DNA from a panel of seven human cancer cell lines revealed that CpG dinucleotides in STC2 promoter was methylated in human ovarian epithelial cancer (SKOV3, OVCAR3 and CaOV3), pancreatic cancer (BxP3), colon adenoma (HT29), and leukemia (Jurkat cells).
  • Treatment of these cancer cells with 5-aza-2'-deoxycytidine (5-aza-CdR), an inhibitor of DNA methylation significantly induced STC2 expression.
  • Using SKOV3 cells as a model, the link between DNA demethylation and STC2 expression was consistently demonstrated with hydralazine treatment, which was shown to reduce the protein level of DNA methyltransferase 1 (DNMT1) but stimulated STC2 expression.
  • Two human normal surface ovarian cell-lines (i.e.
  • Hypoxia stimulated STC2 expression in SKOV3 cells was markedly increased in 5-aza-CdR pretreated cells, showing that DNA methylation may hinder the HIF-1 mediated activation.
  • To elucidate this possibility, RNA interference studies confirmed that endogenous HIF-1 alpha was a key factor for STC2 gene activation as well as in the synergistic induction of STC2 expression in 5-aza-CdR pretreated cells.
  • Chromatin immunoprecipitation (ChIP) assay demonstrated the binding of HIF-1 alpha to STC2 promoter.
  • The binding was increased in 5-aza-CdR pretreated cells.
  • Collectively, this is the first report to show that STC2 was aberrantly hypermethylated in human cancer cells.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Gene Silencing. Glycoproteins / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Intercellular Signaling Peptides and Proteins / genetics
  • [MeSH-minor] Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Base Sequence. Cell Hypoxia. Cell Line, Tumor. CpG Islands. DNA Methylation. Humans. Hydralazine / pharmacology. Molecular Sequence Data. Promoter Regions, Genetic. RNA Interference. Transcriptional Activation

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  • (PMID = 18394600.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glycoproteins; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Intercellular Signaling Peptides and Proteins; 0 / STC2 protein, human; 26NAK24LS8 / Hydralazine; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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81. Evans CO, Yao C, Laborde D, Oyesiku NM: Folate receptor expression in pituitary adenomas cellular and molecular analysis. Vitam Horm; 2008;79:235-66
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  • [Title] Folate receptor expression in pituitary adenomas cellular and molecular analysis.
  • Clinically nonfunctional pituitary adenomas cause hypopituitarism or compression of regional structures.
  • Unlike functional tumors, there is no available medical treatment or specific imaging technique for these tumors.
  • We have recently discovered that both folate receptor (FR)alpha mRNA and protein are uniquely overexpressed in nonfunctional pituitary tumors, but not in functional adenomas.
  • Here, we used murine pituitary tumor cell line alphaT3-1 as a model to investigate the biological significance of FRalpha and its mutant FR67.
  • We demonstrate that overexpression of FR facilitated tumor cell growth and anchorage-independent growth in soft agar.
  • More colonies were observed in FR overexpressing cells than in mutant FR67 clones in soft agar.
  • Cell proliferation rate was increased, the percentage of cells in S-phase was increased, and high PCNA staining was detected in cells overexpressing the receptor.
  • In alphaT3-1 cells transfected with mutant FR67, cell proliferation rate was reduced, the percentage of cells residing in S-phase was slightly decreased, and low PCNA staining was observed.
  • By real-time quantitative PCR, the genes involved in NOTCH3 pathway including NOTCH3, HES-1, and TLE2 were altered; the mRNA expression of FGFR1 was upregulated, and ERbeta mRNA was downregulated in FR overexpressing cells.
  • Our findings suggest that FRalpha plays a role in pituitary tumor formation, and this effect may in part be due to its regulation of the NOTCH3 pathway.
  • [MeSH-major] Adenoma / metabolism. Pituitary Neoplasms / metabolism. Receptors, Cell Surface / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Cell Line. Cell Proliferation. Female. Folate Receptor 1. Folic Acid / metabolism. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Male. Mice. Middle Aged. Mutation. Protein Binding. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Notch / metabolism

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  • (PMID = 18804697.001).
  • [ISSN] 0083-6729
  • [Journal-full-title] Vitamins and hormones
  • [ISO-abbreviation] Vitam. Horm.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01-NS5143901
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Folate Receptor 1; 0 / Folr1 protein, mouse; 0 / Notch3 protein, mouse; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / Receptors, Notch; 935E97BOY8 / Folic Acid
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82. Tomita T, Masuzaki H, Noguchi M, Iwakura H, Fujikura J, Tanaka T, Ebihara K, Kawamura J, Komoto I, Kawaguchi Y, Fujimoto K, Doi R, Shimada Y, Hosoda K, Imamura M, Nakao K: GPR40 gene expression in human pancreas and insulinoma. Biochem Biophys Res Commun; 2005 Dec 30;338(4):1788-90
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  • [Title] GPR40 gene expression in human pancreas and insulinoma.
  • To assess gene expression of a membrane-bound G-protein-coupled fatty acid receptor, GPR40, in the human pancreas and islet cell tumors obtained at surgery were analyzed.
  • The mRNA level of the GPR40 gene in isolated pancreatic islets was approximately 20-fold higher than that in the pancreas, and the level was comparable to or rather higher than that of the sulfonylurea receptor 1 gene, which is known to be expressed abundantly in human pancreatic beta cells.
  • A large amount of GPR40 mRNA was detected in tissue extracts from two cases of insulinoma, whereas the expression was undetectable in glucagonoma or gastrinoma.
  • The present study demonstrates that GPR40 mRNA is expressed predominantly in pancreatic islets in humans and that GPR40 mRNA is expressed solely in human insulinoma among islet cell tumors.
  • These results indicate that GPR40 is probably expressed in pancreatic beta cells in the human pancreas.
  • [MeSH-major] Insulinoma / metabolism. Pancreas / metabolism. Pancreatic Neoplasms / metabolism. Receptors, G-Protein-Coupled / biosynthesis

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  • (PMID = 16289108.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FFAR1 protein, human; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled
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83. Freda PU, Chung WK, Matsuoka N, Walsh JE, Kanibir MN, Kleinman G, Wang Y, Bruce JN, Post KD: Analysis of GNAS mutations in 60 growth hormone secreting pituitary tumors: correlation with clinical and pathological characteristics and surgical outcome based on highly sensitive GH and IGF-I criteria for remission. Pituitary; 2007;10(3):275-82
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  • [Title] Analysis of GNAS mutations in 60 growth hormone secreting pituitary tumors: correlation with clinical and pathological characteristics and surgical outcome based on highly sensitive GH and IGF-I criteria for remission.
  • Although the molecular mechanisms underlying GH secreting pituitary tumor formation are not well understood, mutations in the alpha-subunit of the stimulatory G gene, GNAS, have been identified in up to 40%.
  • As these mutations could play a role in tumor growth, we screened 60 GH secreting tumors for GNAS mutations and assessed whether mutation status correlated with their clinical and pathological characteristics.
  • Tumor specimens obtained at surgery were snap frozen.
  • Tumor DNA was extracted, and PCR was used to amplify regions containing 2 sites of recurrent activating somatic mutations in codons 201 and 227 in GNAS.
  • GNAS mutations were present in 24/60 (40%) of tumors; these were arg201cys(n = 15), arg201ser(n = 2), arg201his(n = 2), gln227leu(n = 4), gln227arg(n = 1).
  • Mutation positive tumors were somewhat smaller than negative tumors (p = 0.07).
  • The proportion of tumors >2 cm was somewhat less among positive (8.3%) vs. negative tumors (25%) (p = 0.10).
  • Neither mib proliferation index, the proportion of invasive tumors nor surgical remission rates differed in the groups.
  • GH secreting tumors harboring GNAS mutations had higher preoperative IGF-I levels, somewhat higher preoperative GH levels and tended to be smaller than tumors without mutations.
  • Presence of a GNAS mutation did not predict a difference in a proliferation marker, surgical remission or response to somatostatin analog therapy.
  • [MeSH-major] GTP-Binding Protein alpha Subunits, Gs / genetics. Growth Hormone-Secreting Pituitary Adenoma / genetics. Growth Hormone-Secreting Pituitary Adenoma / pathology. Human Growth Hormone / blood. Insulin-Like Growth Factor I / metabolism. Mutation / physiology. Pituitary Neoplasms / genetics. Pituitary Neoplasms / pathology
  • [MeSH-minor] Acromegaly / etiology. Adult. Aged. Cell Proliferation / drug effects. Chromogranins. Cohort Studies. Female. Humans. Male. Middle Aged. Remission Induction. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Treatment Outcome

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  • (PMID = 17594522.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK 073040; United States / NIDDK NIH HHS / DK / DK02561; United States / NIDDK NIH HHS / DK / DK064720; United States / NCRR NIH HHS / RR / RR-00645; United States / NIDDK NIH HHS / DK / R01 DK064720; United States / NIDDK NIH HHS / DK / K24 DK073040
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromogranins; 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; EC 3.6.1.- / GNAS protein, human; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
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84. Deng J, Fujimoto J, Ye XF, Men TY, Van Pelt CS, Chen YL, Lin XF, Kadara H, Tao Q, Lotan D, Lotan R: Knockout of the tumor suppressor gene Gprc5a in mice leads to NF-kappaB activation in airway epithelium and promotes lung inflammation and tumorigenesis. Cancer Prev Res (Phila); 2010 Apr;3(4):424-37
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  • [Title] Knockout of the tumor suppressor gene Gprc5a in mice leads to NF-kappaB activation in airway epithelium and promotes lung inflammation and tumorigenesis.
  • We explored the role of inflammation in lung tumor development in mice with knockout of the tumor suppressor Gprc5a.
  • Examination of normal lung tissue and tumors from 51 Gprc5a(+/+) (adenoma incidence, 9.8%; adenocarcinoma, 0%) and 38 Gprc5a(-/-) mice (adenoma, 63%; adenocarcinoma, 21%) revealed macrophage infiltration into lungs of 45% of the Gprc5a(-/-) mice and 8% of Gprc5a(+/+) mice and the direct association of macrophages with 42% of adenomas and 88% of adenocarcinomas in the knockout mice.
  • Studies with epithelial cells cultured from tracheas of Gprc5a(-/-) and Gprc5a(+/+) mice revealed that Gprc5a loss is associated with increased cell proliferation, resistance to cell death in suspension, and increased basal, tumor necrosis factor alpha-induced, and lipopolysaccharide-induced NF-kappaB activation, which were reversed partially in Gprc5a(-/-) adenocarcinoma cells by reexpression of Gprc5a.
  • Compared with Gprc5a(+/+) cells, the Gprc5a(-/-) cells produced higher levels of chemokines and cytokines and their conditioned medium induced more extensive macrophage migration.
  • Silencing Gprc5a and the p65 subunit of NF-kappaB in Gprc5a(+/+) and Gprc5a(-/-) cells, respectively, reversed these effects.
  • Thus, Gprc5a loss enhances NF-kappaB activation in lung epithelial cells, leading to increased autocrine and paracrine interactions, cell autonomy, and enhanced inflammation, which may synergize in the creation of a tumor-promoting microenvironment.

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  • [Copyright] (c) 2010 AACR.
  • [CommentIn] Cancer Prev Res (Phila). 2010 Apr;3(4):403-5 [20354166.001]
  • (PMID = 20354164.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P30 CA16672
  • [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 / NF-kappa B; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, G-Protein-Coupled
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85. Kress E, Skah S, Sirakov M, Nadjar J, Gadot N, Scoazec JY, Samarut J, Plateroti M: Cooperation between the thyroid hormone receptor TRalpha1 and the WNT pathway in the induction of intestinal tumorigenesis. Gastroenterology; 2010 May;138(5):1863-74
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  • BACKGROUND & AIMS: Colorectal tumorigenesis is a multistep process involving the alteration of oncogenes and tumor suppressor genes, leading to the deregulation of molecular pathways that govern intestinal homeostasis.
  • More precisely, TRalpha1 directly enhances the transcription of several components of this pathway, allowing increased expression of beta-catenin/Tcf4 target genes and stimulation of cell proliferation.
  • Because the WNT pathway is a major player in controlling intestinal homeostasis, we addressed whether the TRalpha1 receptor has tumor-inducing potential.
  • RESULTS: The intestine of vil-TRalpha1 mice presents aberrant intestinal mucosal architecture and increased cell proliferation and develops adenoma at a low rate.
  • This is the first report describing the tumor-inducing function of TRalpha1 in the intestine.
  • [MeSH-major] Adenoma / metabolism. Cell Transformation, Neoplastic / metabolism. Intestinal Mucosa / metabolism. Intestinal Neoplasms / metabolism. Signal Transduction. Thyroid Hormone Receptors alpha / metabolism. Wnt Proteins / metabolism
  • [MeSH-minor] Animals. Cell Proliferation. Disease Models, Animal. Gene Expression Regulation, Neoplastic. Genes, APC. Genotype. Mice. Mice, Inbred C57BL. Mice, Transgenic. Phenotype. Time Factors. beta Catenin / metabolism

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  • [Copyright] Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20114049.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, mouse; 0 / Thyroid Hormone Receptors alpha; 0 / Wnt Proteins; 0 / beta Catenin
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86. Vanderlan WB, Zhang Z, Abouljoud MS: Duodenal enteroglucagonoma revealed by differential comparison of serum and tissue glucagon reactivity with Siemens' Double Glucagon Antibody and DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon: a case report. J Med Case Rep; 2010;4:178
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  • [Title] Duodenal enteroglucagonoma revealed by differential comparison of serum and tissue glucagon reactivity with Siemens' Double Glucagon Antibody and DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon: a case report.
  • INTRODUCTION: This case report demonstrates that the differential immunohistochemical reactivities of Siemens' Double Antibody Glucagon compared to DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon allow for pathologic distinction of enteral versus pancreatic glucagonoma.
  • He had a low serum glucagon level using Siemens' Double Antibody Glucagon, a clinical syndrome consistent with glucagon hypersecretion.
  • A periampullary mass biopsy proved to be a neuroendocrine tumor, with positive immunohistochemical reactivity to DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon.
  • CONCLUSIONS: Differential comparison of the immunohistochemical reactivities of Siemens' Double Antibody Glucagon and DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon discerns enteroglucagon from pancreatic glucagon.

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  • [ISO-abbreviation] J Med Case Rep
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87. Chen M: Amended final report of the safety assessment of t-Butyl Alcohol as used in cosmetics. Int J Toxicol; 2005;24 Suppl 2:1-20
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  • Subchronic oral dosing with t-BuOH increased the mineralization of the kidney, nephropathy, and urinary bladder transitional cell epithelial hyperplasia in rats; and liver damage, chronic inflammation, hyperplasia of transitional cell epithelium urinary, and proliferative changes including hyperplasia and neoplasia in the thyroid in mice.
  • Male rats exposed to t-BuOH were susceptible to alpha 2mu-globulin nephropathy. t-BuOH (99.9%) was a moderate to severe ocular irritant to rabbits and caused mild to moderate dermal irritation to rabbits.
  • The principal effects from 2 years of exposure to t-BuOH in drinking water (up to 10 mg/ml for rats and 20 mg/ml for mice) were proliferative lesions (hyperplasia, adenoma, and carcinoma) in the kidneys of exposed male rats, and nephropathy in all exposed groups of female rats.
  • In addition, the renal tubule effects found in male rats were likely an effect of alpha 2mu-globulin.

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  • (PMID = 16154913.001).
  • [ISSN] 1091-5818
  • [Journal-full-title] International journal of toxicology
  • [ISO-abbreviation] Int. J. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cosmetics; 0 / Irritants; 0 / Teratogens; MD83SFE959 / tert-Butyl Alcohol
  • [Number-of-references] 110
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88. Mizokami Y, Egashira N, Takekoshi S, Itoh J, Itoh Y, Osamura RY, Matsumae M: Expression of MSX1 in human normal pituitaries and pituitary adenomas. Endocr Pathol; 2008;19(1):54-61
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  • [Title] Expression of MSX1 in human normal pituitaries and pituitary adenomas.
  • Transcription factors play specific roles in the development and differentiation of normal pituitary tissues and pituitary adenoma.
  • The transcription factor, muscle segment homeobox 1 (MSX1), which belongs to the homeobox gene family, binds the promoter region of the glycoprotein hormone alpha-subunit (SU) in TSH-producing cells in the mouse pituitary and regulates alpha-SU expression.
  • In addition, 50 pituitary adenomas were examined using immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) to clarify the role of MSX1 in the development and functional differentiation of pituitary adenoma cells.
  • In the normal pituitary, MSX1 was predominantly expressed in the cytoplasm of GH-producing cells.
  • Furthermore, MSX1 immunoreactivity was observed in the cytoplasm of some alpha-SU-producing cells.
  • It is interesting to note that, in the pituitary adenoma, MSX1 was expressed in the nucleus of GH- and TSH-producing adenomas.
  • RT-PCR using RNA extracted and purified from formalin-fixed paraffin-embedded pituitary adenoma specimens revealed MSX1 mRNA expressed in GH- and TSH-producing adenomas.
  • These results suggest that MSX1 plays a specific role in human pituitary adenoma.
  • [MeSH-major] Adenoma / genetics. MSX1 Transcription Factor / genetics. Pituitary Gland / physiology. Pituitary Neoplasms / genetics
  • [MeSH-minor] Animals. Autopsy. Blotting, Western. Cell Differentiation. DNA Primers. Humans. Immunohistochemistry. Mice. Microscopy, Immunoelectron. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18379900.001).
  • [ISSN] 1559-0097
  • [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 / DNA Primers; 0 / MSX1 Transcription Factor; 0 / MSX1 protein, human; 0 / Msx1 protein, mouse; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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89. Yen TH, Chen Y, Fu JF, Weng CH, Tian YC, Hung CC, Lin JL, Yang CW: Proliferation of myofibroblasts in the stroma of renal oncocytoma. Cell Prolif; 2010 Jun;43(3):287-96
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  • RESULTS: Renal oncocytomas were composed of oncocytes, large cells with granular eosinophilic cytoplasm, arranged mostly in sheets, in tubulocystic or combined pattern.
  • MIB-1 and active caspase 3 indices were low, but higher in tumour than in surrounding non-tumour parenchyma (MIB-1: 0.93 +/- 0.09 versus 0.46 +/- 0.07, P < 0.001 and active caspase 3: 0.76 +/- 0.08 versus 0.41 +/- 0.09, P < 0.001).
  • Wnt/beta-catenin signalling was not implicated in this neoplasm, as there was no loss of E-cadherin membranous localization or expression of intranuclear beta-catenin in the cells.
  • Importantly, alpha-smooth muscle actin (SMA)-immunostaining established the myofibroblastic nature of many of the stromal cells.
  • [MeSH-major] Adenoma, Oxyphilic / pathology. Fibroblasts / pathology. Kidney Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Cell Proliferation. Extracellular Matrix / metabolism. Extracellular Matrix / pathology. Extracellular Matrix Proteins / metabolism. Female. Humans. Male. Middle Aged. Myoblasts / metabolism. Myoblasts / pathology. Neoplasm Invasiveness / pathology. Neoplasm Invasiveness / physiopathology. Stromal Cells / metabolism. Stromal Cells / pathology

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  • (PMID = 20412129.001).
  • [ISSN] 1365-2184
  • [Journal-full-title] Cell proliferation
  • [ISO-abbreviation] Cell Prolif.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Extracellular Matrix Proteins
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90. McGevna L, McFadden D, Ritvo J, Rabinowitz T: Glucagonoma-associated neuropsychiatric and affective symptoms: diagnostic dilemmas raised by paraneoplastic phenomena. Psychosomatics; 2009 Sep-Oct;50(5):548-50
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  • [Title] Glucagonoma-associated neuropsychiatric and affective symptoms: diagnostic dilemmas raised by paraneoplastic phenomena.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis. Paraneoplastic Syndromes / diagnosis
  • [MeSH-minor] Bipolar Disorder / diagnosis. Diagnosis, Differential. Female. Humans. Lupus Erythematosus, Systemic / diagnosis. Middle Aged

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  • (PMID = 19855043.001).
  • [ISSN] 1545-7206
  • [Journal-full-title] Psychosomatics
  • [ISO-abbreviation] Psychosomatics
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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91. 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.
  • In order to elucidate the roles of Wnt signaling in human pituitary adenomas, we examined the expression of Wnt4 and its putative receptor Frizzled6 (Fzd6) by immunohistochemistry in pituitary adenomas and normal pituitaries.
  • Expression of Wnt4 was higher in growth hormone-producing adenomas (GHomas), prolactin-producing adenomas (PRLomas), and thyroid-stimulating hormone-producing adenomas (TSHomas) than in the normal pituitary.
  • Fzd6 was widely expressed in GHomas, PRLomas, TSHomas, and gonadotropin subunit (GnSU)-positive adenomas.
  • In normal pituitary glands, Wnt4 and Fzd6 were colocalized predominantly in follicle-stimulating hormone-, luteinizing hormone-, and alpha-subunits of glycoprotein hormone-positive cells.
  • 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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92. Wang D, Wang H, Brown J, Daikoku T, Ning W, Shi Q, Richmond A, Strieter R, Dey SK, DuBois RN: CXCL1 induced by prostaglandin E2 promotes angiogenesis in colorectal cancer. J Exp Med; 2006 Apr 17;203(4):941-51
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  • Proinflammatory mediators such as prostaglandin E2 (PGE2) promote colorectal tumor growth by stimulating angiogenesis, cell invasion, and cell growth, and inhibiting apoptosis.
  • Molecules that regulate tumor-associated angiogenesis provide promising therapeutic targets for treatment of colorectal cancer (CRC) as indicated by the recent development of the novel anti-angiogenic agent bevacizumab (Avastin).
  • However, use of this drug only prolongs survival by several months, highlighting the importance of finding more effective treatment regimens.
  • We report here that PGE2 induces expression of CXCL1 (growth-regulated oncogene alpha), a pro-angiogenic chemokine, in human CRC cells.
  • More importantly, CXCL1 released from carcinoma cells induces microvascular endothelial cell migration and tube formation in vitro.
  • Furthermore, PGE2 promotes tumor growth in vivo by induction of CXCL1 expression, which results in increased tumor microvessel formation.